Nowotwór kręgosłupa – Patofizjologia i mechanizm

Nowotwór kręgosłupa
Patofizjologia i mechanizm

Nowotwory kręgosłupa, zarówno pierwotne, jak i przerzutowe, charakteryzują się złożoną patofizjologią obejmującą mechanizmy molekularne i genetyczne. Przerzuty stanowią około 97% przypadków i najczęściej pochodzą z raka piersi, prostaty czy płuc, rozprzestrzeniając się głównie przez splot żylny Batsona, układ tętniczy lub limfatyczny. Komórki nowotworowe osadzają się w szpiku kostnym kręgów, gdzie poprzez produkcję cytokin (m.in. IL-1, IL-6, IL-8, IL-11, PTHrP, TGF-β, VEGF) stymulują aktywność osteoklastów i osteoblastów, prowadząc do zmian osteolitycznych, osteoblastycznych lub mieszanych. Przykładowo, przerzuty raka piersi indukują głównie osteolizę poprzez PTHrP i RANKL, natomiast przerzuty raka prostaty wywołują osteoblastyczne zmiany za pośrednictwem endoteliny 1 (ET-1) i szlaku WNT. Pierwotne nowotwory kręgosłupa, choć rzadsze, wykazują specyficzne mutacje genetyczne (np. fuzje ZFTA, MYCN) oraz są powiązane z chorobami genetycznymi takimi jak NF1, NF2 i zespół von Hippel-Lindau. Ucisk rdzenia kręgowego (SCC) przez guz prowadzi do demielinizacji, uszkodzenia aksonów oraz zaburzeń naczyniowych, co może skutkować trwałymi deficytami neurologicznymi, jeśli nie zostanie szybko podjęte leczenie.

Patogeneza nowotworów kręgosłupa

Mechanizmy przerzutowania do kręgosłupa
Mechanizmy molekularne w patogenezie nowotworów kręgosłupa
Mechanizm uszkodzenia kości w nowotworach kręgosłupa
Mechanizm powstawania pierwotnych nowotworów kręgosłupa

Mechanizmy uszkodzenia rdzenia kręgowego w nowotworach kręgosłupa

Mechanizmy uszkodzenia bezpośredniego i naczyniowego
Rola lokalizacji nowotworów w uszkodzeniu neurologicznym

Rola uwarunkowań genetycznych w rozwoju nowotworów kręgosłupa

Uwarunkowania genetyczne pierwotnych nowotworów kręgosłupa
Zespoły genetyczne związane z nowotworami kręgosłupa

Znaczenie patogenezy nowotworów kręgosłupa w diagnostyce i leczeniu

Implikacje dla diagnostyki
Implikacje dla leczenia
Implikacje dla leczenia chirurgicznego
Kolejne rozdziały

Patogeneza nowotworów kręgosłupa

Nowotwór kręgosłupa to nieprawidłowy rozrost komórek, który występuje w kościach kręgosłupa, kanale kręgowym lub rdzeniu kręgowym. Nowotwory te mogą być łagodne (niezłośliwe) lub złośliwe. Większość złośliwych nowotworów kręgosłupa powstaje w wyniku rozprzestrzeniania się raka z innych części ciała, co określa się mianem przerzutów¹². Około 97% nowotworów kręgosłupa ma charakter przerzutowy, co jest związane z bogatym unaczynieniem kręgosłupa oraz jego bliskim sąsiedztwem z dużymi układami żylnymi i limfatycznymi³⁴.

Mechanizmy przerzutowania do kręgosłupa

Rozprzestrzenianie się komórek nowotworowych do kręgosłupa może następować kilkoma drogami⁵⁶:

Przez układ żylny Batsona – główny mechanizm przerzutów do kręgosłupa
Przez układ tętniczy – rozprzestrzenianie drogą krwionośną
Przez układ limfatyczny
Przez ciągłość tkanek – bezpośrednie naciekanie z okolicznych struktur

⁵⁷

Teoria „ziarna i gleby” (seed-soil theory) potwierdzona przez Harta i Fidlera w 1984 roku wyjaśnia, że potencjalnie przerzutowe komórki z dowolnego guza mogą dotrzeć do kręgosłupa przez układ krążenia, ale rozwój przerzutu następuje tylko wtedy, gdy komórka nowotworowa ma szczególne powinowactwo do kości, a kość może zapewnić sprzyjające środowisko dla wzrostu komórek nowotworowych⁸.

Badania eksperymentalne wykazały, że komórki nowotworowe osadzają się i rosną w szpiku kostnym kręgów. Następnie komórki nowotworowe znajdujące się w jamie szpiku kręgów naciekają do kanału kręgowego przez otwory żył kręgowych, a nie przez niszczenie kości korowej⁹. Linie komórek nowotworowych, które rosną w sposób naciekający, migrują w kierunku tylnej lokalizacji w kanale kręgowym i uciskają rdzeń kręgowy od strony tylnej. Z kolei linie komórek nowotworowych, które rosną jako zwarte guzy, tworzą masę guza w tym samym miejscu, z którego komórki wyłaniają się z kręgu, i uciskają rdzeń głównie od strony przedniej¹⁰.

Mechanizmy molekularne w patogenezie nowotworów kręgosłupa

Rozwój przerzutów do kości jest procesem wieloetapowym. Najpierw komórki nowotworowe odłączają się od swojego pierwotnego miejsca poprzez utratę ekspresji E-kadheryny, cząsteczki adhezyjnej powierzchni komórki, co obserwuje się w rakach piersi, prostaty, jelita grubego i trzustki¹¹.

Po inwazji komórek nowotworowych do kości, produkują one czynniki wzrostu, które bezpośrednio stymulują aktywność osteoklastów i/lub osteoblastów, powodując przebudowę kości i dalsze uwalnianie czynników wzrostu, co prowadzi do błędnego koła niszczenia kości i wzrostu lokalnego guza¹².

Komórki nowotworowe produkują szereg cytokin i czynników wzrostu, takich jak¹³:

Interleukiny (IL-1, IL-6, IL-8, IL-11)
Prostaglandyna E2 (PgE2)
Transformujący czynnik wzrostu (TGF, TGF-β)
Nabłonkowy czynnik wzrostu (EGF)
Naczyniowo-śródbłonkowy czynnik wzrostu (VEGF)
Czynnik martwicy nowotworu (TNF)
Czynnik stymulujący kolonie (CSF-1, GM-CSF, M-CSF)

¹³¹⁴

Czynniki te mogą bezpośrednio lub pośrednio stymulować aktywność osteoklastyczną, a następnie resorpcję kości¹⁵. PTHrP (białko podobne do parathormonu) produkowane przez komórki raka piersi odgrywa kluczową rolę w resorpcji kości, stymulując aktywność osteoklastyczną¹⁶¹⁷.

Mechanizm uszkodzenia kości w nowotworach kręgosłupa

Przerzuty zaburzają szlak transdukcji sygnału OPG-RANKL-RANK. Równowaga interakcji między OPG, RANK i RANKL determinuje charakter zmiany i jej odpowiedni wygląd radiograficzny, a mianowicie osteolityczny, osteoblastyczny lub mieszany¹⁸.

Mechanizm osteolityczny (niszczenie kości):

Osteolityczne zmiany kostne są powodowane aktywacją osteoklastów indukowaną przez guza
Proces ten zachodzi poprzez szlak RANK, RANK ligand (RANKL), osteoprotegeryna
Komórki raka piersi pozytywne dla PTHrP aktywują produkcję RANKL przez osteoblasty
Komórki onkogenne uwalniają cytokiny TNF-alfa, IL-6, IL-11, PTHrP, TGF-beta
PTHrP i TGF-beta aktywują osteoblasty
Osteoblasty wydzielają RANKL, który wiąże się z RANK na osteoklastach i aktywuje osteoklasty

¹⁹²⁰

Zmiany osteolityczne są powodowane stymulacją aktywności osteoklastycznej z towarzyszącym zmniejszeniem aktywności osteoblastycznej, a nie bezpośrednim wpływem komórek nowotworowych na kość²¹.

Mechanizm osteoblastyczny (tworzenie kości):

Charakterystyczny szczególnie dla przerzutów raka prostaty
Komórki raka prostaty wydzielają endotelinę 1 (ET-1)
ET-1 wiąże się z receptorem endoteliny A (ETAR) na osteoblastach i stymuluje osteoblasty
ET-1 zmniejsza supresor WNT DKK-1
Aktywuje szlak WNT, zwiększając aktywność osteoblastów

²²²³

Czynniki wzrostu takie jak TFG, PDGF, BMPs, IGFs, FGFs i u-PA (który stymuluje uwalnianie TGF) zostały wyizolowane w komórkach raka prostaty i stymulują różnicowanie osteoblastyczne oraz odgrywają rolę we wzroście i przeżyciu samych komórek nowotworowych²⁴. Wykazano, że poziom endoteliny 1 jest podwyższony w przerzutach do kości raka prostaty w porównaniu z guzami bez przerzutów²⁵.

Mechanizm powstawania pierwotnych nowotworów kręgosłupa

Pierwotne nowotwory kręgosłupa, które zaczynają się w kręgosłupie i nie rozprzestrzeniły się z innego miejsca, są rzadkie²⁶. Nowotwory te powstają, gdy komórki w kościach kręgosłupa rozwijają zmiany w swoim DNA²⁷²⁸.

DNA komórki zawiera instrukcje, które mówią komórce, co ma robić. W zdrowych komórkach DNA daje instrukcje, aby rosnąć i namnażać się w ustalonym tempie. Instrukcje nakazują komórkom umierać w określonym czasie. W komórkach nowotworowych zmiany DNA dają inne instrukcje. Zmiany nakazują komórkom nowotworowym wytwarzanie znacznie większej liczby komórek w szybkim tempie. Komórki nowotworowe mogą nadal żyć, gdy zdrowe komórki obumierałyby. Powoduje to nadmiar komórek, które tworzą guz mogący uciskać okoliczne nerwy²⁹³⁰.

Czasami komórki rozwijają zmiany w DNA, które przekształcają je w komórki nowotworowe. Komórki nowotworowe mogą naciąć i zniszczyć zdrową tkankę organizmu. Mogą one oderwać się i rozprzestrzenić do innych części ciała³¹.

Przyczyny pierwotnych nowotworów kręgosłupa nie są do końca jasne. Wiadomo jednak, że nowotwory kręgosłupa występują częściej u osób z pewnymi chorobami genetycznymi, w tym z nerwiakowłókniakowatością typu 1 (NF1), nerwiakowłókniakowatością typu 2 (NF2) i chorobą von Hippel-Lindau (VHL)³²³³.

Mechanizmy uszkodzenia rdzenia kręgowego w nowotworach kręgosłupa

Nowotwory kręgosłupa powodują uszkodzenia neurologiczne poprzez naciekanie lub ucisk tkanek nerwowych rdzenia kręgowego lub nerwów rdzeniowych. Obrzęk wokół guza może zwiększać ucisk³⁴. Zarówno inwazja, jak i ucisk rdzenia mogą prowadzić do klinicznej prezentacji urazu rdzenia kręgowego³⁵.

Mechanizmy uszkodzenia bezpośredniego i naczyniowego

Ucisk rdzenia kręgowego (SCC – Spinal Cord Compression) uszkadza rdzeń kręgowy na dwa główne sposoby³⁶:

Bezpośredni ucisk – powoduje demielinizację i uszkodzenie aksonów
Ucisk naczyniowy – powoduje zaburzenia krążenia krwi

³⁶

Jeśli bezpośredni ucisk rdzenia trwa krótko, jego skutki są odwracalne i możliwe jest wyzdrowienie. Jednakże dłuższy okres ucisku toruje drogę do wtórnego uszkodzenia naczyniowego³⁷.

Zaburzenia naczyniowe powodują uszkodzenie bariery krew-rdzeń kręgowy, prowadząc do obrzęku naczyniopochodnego i zawału rdzenia kręgowego³⁸. Ostry ucisk rdzenia kręgowego, niezależnie od przyczyny, może prowadzić do obrzęku i zmniejszonego przepływu krwi, potencjalnie skutkując trwałymi deficytami neurologicznymi, jeśli nie zostanie szybko rozwiązany³⁹.

Dodatkowo, procesy zapalne, zmieniona perfuzja krwi i stres oksydacyjny przyczyniają się do dynamicznego charakteru urazów rdzenia kręgowego, co wymaga szybkiej interwencji w celu złagodzenia progresji⁴⁰.

Oprócz efektu masy, guz zewnątrzoponowy może powodować zniekształcenie rdzenia, powodujące demielinizację lub zniszczenie aksonalne. Zakłócenie naczyniowe prowadzi do przekrwienia żylnego i obrzęku naczyniopochodnego rdzenia kręgowego, powodując zawał żylny i krwotok⁴¹.

Rola lokalizacji nowotworów w uszkodzeniu neurologicznym

Lokalne zniszczenie kręgosłupa może prowadzić do bólu w wyniku niestabilności kręgosłupa. Podobnie guzy mogą powiększać się poza kręgosłup i uciskać elementy nerwowe. Uszkodzenie elementów nerwowych może objawiać się bólem, zmienionymi odczuciami, osłabieniem mięśni, spastycznością lub innymi zaburzeniami neurologicznymi⁴².

Guzy przerzutowe mogą przemieszczać się do kręgosłupa przez splot żylny zewnątrzoponowy, rosnąć w przestrzeni zewnątrzoponowej i powodować objawy neurologiczne⁴³. Guzy pierwotne elementów nerwowych mogą być przenoszone przez płyn mózgowo-rdzeniowy i powodować podobny ucisk elementów nerwowych z wnętrza worka oponowego⁴⁴.

Większość zmian zlokalizowana jest w przedniej części trzonu kręgu (60%). W 30% przypadków zmiana nacieka nasadę lub blaszkę. U niewielu pacjentów choroba występuje zarówno w tylnej, jak i przedniej części kręgosłupa⁴⁵.

Rola uwarunkowań genetycznych w rozwoju nowotworów kręgosłupa

Zmiany genetyczne w komórkach nowotworów wewnątrztwardówkowych kręgosłupa mogą mieć znaczący wpływ na opcje leczenia, poradnictwo i prognozę dla pacjentów⁴⁶. Niedawne badania pomogły określić konkretne różnice genetyczne i molekularne między nowotworami wewnątrztwardówkowymi kręgosłupa a ich odpowiednikami wewnątrzczaszkowymi oraz zidentyfikowały znaczne zróżnicowanie efektów terapeutycznych na te guzy⁴⁷.

Uwarunkowania genetyczne pierwotnych nowotworów kręgosłupa

Zmiany genetyczne dostarczają informacji o patofizjologicznym pochodzeniu guza i mogą również służyć jako markery do oceny wyników klinicznych⁴⁸. Zmienność zmian genetycznych może również informować o klasyfikacji guzów i identyfikować komórki pochodzenia różnych typów guzów, co wykazano w przypadku rdzeniaków⁴⁹.

Najnowsza klasyfikacja WHO z 2021 roku doprecyzowała patologię molekularną wyściółczaków. Guzy znane wcześniej jako wyściółczaki ST-RELA są obecnie nazywane wyściółczakami ST-ZFTA, a dodano nową klasyfikację rzadkiego, ale agresywnego guza kręgosłupa: wyściółczaka SP-MYCN⁵⁰.

Fuzja RELA prowadzi do niekontrolowanej aktywacji specyficznego szlaku komórkowego guza zwanego szlakiem NF-kB. NF-kB przyczynia się do powstawania guza i jego niekontrolowanego wzrostu⁵¹.

Naukowcy zaczynają identyfikować charakterystyczne zmiany w guzach dołu tylnego, a specyficzne profile epigenetyczne i ekspresji genów zostały zidentyfikowane jako potencjalne markery do rozdzielenia wyściółczaków dołu tylnego na odrębne grupy kliniczne⁵².

Zespoły genetyczne związane z nowotworami kręgosłupa

Istnieje wiele czynników genetycznych związanych z guzami wewnątrztwardówkowymi, najczęściej⁵³:

Nerwiakowłókniakowatość typu 1 (NF1)
Nerwiakowłókniakowatość typu 2 (NF2)
Zespół von Hippel-Lindau (VHL)

⁵³⁵⁴

Osoby z określonymi dziedzicznymi chorobami genetycznymi, takimi jak nerwiakowłókniakowatość typu 2 lub choroba Von Hipple-Lindau (stan, który wpływa na sposób, w jaki komórki rosną, dzielą się i umierają), mają wyższe ryzyko rozwoju guzów rdzenia kręgowego⁵⁵.

Badacze uważają, że w większości przypadków podczas normalnego rozwoju czegoś brakuje. W szczególności komórki w rdzeniu kręgowym rosną i dzielą się w miarę rozwoju organizmu. Podczas tego procesu podziału komórkowego komórki muszą replikować swój materiał genetyczny. Podczas tego procesu mogą wystąpić błędy, prowadzące do mutacji, które mogą pozwolić komórkom rozwinąć się w guzy. Te błędy generalnie występują losowo i nie można im zapobiec⁵⁶.

Znaczenie patogenezy nowotworów kręgosłupa w diagnostyce i leczeniu

Zrozumienie patofizjologii nowotworów kręgosłupa ma kluczowe znaczenie dla wczesnej diagnostyki, oceny zaangażowania struktur nerwowych oraz planowania leczenia⁵⁷.

Implikacje dla diagnostyki

Radiologiczne dowody przerzutów do kręgosłupa są późnym zdarzeniem i zwykle związane ze znacznym uciskiem rdzenia i guzem pozakostnym⁵⁸. Dlatego kluczowe jest wczesne rozpoznanie objawów klinicznych i szybkie wdrożenie badań obrazowych.

Rezonans magnetyczny (MRI) jest metodą obrazowania z wyboru do diagnostyki ucisku rdzenia kręgowego, z czułością 93% i swoistością 97%⁵⁹. Za pomocą zaawansowanych technologii, lekarz może zidentyfikować, czy guz jest łagodny czy złośliwy i wybrać zindywidualizowane leczenie dla każdego pacjenta⁶⁰.

Dla radiologów wartościowe jest zrozumienie patofizjologii przerzutów do kręgosłupa i ocena zajęcia struktury nerwowej oraz utraty stabilności kręgosłupa związanej z patofizjologią⁶¹.

Implikacje dla leczenia

Znajomość mechanizmów molekularnych zaangażowanych w patogenezę pomaga badaczom opracować nowe cząsteczki docelowe, które mogą pomóc zmniejszyć obciążenie guzem⁶².

Najnowszy rozwój ukierunkowanego inhibitora to inhibitor PD-1 niwolumab do leczenia pacjentów z czerniakiem⁶³. Chociaż poprawa wiedzy na temat molekularnych mechanizmów działania guzów prawdopodobnie nie zakwestionuje prymatu leczenia chirurgicznego w najbliższej przyszłości, lepsze zrozumienie genetyki guzów może prowadzić do lepszego leczenia nowotworów wewnątrztwardówkowych kręgosłupa⁶⁴.

Te specyficzne różnice w genetycznym składzie sugerują potencjalnie inną patogenezę, która wymaga rozważenia określonych modalności leczenia⁶⁵. Zastosowanie aktualnej wiedzy uzyskanej z badań guzów czaszki będzie odgrywać ważną rolę w leczeniu guzów rdzenia kręgowego, pomimo różnic genetycznych między guzami kręgosłupa a ich odpowiednikami wewnątrzczaszkowymi⁶⁶.

Dalsze wyjaśnienie cech genetycznych tych guzów pomoże w przyszłym projektowaniu opcji leczenia i podejmowaniu decyzji klinicznych⁶⁷.

Implikacje dla leczenia chirurgicznego

Koncepcja stabilności kręgosłupa opiera się na anatomicznej i funkcjonalnej złożoności struktury kręgosłupa⁶⁸. Prezentacja kliniczna niestabilności kręgosłupa jest niuansowana, gdy jest spowodowana przez nowotwór, z których każdy postępuje z własnym zestawem zaangażowania kostnego i więzadłowego, objawów neurologicznych, jakości kości i perspektyw skutecznej naprawy⁶⁹.

Ryzyko złamania kompresyjnego również wzrasta wraz z wielkością guza⁷⁰. Historycznie operacja w postaci prostej tylnej laminektomii (usunięcia grzbietowych elementów kręgosłupa) bez instrumentacji była wykonywana w celu odbarczenia rdzenia kręgowego⁷¹. Jednak kilka badań wykazało, że sama laminektomia lub w połączeniu z radioterapią nie dawała żadnej przewagi⁷².

W rzeczywistości laminektomia nie jest najlepszą opcją u wielu pacjentów z przerzutowym SCC, których przerzuty do kręgosłupa naciekają trzon kręgu od przodu⁷³. Rozwinięto więc inną technikę chirurgiczną polegającą na dostępie przednim w celu usunięcia guza z natychmiastowym tylnym odbarczeniem poprzez laminektomię, a następnie instrumentację kręgosłupa w celu odnowienia stabilności⁷⁴.

Obecnie rola chirurgii jest dobrze ugruntowana u pacjentów z przerzutową chorobą kręgosłupa z deficytem neurologicznym lub SCC wysokiego stopnia bez deficytów⁷⁵. W takich przypadkach operacja jest wskazana niezależnie od wyniku SINS⁷⁶.

Nie można kwestionować pilności chirurgicznego leczenia SCC⁷⁷. Czynnikami ryzyka przewidującymi utratę chodzenia po chirurgicznym odbarczeniu były przedoperacyjna utrata chodzenia, nawracający lub przetrwały guz po radioterapii w miejscu operacji, procedura inna niż korpektomia kręgowa oraz guz pierwotny inny niż rak piersi⁷⁸. Dodatkowo wykazano, że operacja w ciągu 48 godzin od wystąpienia deficytów ruchowych zapewnia lepsze wyniki w zakresie chodzenia⁷⁹.

Rodzaj nowotworu	Mechanizm rozwoju	Charakter zmian kostnych	Główne czynniki molekularne
Przerzuty raka piersi	Rozrost komórek w szpiku kostnym, inwazja do kanału kręgowego	Głównie osteolityczne	PTHrP, RANKL, IL-6, IL-8, TNF-α
Przerzuty raka prostaty	Rozprzestrzenianie przez splot Batsona	Głównie osteoblastyczne	Endotelina 1 (ET-1), TGF, PDGF, BMPs
Przerzuty raka płuc	Rozprzestrzenianie drogą krwionośną	Często osteolityczne	RANKL, IL-6, różne cytokiny prozapalne
Pierwotne nowotwory kręgosłupa	Mutacje w DNA komórek kręgosłupa	Zależnie od typu guza	Mutacje specyficzne dla typu guza (np. ZFTA, MYCN)
Chłoniaki	Często bezpośrednie naciekanie	Mieszane	Specyficzne dla typu chłoniaka

Podsumowując, zrozumienie patogenezy nowotworów kręgosłupa ma kluczowe znaczenie dla ich wczesnego wykrywania, właściwej diagnostyki i skutecznego leczenia. Złożoność mechanizmów molekularnych biorących udział w rozwoju i progresji tych nowotworów stwarza wyzwania, ale jednocześnie otwiera nowe możliwości terapeutyczne. Badania genetyczne i molekularne mogą w przyszłości pomóc w opracowaniu bardziej spersonalizowanych i skutecznych metod leczenia dla pacjentów z nowotworami kręgosłupa⁸⁰.

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

Materiały źródłowe

#1 Vertebral tumor – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/vertebral-tumor/symptoms-causes/syc-20350123
A vertebral tumor is a growth of cells that happens in the bones of the spine. A vertebral tumor also is called a spinal tumor. […] Vertebral tumors can be cancerous or not cancerous. A noncancerous vertebral tumor also is called a benign vertebral tumor. Vertebral tumors that are cancerous are called malignant vertebral tumors. […] Most malignant vertebral tumors are caused by cancer that starts somewhere else in the body and spreads to the spine. Cancer that spreads from an organ to another part of the body is called metastatic cancer. Cancers that affect the blood cells and bone marrow also can cause malignant vertebral tumors. […] Vertebral tumors that start in the bones of the spine and haven’t spread from somewhere else are rare. Another name for these tumors is primary bone tumors.
#2 Spinal Tumors: Practice Essentials, Anatomy, Pathophysiology
https://emedicine.medscape.com/article/1267223-overview
In general, tumors (neoplasms) are considered to be either primary or metastatic. Primary tumors arise from the tissue itself for example, a chordoma is a tumor formed from tissues of the spinal column. In contrast, metastatic tumors form in other tissues and either directly invade nearby structures or travel distantly through the body via the blood stream or lymphatic drainage. The spine is highly vascularized, with many slow-flowing channels, and is in intimate proximity with large venous and lymphatic systems; these characteristics make the spine a fertile location for metastatic disease. Approximately 97% of the tumors found in the spine are metastatic. […] Local destruction of the bony spinal column can lead to pain as a consequence of instability of the spine. Similarly, tumors may expand out of the bony spine and impinge on the neural elements. Injury to the neural elements can present as pain, altered sensation, muscular weakness, spasticity, or other neurologic derangements. Metastatic tumors can travel to the spine via the epidural venous plexus, growing in the epidural space and causing neurologic symptoms. Primary tumors of the neural elements may be transmitted through the cerebrospinal fluid and cause similar compression of the neural elements from within the thecal sac itself.
#3 Spinal Tumors: Practice Essentials, Anatomy, Pathophysiology
https://emedicine.medscape.com/article/1267223-overview
In general, tumors (neoplasms) are considered to be either primary or metastatic. Primary tumors arise from the tissue itself for example, a chordoma is a tumor formed from tissues of the spinal column. In contrast, metastatic tumors form in other tissues and either directly invade nearby structures or travel distantly through the body via the blood stream or lymphatic drainage. The spine is highly vascularized, with many slow-flowing channels, and is in intimate proximity with large venous and lymphatic systems; these characteristics make the spine a fertile location for metastatic disease. Approximately 97% of the tumors found in the spine are metastatic. […] Local destruction of the bony spinal column can lead to pain as a consequence of instability of the spine. Similarly, tumors may expand out of the bony spine and impinge on the neural elements. Injury to the neural elements can present as pain, altered sensation, muscular weakness, spasticity, or other neurologic derangements. Metastatic tumors can travel to the spine via the epidural venous plexus, growing in the epidural space and causing neurologic symptoms. Primary tumors of the neural elements may be transmitted through the cerebrospinal fluid and cause similar compression of the neural elements from within the thecal sac itself.
#4 Spinal Tumors Radiation Therapy – Innovative Cancer Institute
https://www.innovativecancer.com/spinal-tumors/
About 90% of all spine tumors (cord + vertebral) are metastatic resulting from the spread of cancer cells from the initial tumor to another part of the body. […] The mechanism of metastatic spread of malignant tumors to the region is variable and includes: […] Breast cancer, lung cancer and melanoma are common sources of spine metastases. Renal tumors, prostate cancer, multiple myeloma and lymphoma are other primaries that can metastasize to the spine. It is estimated that every year over 200,000 patients will develop vertebral metastasis, of which 10% can have epidural spinal extension with cord compression. This progression of the cancer is considered an emergency and if left untreated can rapidly progress to paralysis. […] Spinal radiosurgery provides greater dosage of radiation to a lesion compared to conventional radiotherapy. This translates into a high-rate of tumor control and faster pain-relief for the patients. […] Spinal and paraspinal metastases are common complications of advanced cancer. The incidence of spinal metastasis is increasing because patients are living longer due to recent advances in systemic therapy.
#5 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
The diffusion through Batson venous system is the principal process of spinal metastasis, but the dissemination is possible also through arterial and lymphatic system or by contiguity. […] Once cancer cells have invaded the bone, they produce growth factors that stimulate osteoblastic or osteolytic activity resulting in bone remodeling with release of other growth factors that lead to a vicious cycle of bone destruction and growth of local tumour. […] The osteolytic lesions are caused by stimulation of osteoclastic activity accompanied by reduced osteoblastic activity not by direct effects of tumour cells on the bone. […] Once cancer cells have invaded the bone, they produce growth factors that directly stimulate osteoclastic activity and/or osteoblastic activity resulting in bone remodelling and further release of growth factors that lead to a vicious cycle of bone destruction and growth of local tumour.
#6 Comprehensive Insights into Metastasis-Associated Spinal Cord Compression: Pathophysiology, Diagnosis, Treatment, and Prognosis: A State-of-the-Art Systematic Review
https://www.mdpi.com/2077-0383/13/12/3590
Metastatic cancer cells can spread to the spinal cord through arteries, more specifically retrograde through the Batson plexus, or by direct invasion through the intervertebral foramina, like in non-Hodgkinâs lymphoma where there is direct tumour extension. […] Acute spinal cord compression, regardless of cause, can lead to oedema and diminished blood perfusion, potentially resulting in permanent neurological deficits if not promptly addressed. […] The intricate nature of spinal cord involvement necessitates a comprehensive understanding of the underlying pathophysiology, optimal diagnostic approaches, and multidisciplinary treatment strategies. Prompt diagnosis and treatment are essential to preventing irreversible neurological deficits and improving patientsâ quality of life.
#7 Spinal Metastasis: Background, Pathophysiology, Prognosis
https://emedicine.medscape.com/article/1157987-overview
Spread from primary tumors is mainly by the arterial route. Retrograde spread through the Batson plexus during Valsalva maneuver is postulated. Direct invasion through the intervertebral foramina can also occur. Besides the mass effect, an epidural mass can cause cord distortion, resulting in demyelination or axonal destruction. Vascular compromise produces venous congestion and vasogenic edema of the spinal cord, resulting in venous infarction and hemorrhage. […] Intramural and intramedullary metastases are not as common as those of the vertebral body and the epidural space. Isolated epidural involvement accounts for less than 10% of cases; it is particularly common in lymphoma and renal cell carcinoma. Most of the lesions are localized at the anterior portion of the vertebral body (60%). In 30% of cases, the lesion infiltrates the pedicle or lamina. A few patients have disease in both posterior and anterior parts of the spine.
#8
https://journals.lww.com/isoj/fulltext/2022/05020/epidemiology,_pathogenesis,_clinical_presentation,.3.aspx
Spinal metastasis has become a major public health problem worldwide and seriously affects patients quality of life. […] In 1984, Hart and Fidler disproved Ewings theory and conclusively proved the seed-soil theory of metastasis. Thus, the fact is that potentially metastatic cells from any tumor can reach the spine via the circulatory system, but the development of metastasis occurs only if the tumor cell has a special affinity for bone and in turn if the bone can provide a conducive environment for the tumor cells to grow. […] Development of bony metastasis is a multistep process. First, the cancer cells disengage from their primary site by loss of expression of E-cadherin, a cell-surface adhesion molecule, as seen in breast, prostate, colorectal, and pancreatic carcinomas. […] The growth factor and cytokines released by the tumor cells activate both osteoclasts and osteoblasts.
#9 Pathogenesis of vertebral metastasis and epidural spinal cord compression – PubMed
https://pubmed.ncbi.nlm.nih.gov/2293874/
The authors have studied the sequential events in the process of vertebral metastasis that result in spinal cord compression. […] Different tumor cell lines were injected into the systemic arterial circulation of syngeneic or nude mice, and they were killed at timed intervals after injection or when they became paraplegic. […] The tumor cells lodged and grew in the hematopoietic bone marrow of the vertebrae. […] Cancer cells in the vertebral marrow cavity invaded into the spinal canal through the foramina of the vertebral veins rather than destroying the cortical bone. […] Tumor cell lines that grew in an infiltrative fashion migrated toward a posterior location in the spinal canal, and compressed the spinal cord from a posterior direction. […] Tumor cell lines that grew as compact tumors formed a tumor mass at the same location from which the cells emerged from the vertebra, and compressed the cord predominantly from an anterior direction.
#10 Pathogenesis of vertebral metastasis and epidural spinal cord compression – PubMed
https://pubmed.ncbi.nlm.nih.gov/2293874/
The authors have studied the sequential events in the process of vertebral metastasis that result in spinal cord compression. […] Different tumor cell lines were injected into the systemic arterial circulation of syngeneic or nude mice, and they were killed at timed intervals after injection or when they became paraplegic. […] The tumor cells lodged and grew in the hematopoietic bone marrow of the vertebrae. […] Cancer cells in the vertebral marrow cavity invaded into the spinal canal through the foramina of the vertebral veins rather than destroying the cortical bone. […] Tumor cell lines that grew in an infiltrative fashion migrated toward a posterior location in the spinal canal, and compressed the spinal cord from a posterior direction. […] Tumor cell lines that grew as compact tumors formed a tumor mass at the same location from which the cells emerged from the vertebra, and compressed the cord predominantly from an anterior direction.
#11
https://journals.lww.com/isoj/fulltext/2022/05020/epidemiology,_pathogenesis,_clinical_presentation,.3.aspx
Spinal metastasis has become a major public health problem worldwide and seriously affects patients quality of life. […] In 1984, Hart and Fidler disproved Ewings theory and conclusively proved the seed-soil theory of metastasis. Thus, the fact is that potentially metastatic cells from any tumor can reach the spine via the circulatory system, but the development of metastasis occurs only if the tumor cell has a special affinity for bone and in turn if the bone can provide a conducive environment for the tumor cells to grow. […] Development of bony metastasis is a multistep process. First, the cancer cells disengage from their primary site by loss of expression of E-cadherin, a cell-surface adhesion molecule, as seen in breast, prostate, colorectal, and pancreatic carcinomas. […] The growth factor and cytokines released by the tumor cells activate both osteoclasts and osteoblasts.
#12 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
The diffusion through Batson venous system is the principal process of spinal metastasis, but the dissemination is possible also through arterial and lymphatic system or by contiguity. […] Once cancer cells have invaded the bone, they produce growth factors that stimulate osteoblastic or osteolytic activity resulting in bone remodeling with release of other growth factors that lead to a vicious cycle of bone destruction and growth of local tumour. […] The osteolytic lesions are caused by stimulation of osteoclastic activity accompanied by reduced osteoblastic activity not by direct effects of tumour cells on the bone. […] Once cancer cells have invaded the bone, they produce growth factors that directly stimulate osteoclastic activity and/or osteoblastic activity resulting in bone remodelling and further release of growth factors that lead to a vicious cycle of bone destruction and growth of local tumour.
#13 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
Tumour cells produce IL-1-6-8-11, PgE2, TGF, TGF, EGF, VEGF, TNF, CSF-1, GM-CSF, and M-CSF, which can directly or indirectly stimulate osteoclastic activity and then bone resorption. […] PTHrP produced by breast cancer cells plays a key role in bone resorption stimulating osteoclastic activity. […] The bone damage consequently obtained facilitates the growth factors release causing tumour cells proliferation, as TGF, IGFs, FGFs, PDGF, BMPs, which stimulates PTHrP production and then osteolysis. […] So a vicious circle is present: osteolysis and growth factors release stimulate tumour cells proliferation and then metastatic cells growth. […] Bone blastic metastasis is usually present in prostate cancer. […] Growth factors as TFG, PDGF, BMPs, IGFs, FGFs, and l’u-PA (which stimulates TGF release) have been isolated in prostate cancer cells and stimulate osteoblastic differentiation and they have a role in growing and survival tumour cells itself. […] It has been demonstrated that endothelin 1 level is elevated in bone metastatic prostate tumours than in nonmetastatic ones.
#14
https://www.orthobullets.com/pathology/2009/metastatic-disease-of-spine
Metastatic disease to the spine the the most common location for metastases to bone that can lead to significant morbidity. This condition typically occurs in older cancer patients and presents with axial night pain and/or neurologic deficits. […] Diagnosis is typically made with MRI with contrast which shows a soft tissue mass with possible cord compression or vertebral fractures. […] Mechanism of bone destruction (osteolysis) […] osteolytic bone lesions are caused by tumor-induced activation of osteoclasts […] occurs through the RANK, RANK ligand (RANKL), osteoprotegerin pathway. […] PTHrP positive breast cancer cells activate osteoblastic RANKL production. […] Mechanism of bone lysis […] oncogenic cell releases cytokines TNF-alpha, IL-6, IL-11, PTHrP, TGF-beta. […] PTHrP and TGF-beta activate osteoblasts.
#15 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
Tumour cells produce IL-1-6-8-11, PgE2, TGF, TGF, EGF, VEGF, TNF, CSF-1, GM-CSF, and M-CSF, which can directly or indirectly stimulate osteoclastic activity and then bone resorption. […] PTHrP produced by breast cancer cells plays a key role in bone resorption stimulating osteoclastic activity. […] The bone damage consequently obtained facilitates the growth factors release causing tumour cells proliferation, as TGF, IGFs, FGFs, PDGF, BMPs, which stimulates PTHrP production and then osteolysis. […] So a vicious circle is present: osteolysis and growth factors release stimulate tumour cells proliferation and then metastatic cells growth. […] Bone blastic metastasis is usually present in prostate cancer. […] Growth factors as TFG, PDGF, BMPs, IGFs, FGFs, and l’u-PA (which stimulates TGF release) have been isolated in prostate cancer cells and stimulate osteoblastic differentiation and they have a role in growing and survival tumour cells itself. […] It has been demonstrated that endothelin 1 level is elevated in bone metastatic prostate tumours than in nonmetastatic ones.
#16 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
Tumour cells produce IL-1-6-8-11, PgE2, TGF, TGF, EGF, VEGF, TNF, CSF-1, GM-CSF, and M-CSF, which can directly or indirectly stimulate osteoclastic activity and then bone resorption. […] PTHrP produced by breast cancer cells plays a key role in bone resorption stimulating osteoclastic activity. […] The bone damage consequently obtained facilitates the growth factors release causing tumour cells proliferation, as TGF, IGFs, FGFs, PDGF, BMPs, which stimulates PTHrP production and then osteolysis. […] So a vicious circle is present: osteolysis and growth factors release stimulate tumour cells proliferation and then metastatic cells growth. […] Bone blastic metastasis is usually present in prostate cancer. […] Growth factors as TFG, PDGF, BMPs, IGFs, FGFs, and l’u-PA (which stimulates TGF release) have been isolated in prostate cancer cells and stimulate osteoblastic differentiation and they have a role in growing and survival tumour cells itself. […] It has been demonstrated that endothelin 1 level is elevated in bone metastatic prostate tumours than in nonmetastatic ones.
#17
https://journals.lww.com/isoj/fulltext/2022/05020/epidemiology,_pathogenesis,_clinical_presentation,.3.aspx
Metastases disrupt the OPG-RANKL-RANK signal transduction pathway. The balance of the interaction between OPG, RANK, and RANKL determines the nature of the lesion and its corresponding radiographic appearance, namely, osteolytic, osteoblastic, or mixed. […] Bone metastases from breast cancer are predominantly osteolytic. […] Metastatic breast cancer cells produce factors like parathyroid hormone-related peptide (PTHrP) that shares molecular similarities with parathyroid hormone (PTH) and has the same effect on osteoclasts as PTH, which is stimulation of osteoclastogenesis via RANKL. […] The presence of tumor cells in spine results in a disruption of the homeostasis between bone formation and remodeling, thereby producing osteoblastic, osteolytic, and mixed lesions. […] Understanding the molecular mechanisms involved in pathogenesis helps researchers develop new target molecules that can help reduce the tumor burden.
#18
https://journals.lww.com/isoj/fulltext/2022/05020/epidemiology,_pathogenesis,_clinical_presentation,.3.aspx
Metastases disrupt the OPG-RANKL-RANK signal transduction pathway. The balance of the interaction between OPG, RANK, and RANKL determines the nature of the lesion and its corresponding radiographic appearance, namely, osteolytic, osteoblastic, or mixed. […] Bone metastases from breast cancer are predominantly osteolytic. […] Metastatic breast cancer cells produce factors like parathyroid hormone-related peptide (PTHrP) that shares molecular similarities with parathyroid hormone (PTH) and has the same effect on osteoclasts as PTH, which is stimulation of osteoclastogenesis via RANKL. […] The presence of tumor cells in spine results in a disruption of the homeostasis between bone formation and remodeling, thereby producing osteoblastic, osteolytic, and mixed lesions. […] Understanding the molecular mechanisms involved in pathogenesis helps researchers develop new target molecules that can help reduce the tumor burden.
#19
https://www.orthobullets.com/pathology/2009/metastatic-disease-of-spine
Metastatic disease to the spine the the most common location for metastases to bone that can lead to significant morbidity. This condition typically occurs in older cancer patients and presents with axial night pain and/or neurologic deficits. […] Diagnosis is typically made with MRI with contrast which shows a soft tissue mass with possible cord compression or vertebral fractures. […] Mechanism of bone destruction (osteolysis) […] osteolytic bone lesions are caused by tumor-induced activation of osteoclasts […] occurs through the RANK, RANK ligand (RANKL), osteoprotegerin pathway. […] PTHrP positive breast cancer cells activate osteoblastic RANKL production. […] Mechanism of bone lysis […] oncogenic cell releases cytokines TNF-alpha, IL-6, IL-11, PTHrP, TGF-beta. […] PTHrP and TGF-beta activate osteoblasts.
#20
https://www.orthobullets.com/pathology/2009/metastatic-disease-of-spine
osteoblasts secrete RANKL, that binds to RANK on osteoclasts and activates osteoclasts. […] Mechanism of bone sclerosis (prostate and breast mets) […] prostate cancer cells secrete endothelin 1 (ET-1). […] ET-1 binds to endothelin A receptor (ETAR) on osteoblasts and stimulates osteoblasts. […] ET-1 decreases WNT suppressor DKK-1 […] activates WNT pathway, increasing osteoblast activity. […] breast cancers can produce sclerosis which represses osteoblasts.
#21 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
The diffusion through Batson venous system is the principal process of spinal metastasis, but the dissemination is possible also through arterial and lymphatic system or by contiguity. […] Once cancer cells have invaded the bone, they produce growth factors that stimulate osteoblastic or osteolytic activity resulting in bone remodeling with release of other growth factors that lead to a vicious cycle of bone destruction and growth of local tumour. […] The osteolytic lesions are caused by stimulation of osteoclastic activity accompanied by reduced osteoblastic activity not by direct effects of tumour cells on the bone. […] Once cancer cells have invaded the bone, they produce growth factors that directly stimulate osteoclastic activity and/or osteoblastic activity resulting in bone remodelling and further release of growth factors that lead to a vicious cycle of bone destruction and growth of local tumour.
#22
https://www.orthobullets.com/pathology/2009/metastatic-disease-of-spine
osteoblasts secrete RANKL, that binds to RANK on osteoclasts and activates osteoclasts. […] Mechanism of bone sclerosis (prostate and breast mets) […] prostate cancer cells secrete endothelin 1 (ET-1). […] ET-1 binds to endothelin A receptor (ETAR) on osteoblasts and stimulates osteoblasts. […] ET-1 decreases WNT suppressor DKK-1 […] activates WNT pathway, increasing osteoblast activity. […] breast cancers can produce sclerosis which represses osteoblasts.
#23 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
Tumour cells produce IL-1-6-8-11, PgE2, TGF, TGF, EGF, VEGF, TNF, CSF-1, GM-CSF, and M-CSF, which can directly or indirectly stimulate osteoclastic activity and then bone resorption. […] PTHrP produced by breast cancer cells plays a key role in bone resorption stimulating osteoclastic activity. […] The bone damage consequently obtained facilitates the growth factors release causing tumour cells proliferation, as TGF, IGFs, FGFs, PDGF, BMPs, which stimulates PTHrP production and then osteolysis. […] So a vicious circle is present: osteolysis and growth factors release stimulate tumour cells proliferation and then metastatic cells growth. […] Bone blastic metastasis is usually present in prostate cancer. […] Growth factors as TFG, PDGF, BMPs, IGFs, FGFs, and l’u-PA (which stimulates TGF release) have been isolated in prostate cancer cells and stimulate osteoblastic differentiation and they have a role in growing and survival tumour cells itself. […] It has been demonstrated that endothelin 1 level is elevated in bone metastatic prostate tumours than in nonmetastatic ones.
#24 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
Tumour cells produce IL-1-6-8-11, PgE2, TGF, TGF, EGF, VEGF, TNF, CSF-1, GM-CSF, and M-CSF, which can directly or indirectly stimulate osteoclastic activity and then bone resorption. […] PTHrP produced by breast cancer cells plays a key role in bone resorption stimulating osteoclastic activity. […] The bone damage consequently obtained facilitates the growth factors release causing tumour cells proliferation, as TGF, IGFs, FGFs, PDGF, BMPs, which stimulates PTHrP production and then osteolysis. […] So a vicious circle is present: osteolysis and growth factors release stimulate tumour cells proliferation and then metastatic cells growth. […] Bone blastic metastasis is usually present in prostate cancer. […] Growth factors as TFG, PDGF, BMPs, IGFs, FGFs, and l’u-PA (which stimulates TGF release) have been isolated in prostate cancer cells and stimulate osteoblastic differentiation and they have a role in growing and survival tumour cells itself. […] It has been demonstrated that endothelin 1 level is elevated in bone metastatic prostate tumours than in nonmetastatic ones.
#25 Physiopathology of Spine Metastasis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3265280/
Tumour cells produce IL-1-6-8-11, PgE2, TGF, TGF, EGF, VEGF, TNF, CSF-1, GM-CSF, and M-CSF, which can directly or indirectly stimulate osteoclastic activity and then bone resorption. […] PTHrP produced by breast cancer cells plays a key role in bone resorption stimulating osteoclastic activity. […] The bone damage consequently obtained facilitates the growth factors release causing tumour cells proliferation, as TGF, IGFs, FGFs, PDGF, BMPs, which stimulates PTHrP production and then osteolysis. […] So a vicious circle is present: osteolysis and growth factors release stimulate tumour cells proliferation and then metastatic cells growth. […] Bone blastic metastasis is usually present in prostate cancer. […] Growth factors as TFG, PDGF, BMPs, IGFs, FGFs, and l’u-PA (which stimulates TGF release) have been isolated in prostate cancer cells and stimulate osteoblastic differentiation and they have a role in growing and survival tumour cells itself. […] It has been demonstrated that endothelin 1 level is elevated in bone metastatic prostate tumours than in nonmetastatic ones.
#26 Vertebral tumor – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/vertebral-tumor/symptoms-causes/syc-20350123
A vertebral tumor is a growth of cells that happens in the bones of the spine. A vertebral tumor also is called a spinal tumor. […] Vertebral tumors can be cancerous or not cancerous. A noncancerous vertebral tumor also is called a benign vertebral tumor. Vertebral tumors that are cancerous are called malignant vertebral tumors. […] Most malignant vertebral tumors are caused by cancer that starts somewhere else in the body and spreads to the spine. Cancer that spreads from an organ to another part of the body is called metastatic cancer. Cancers that affect the blood cells and bone marrow also can cause malignant vertebral tumors. […] Vertebral tumors that start in the bones of the spine and haven’t spread from somewhere else are rare. Another name for these tumors is primary bone tumors.
#27 Vertebral tumor – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/vertebral-tumor/symptoms-causes/syc-20350123
Most vertebral tumors are caused by cancer that starts somewhere else in the body. Cancer that spreads from an organ to somewhere else in the body is called metastatic cancer. Any cancer can spread to the spine. Most vertebral tumors are caused by cancer that spreads from the breasts, lungs or prostate. Other cancers that tend to spread to the spine include kidney cancer and thyroid cancer. […] Vertebral tumors that start in the spine happen when cells in the bones of the spine develop changes in their DNA. A cell’s DNA holds the instructions that tell the cell what to do. In healthy cells, the DNA gives instructions to grow and multiply at a set rate. The instructions tell the cells to die at a set time. In the tumor cells, the DNA changes give different instructions. The changes tell the tumor cells to make many more cells quickly. Tumor cells can keep living when healthy cells would die. This causes too many cells. […] Sometimes cells develop changes in their DNA that turn them into cancer cells. Cancer cells can invade and destroy healthy body tissue. They can break away and spread to other parts of the body. […] Vertebral tumors that start in the spine are rare. It’s not clear what causes them.
#28 Spinal cord tumor – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/spinal-cord-tumor/symptoms-causes/syc-20350103
A spinal cord tumor starts when cells in the spinal cord or in the tissue around it develop changes in their DNA. […] A cell’s DNA holds the instructions that tell the cell what to do. In healthy cells, the DNA tells the cells to grow and multiply at a set rate. The DNA also tells the cells to die at a set time. […] In tumor cells, the DNA changes give different instructions. The changes tell the tumor cells to grow and multiply quickly. Tumor cells can keep living when healthy cells would die. This causes too many cells. The tumor cells form a growth that can press on the nearby nerves. […] Sometimes the cells develop DNA changes that turn them into cancer cells. Cancer cells can invade and destroy healthy body tissue.
#29 Vertebral tumor – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/vertebral-tumor/symptoms-causes/syc-20350123
Most vertebral tumors are caused by cancer that starts somewhere else in the body. Cancer that spreads from an organ to somewhere else in the body is called metastatic cancer. Any cancer can spread to the spine. Most vertebral tumors are caused by cancer that spreads from the breasts, lungs or prostate. Other cancers that tend to spread to the spine include kidney cancer and thyroid cancer. […] Vertebral tumors that start in the spine happen when cells in the bones of the spine develop changes in their DNA. A cell’s DNA holds the instructions that tell the cell what to do. In healthy cells, the DNA gives instructions to grow and multiply at a set rate. The instructions tell the cells to die at a set time. In the tumor cells, the DNA changes give different instructions. The changes tell the tumor cells to make many more cells quickly. Tumor cells can keep living when healthy cells would die. This causes too many cells. […] Sometimes cells develop changes in their DNA that turn them into cancer cells. Cancer cells can invade and destroy healthy body tissue. They can break away and spread to other parts of the body. […] Vertebral tumors that start in the spine are rare. It’s not clear what causes them.
#30 Spinal cord tumor – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/spinal-cord-tumor/symptoms-causes/syc-20350103
A spinal cord tumor starts when cells in the spinal cord or in the tissue around it develop changes in their DNA. […] A cell’s DNA holds the instructions that tell the cell what to do. In healthy cells, the DNA tells the cells to grow and multiply at a set rate. The DNA also tells the cells to die at a set time. […] In tumor cells, the DNA changes give different instructions. The changes tell the tumor cells to grow and multiply quickly. Tumor cells can keep living when healthy cells would die. This causes too many cells. The tumor cells form a growth that can press on the nearby nerves. […] Sometimes the cells develop DNA changes that turn them into cancer cells. Cancer cells can invade and destroy healthy body tissue.
#31 Vertebral tumor – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/vertebral-tumor/symptoms-causes/syc-20350123
Most vertebral tumors are caused by cancer that starts somewhere else in the body. Cancer that spreads from an organ to somewhere else in the body is called metastatic cancer. Any cancer can spread to the spine. Most vertebral tumors are caused by cancer that spreads from the breasts, lungs or prostate. Other cancers that tend to spread to the spine include kidney cancer and thyroid cancer. […] Vertebral tumors that start in the spine happen when cells in the bones of the spine develop changes in their DNA. A cell’s DNA holds the instructions that tell the cell what to do. In healthy cells, the DNA gives instructions to grow and multiply at a set rate. The instructions tell the cells to die at a set time. In the tumor cells, the DNA changes give different instructions. The changes tell the tumor cells to make many more cells quickly. Tumor cells can keep living when healthy cells would die. This causes too many cells. […] Sometimes cells develop changes in their DNA that turn them into cancer cells. Cancer cells can invade and destroy healthy body tissue. They can break away and spread to other parts of the body. […] Vertebral tumors that start in the spine are rare. It’s not clear what causes them.
#32 Spinal Tumors > Fact Sheets > Yale Medicine
https://www.yalemedicine.org/conditions/spinal-tumors
Tumors, both benign (noncancerous) and malignant (cancerous), can develop in or around the spinal cord or the spinal column. […] The tumors compression of the spinal cord and nerves can also cause muscle weakness, numbness, and, in some cases, paralysis. […] Researchers do not yet know what causes primary spinal tumors. It is known, however, that spinal tumors occur more frequently in people who have certain genetic conditions, including neurofibromatosis type 1 (NF1), neurofibromatosis type 2 (NF2), and von Hippel-Lindau (VHL) disease. […] Most spinal tumors are metastatic tumors, meaning they originated from cancer elsewhere in the body. Several types of cancer are known to spread to the spine including lung, breast, and prostate cancers, as well as blood cancers such as lymphoma and myeloma.
#33 Spinal tumor – Wikipedia
https://en.wikipedia.org/wiki/Spinal_tumor
The cause of spinal tumors is unknown. Most extradural tumors are metastatic commonly from breast, prostate, lung, and kidney cancer. […] There are many genetic factors associated with intradural tumors, most commonly neurofibromatosis 1 (NF1), neurofibromatosis 2 (NF2), and Von-Hippel Lindau (VHL) syndrome. […] Most symptoms from spinal tumors occur due to compression of the spinal cord as it plays a primary role in motor and sensory function. […] It is important to diagnose and promptly treat metastatic tumors as they can lead to long-term neurologic deficit from epidural spinal cord compression. […] Primary extradural tumors are rare and most arise from surrounding bony and soft tissue structures, including Ewing’s sarcoma, osteosarcoma, and vertebral hemangioblastomas.
#34 Spinal Tumors | PM&R KnowledgeNow
https://now.aapmr.org/spinal-tumors/
All malignant and most benign tumors are the result of abnormal, excessive tissue growth following damages to genes. […] Spinal tumors cause neurologic injury by invading or compressing nerve tissues of the spinal cord or spinal nerves. Edema around the tumor can increase compression. Both invasion and compression of the cord can result in clinical presentation of a spinal cord injury. […] Cancer stem cells and their roles in chemoresistance, radiation resistance, and metastasis have aroused significant scientific interests in novel therapies targeting these cells. […] There are many proposed modalities for neurorehabilitation. These include partial or full body-weight-supported treadmill, functional electrical stimulation, and other complementary modalities, such as acupuncture. However, no clear scientific studies have been conducted to show definitive effects of these treatments for recovery from spinal tumors. […] Further studies are needed to determine the efficacy and safety of various minimally invasive surgical techniques, radiosurgery, and optimal dosage of radiation therapy in the primary treatment of both primary and secondary spinal tumors.
#35 Spinal Tumors | PM&R KnowledgeNow
https://now.aapmr.org/spinal-tumors/
All malignant and most benign tumors are the result of abnormal, excessive tissue growth following damages to genes. […] Spinal tumors cause neurologic injury by invading or compressing nerve tissues of the spinal cord or spinal nerves. Edema around the tumor can increase compression. Both invasion and compression of the cord can result in clinical presentation of a spinal cord injury. […] Cancer stem cells and their roles in chemoresistance, radiation resistance, and metastasis have aroused significant scientific interests in novel therapies targeting these cells. […] There are many proposed modalities for neurorehabilitation. These include partial or full body-weight-supported treadmill, functional electrical stimulation, and other complementary modalities, such as acupuncture. However, no clear scientific studies have been conducted to show definitive effects of these treatments for recovery from spinal tumors. […] Further studies are needed to determine the efficacy and safety of various minimally invasive surgical techniques, radiosurgery, and optimal dosage of radiation therapy in the primary treatment of both primary and secondary spinal tumors.
#36 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The clinical onset of SCC can be gradual or acute. […] SCC injures the spinal cord either directly through demyelination and axonal damage, or by vascular compression. […] If direct cord compression is of short duration, the effects are reversible and recovery is possible. […] However, a longer period of compression paves the way for secondary vascular injury. […] Vascular compromise causes breakdown in the blood-spinal cord barrier leading to vasogenic edema and spinal cord infarction. […] About 2.55% of patients with terminal cancer have SCC within the last 2 years of their illness. […] Incidence of SCC varies with age and primary disease histology. […] Any systemic cancer can metastasize to the spinal column, but prostate, breast, and lung cancers are those most commonly associated with SCC.
#37 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The clinical onset of SCC can be gradual or acute. […] SCC injures the spinal cord either directly through demyelination and axonal damage, or by vascular compression. […] If direct cord compression is of short duration, the effects are reversible and recovery is possible. […] However, a longer period of compression paves the way for secondary vascular injury. […] Vascular compromise causes breakdown in the blood-spinal cord barrier leading to vasogenic edema and spinal cord infarction. […] About 2.55% of patients with terminal cancer have SCC within the last 2 years of their illness. […] Incidence of SCC varies with age and primary disease histology. […] Any systemic cancer can metastasize to the spinal column, but prostate, breast, and lung cancers are those most commonly associated with SCC.
#38 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The clinical onset of SCC can be gradual or acute. […] SCC injures the spinal cord either directly through demyelination and axonal damage, or by vascular compression. […] If direct cord compression is of short duration, the effects are reversible and recovery is possible. […] However, a longer period of compression paves the way for secondary vascular injury. […] Vascular compromise causes breakdown in the blood-spinal cord barrier leading to vasogenic edema and spinal cord infarction. […] About 2.55% of patients with terminal cancer have SCC within the last 2 years of their illness. […] Incidence of SCC varies with age and primary disease histology. […] Any systemic cancer can metastasize to the spinal column, but prostate, breast, and lung cancers are those most commonly associated with SCC.
#39 Comprehensive Insights into Metastasis-Associated Spinal Cord Compression: Pathophysiology, Diagnosis, Treatment, and Prognosis: A State-of-the-Art Systematic Review
https://www.mdpi.com/2077-0383/13/12/3590
Metastatic cancer cells can spread to the spinal cord through arteries, more specifically retrograde through the Batson plexus, or by direct invasion through the intervertebral foramina, like in non-Hodgkinâs lymphoma where there is direct tumour extension. […] Acute spinal cord compression, regardless of cause, can lead to oedema and diminished blood perfusion, potentially resulting in permanent neurological deficits if not promptly addressed. […] The intricate nature of spinal cord involvement necessitates a comprehensive understanding of the underlying pathophysiology, optimal diagnostic approaches, and multidisciplinary treatment strategies. Prompt diagnosis and treatment are essential to preventing irreversible neurological deficits and improving patientsâ quality of life.
#40 Comprehensive Insights into Metastasis-Associated Spinal Cord Compression: Pathophysiology, Diagnosis, Treatment, and Prognosis: A State-of-the-Art Systematic Review
https://www.mdpi.com/2077-0383/13/12/3590
The pathophysiology of spinal cord metastases involves multifaceted mechanisms, including hematogenous dissemination, direct invasion, and retrograde spread through Batson’s plexus. Tumour cells infiltrate the vertebral column, leading to compression of neural structures, disruption of blood flow, and neurologic dysfunction. Additionally, inflammatory processes, altered blood perfusion, and oxidative stress contribute to the dynamic nature of spinal cord injuries, necessitating prompt intervention to mitigate progression. […] Spinal cord metastatic lesions affect 5% to 10% of the oncology patients in the USA. Approximately 15% of all central nervous system lesions involve the spinal cord, with an incidence rate of 0.5â2.5 cases per 100,000 population. Morbidity and mortality are influenced by the degree and level of spinal cord impairment.
#41 Spinal Metastasis: Background, Pathophysiology, Prognosis
https://emedicine.medscape.com/article/1157987-overview
Spread from primary tumors is mainly by the arterial route. Retrograde spread through the Batson plexus during Valsalva maneuver is postulated. Direct invasion through the intervertebral foramina can also occur. Besides the mass effect, an epidural mass can cause cord distortion, resulting in demyelination or axonal destruction. Vascular compromise produces venous congestion and vasogenic edema of the spinal cord, resulting in venous infarction and hemorrhage. […] Intramural and intramedullary metastases are not as common as those of the vertebral body and the epidural space. Isolated epidural involvement accounts for less than 10% of cases; it is particularly common in lymphoma and renal cell carcinoma. Most of the lesions are localized at the anterior portion of the vertebral body (60%). In 30% of cases, the lesion infiltrates the pedicle or lamina. A few patients have disease in both posterior and anterior parts of the spine.
#42 Spinal Tumors: Practice Essentials, Anatomy, Pathophysiology
https://emedicine.medscape.com/article/1267223-overview
In general, tumors (neoplasms) are considered to be either primary or metastatic. Primary tumors arise from the tissue itself for example, a chordoma is a tumor formed from tissues of the spinal column. In contrast, metastatic tumors form in other tissues and either directly invade nearby structures or travel distantly through the body via the blood stream or lymphatic drainage. The spine is highly vascularized, with many slow-flowing channels, and is in intimate proximity with large venous and lymphatic systems; these characteristics make the spine a fertile location for metastatic disease. Approximately 97% of the tumors found in the spine are metastatic. […] Local destruction of the bony spinal column can lead to pain as a consequence of instability of the spine. Similarly, tumors may expand out of the bony spine and impinge on the neural elements. Injury to the neural elements can present as pain, altered sensation, muscular weakness, spasticity, or other neurologic derangements. Metastatic tumors can travel to the spine via the epidural venous plexus, growing in the epidural space and causing neurologic symptoms. Primary tumors of the neural elements may be transmitted through the cerebrospinal fluid and cause similar compression of the neural elements from within the thecal sac itself.
#43 Spinal Tumors: Practice Essentials, Anatomy, Pathophysiology
https://emedicine.medscape.com/article/1267223-overview
In general, tumors (neoplasms) are considered to be either primary or metastatic. Primary tumors arise from the tissue itself for example, a chordoma is a tumor formed from tissues of the spinal column. In contrast, metastatic tumors form in other tissues and either directly invade nearby structures or travel distantly through the body via the blood stream or lymphatic drainage. The spine is highly vascularized, with many slow-flowing channels, and is in intimate proximity with large venous and lymphatic systems; these characteristics make the spine a fertile location for metastatic disease. Approximately 97% of the tumors found in the spine are metastatic. […] Local destruction of the bony spinal column can lead to pain as a consequence of instability of the spine. Similarly, tumors may expand out of the bony spine and impinge on the neural elements. Injury to the neural elements can present as pain, altered sensation, muscular weakness, spasticity, or other neurologic derangements. Metastatic tumors can travel to the spine via the epidural venous plexus, growing in the epidural space and causing neurologic symptoms. Primary tumors of the neural elements may be transmitted through the cerebrospinal fluid and cause similar compression of the neural elements from within the thecal sac itself.
#44 Spinal Tumors: Practice Essentials, Anatomy, Pathophysiology
https://emedicine.medscape.com/article/1267223-overview
In general, tumors (neoplasms) are considered to be either primary or metastatic. Primary tumors arise from the tissue itself for example, a chordoma is a tumor formed from tissues of the spinal column. In contrast, metastatic tumors form in other tissues and either directly invade nearby structures or travel distantly through the body via the blood stream or lymphatic drainage. The spine is highly vascularized, with many slow-flowing channels, and is in intimate proximity with large venous and lymphatic systems; these characteristics make the spine a fertile location for metastatic disease. Approximately 97% of the tumors found in the spine are metastatic. […] Local destruction of the bony spinal column can lead to pain as a consequence of instability of the spine. Similarly, tumors may expand out of the bony spine and impinge on the neural elements. Injury to the neural elements can present as pain, altered sensation, muscular weakness, spasticity, or other neurologic derangements. Metastatic tumors can travel to the spine via the epidural venous plexus, growing in the epidural space and causing neurologic symptoms. Primary tumors of the neural elements may be transmitted through the cerebrospinal fluid and cause similar compression of the neural elements from within the thecal sac itself.
#45 Spinal Metastasis: Background, Pathophysiology, Prognosis
https://emedicine.medscape.com/article/1157987-overview
Spread from primary tumors is mainly by the arterial route. Retrograde spread through the Batson plexus during Valsalva maneuver is postulated. Direct invasion through the intervertebral foramina can also occur. Besides the mass effect, an epidural mass can cause cord distortion, resulting in demyelination or axonal destruction. Vascular compromise produces venous congestion and vasogenic edema of the spinal cord, resulting in venous infarction and hemorrhage. […] Intramural and intramedullary metastases are not as common as those of the vertebral body and the epidural space. Isolated epidural involvement accounts for less than 10% of cases; it is particularly common in lymphoma and renal cell carcinoma. Most of the lesions are localized at the anterior portion of the vertebral body (60%). In 30% of cases, the lesion infiltrates the pedicle or lamina. A few patients have disease in both posterior and anterior parts of the spine.
#46 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
Genetic alterations in the cells of intradural spinal tumors can have a significant impact on the treatment options, counseling, and prognosis for patients. […] Recent studies have helped delineate specific genetic and molecular differences between intradural spinal tumors and their intracranial counterparts and have also identified significant variation in therapeutic effects on these tumors. […] Importantly, the impact of this knowledge on therapeutic options and its application to clinical practice are discussed. […] Genetic alterations provide information about a tumors pathophysiological origin and may also serve as markers for evaluating clinical outcomes. […] Variation in genetic alterations may also inform tumor classification and identify cells of origin for different tumor types, as has been shown for medulloblastoma.
#47 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
Genetic alterations in the cells of intradural spinal tumors can have a significant impact on the treatment options, counseling, and prognosis for patients. […] Recent studies have helped delineate specific genetic and molecular differences between intradural spinal tumors and their intracranial counterparts and have also identified significant variation in therapeutic effects on these tumors. […] Importantly, the impact of this knowledge on therapeutic options and its application to clinical practice are discussed. […] Genetic alterations provide information about a tumors pathophysiological origin and may also serve as markers for evaluating clinical outcomes. […] Variation in genetic alterations may also inform tumor classification and identify cells of origin for different tumor types, as has been shown for medulloblastoma.
#48 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
Genetic alterations in the cells of intradural spinal tumors can have a significant impact on the treatment options, counseling, and prognosis for patients. […] Recent studies have helped delineate specific genetic and molecular differences between intradural spinal tumors and their intracranial counterparts and have also identified significant variation in therapeutic effects on these tumors. […] Importantly, the impact of this knowledge on therapeutic options and its application to clinical practice are discussed. […] Genetic alterations provide information about a tumors pathophysiological origin and may also serve as markers for evaluating clinical outcomes. […] Variation in genetic alterations may also inform tumor classification and identify cells of origin for different tumor types, as has been shown for medulloblastoma.
#49 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
Genetic alterations in the cells of intradural spinal tumors can have a significant impact on the treatment options, counseling, and prognosis for patients. […] Recent studies have helped delineate specific genetic and molecular differences between intradural spinal tumors and their intracranial counterparts and have also identified significant variation in therapeutic effects on these tumors. […] Importantly, the impact of this knowledge on therapeutic options and its application to clinical practice are discussed. […] Genetic alterations provide information about a tumors pathophysiological origin and may also serve as markers for evaluating clinical outcomes. […] Variation in genetic alterations may also inform tumor classification and identify cells of origin for different tumor types, as has been shown for medulloblastoma.
#50 Pathology | CERN Foundation
https://www.cern-foundation.org/education/diagnosis/pathology
Recently, underlying genetic changes have revealed that ependymoma tumor subtypes may be different based on location. There are three locations thought to be important: those that are supratentorial, infratentorial in the posterior fossa, and those located in the spine. […] This fusion, RELA, results in the uncontrolled activation of a specific tumor cell molecular pathway called the NF-kB pathway. NF-kB contributes to the formation of the tumor and its uncontrolled growth. […] The 2021 WHO classification further refined ependymoma molecular pathology. Tumors previously known as ST-RELA ependymoma are now called ST-ZFTA ependymoma and a new classification has been added for of a rare but aggressive spinal tumor: SP-MYCN ependymoma. […] Scientists are beginning to identify characteristic changes in posterior fossa tumors, and specific epigenetic and gene expression profiles have been identified as potential markers to separate posterior fossa ependymomas into clinically distinct groups.
#51 Pathology | CERN Foundation
https://www.cern-foundation.org/education/diagnosis/pathology
Recently, underlying genetic changes have revealed that ependymoma tumor subtypes may be different based on location. There are three locations thought to be important: those that are supratentorial, infratentorial in the posterior fossa, and those located in the spine. […] This fusion, RELA, results in the uncontrolled activation of a specific tumor cell molecular pathway called the NF-kB pathway. NF-kB contributes to the formation of the tumor and its uncontrolled growth. […] The 2021 WHO classification further refined ependymoma molecular pathology. Tumors previously known as ST-RELA ependymoma are now called ST-ZFTA ependymoma and a new classification has been added for of a rare but aggressive spinal tumor: SP-MYCN ependymoma. […] Scientists are beginning to identify characteristic changes in posterior fossa tumors, and specific epigenetic and gene expression profiles have been identified as potential markers to separate posterior fossa ependymomas into clinically distinct groups.
#52 Pathology | CERN Foundation
https://www.cern-foundation.org/education/diagnosis/pathology
Recently, underlying genetic changes have revealed that ependymoma tumor subtypes may be different based on location. There are three locations thought to be important: those that are supratentorial, infratentorial in the posterior fossa, and those located in the spine. […] This fusion, RELA, results in the uncontrolled activation of a specific tumor cell molecular pathway called the NF-kB pathway. NF-kB contributes to the formation of the tumor and its uncontrolled growth. […] The 2021 WHO classification further refined ependymoma molecular pathology. Tumors previously known as ST-RELA ependymoma are now called ST-ZFTA ependymoma and a new classification has been added for of a rare but aggressive spinal tumor: SP-MYCN ependymoma. […] Scientists are beginning to identify characteristic changes in posterior fossa tumors, and specific epigenetic and gene expression profiles have been identified as potential markers to separate posterior fossa ependymomas into clinically distinct groups.
#53 Spinal tumor – Wikipedia
https://en.wikipedia.org/wiki/Spinal_tumor
The cause of spinal tumors is unknown. Most extradural tumors are metastatic commonly from breast, prostate, lung, and kidney cancer. […] There are many genetic factors associated with intradural tumors, most commonly neurofibromatosis 1 (NF1), neurofibromatosis 2 (NF2), and Von-Hippel Lindau (VHL) syndrome. […] Most symptoms from spinal tumors occur due to compression of the spinal cord as it plays a primary role in motor and sensory function. […] It is important to diagnose and promptly treat metastatic tumors as they can lead to long-term neurologic deficit from epidural spinal cord compression. […] Primary extradural tumors are rare and most arise from surrounding bony and soft tissue structures, including Ewing’s sarcoma, osteosarcoma, and vertebral hemangioblastomas.
#54 Spinal Cord Tumor | Nationwide Children’s Hospital
https://www.nationwidechildrens.org/conditions/spinal-cord-tumor
People with certain inherited genetic diseases, such as neurofibromatosis type 2 or Von Hipple-Lindau disease (a condition that affects how your cells grow, divide and die), have a higher risk of developing spinal cord tumors. […] Researchers believe that in most cases, something is absent during normal development. Specifically, cells in the spinal cord grow and divide as the body develops. During this cell division process, cells need to replicate their genetic material. Errors can take place during this process, leading to mutations, which may allow cells to grow into tumors. These errors generally occur randomly and cannot be prevented.
#55 Spinal Cord Tumor | Nationwide Children’s Hospital
https://www.nationwidechildrens.org/conditions/spinal-cord-tumor
People with certain inherited genetic diseases, such as neurofibromatosis type 2 or Von Hipple-Lindau disease (a condition that affects how your cells grow, divide and die), have a higher risk of developing spinal cord tumors. […] Researchers believe that in most cases, something is absent during normal development. Specifically, cells in the spinal cord grow and divide as the body develops. During this cell division process, cells need to replicate their genetic material. Errors can take place during this process, leading to mutations, which may allow cells to grow into tumors. These errors generally occur randomly and cannot be prevented.
#56 Spinal Cord Tumor | Nationwide Children’s Hospital
https://www.nationwidechildrens.org/conditions/spinal-cord-tumor
People with certain inherited genetic diseases, such as neurofibromatosis type 2 or Von Hipple-Lindau disease (a condition that affects how your cells grow, divide and die), have a higher risk of developing spinal cord tumors. […] Researchers believe that in most cases, something is absent during normal development. Specifically, cells in the spinal cord grow and divide as the body develops. During this cell division process, cells need to replicate their genetic material. Errors can take place during this process, leading to mutations, which may allow cells to grow into tumors. These errors generally occur randomly and cannot be prevented.
#57 :: iMRI :: Investigative Magnetic Resonance Imaging
https://i-mri.org/DOIx.php?id=10.13104/imri.2016.20.1.1
The spine is the most common location for skeletal metastases, and the incidence of spinal metastasis shows an increasing tendency. […] Therefore, it is clinically significant for radiologists to understand the pathophysiology of spinal metastasis and to assess the involvement of neural structures and the disintegration of spinal instability related to the pathophysiology. […] Therefore, we propose two learning objectives in our study. The first is to understand the pathophysiology of the spinal metastasis resulting in clinical symptoms and complications. The second is to evaluate the MR examination while focusing on some analysis points providing practical and useful information regarding the next step for a further developed clinical approach. […] Therefore, it is very valuable for radiologists to understand this pathophysiology of spinal metastasis and to evaluate the neural involvement of the neural structure and loss of spinal stability related to the pathophysiology.
#58 Pathogenesis of vertebral metastasis and epidural spinal cord compression – PubMed
https://pubmed.ncbi.nlm.nih.gov/2293874/
Radiographic evidence of vertebral metastasis was a late event, and commonly associated with significant compression of the cord and extraosseous tumor. […] These experimental findings may help to establish better diagnostic and treatment strategies for patients with metastatic disease of the spine.
#59 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
Neurological deficits may become apparent at the time of presentation and include motor weakness or paraplegia, dermatomal sensory loss, saddle anesthesia, neuropathic pain, and urinary/fecal incontinence. […] Patients with previously stable back pain who present with new pain escalation should trigger both suspicion of SCC and prompt acquisition of imaging within 24 h of presentation to show whether it is present. […] MRI is the imaging method of choice for the diagnosis of SCC with a sensitivity of 93% and specificity of 97%. […] The total dosage and number of fractions used both vary widely in the literature. […] The concept of spinal stability rests on the anatomical and functional complexity of the spinal structure. […] The clinical presentation of spinal instability is nuanced when caused by a neoplasm, each of which proceeds with its own array of bony and ligamentous involvement, neurological symptoms, bone quality, and prospect for effective repair.
#60 Spot The Warning Signs Of Spinal and Spinal Cord Tumors | Bangkok International Hospital (Brain x Bone)
https://www.bangkokinternationalhospital.com/health-articles/disease-treatment/spine-and-medulla-tumor
Patients who have symptoms that are suspicious for a spinal tumor should be comprehensively evaluated by a physician. Evaluation includes a complete medical history, a physical and neurological examination, and a radiographic study of the spine. With technological advancement, the doctor can identify whether a tumor is benign or malignant and select the individualized treatment for each patient.
#61 :: iMRI :: Investigative Magnetic Resonance Imaging
https://i-mri.org/DOIx.php?id=10.13104/imri.2016.20.1.1
The spine is the most common location for skeletal metastases, and the incidence of spinal metastasis shows an increasing tendency. […] Therefore, it is clinically significant for radiologists to understand the pathophysiology of spinal metastasis and to assess the involvement of neural structures and the disintegration of spinal instability related to the pathophysiology. […] Therefore, we propose two learning objectives in our study. The first is to understand the pathophysiology of the spinal metastasis resulting in clinical symptoms and complications. The second is to evaluate the MR examination while focusing on some analysis points providing practical and useful information regarding the next step for a further developed clinical approach. […] Therefore, it is very valuable for radiologists to understand this pathophysiology of spinal metastasis and to evaluate the neural involvement of the neural structure and loss of spinal stability related to the pathophysiology.
#62
https://journals.lww.com/isoj/fulltext/2022/05020/epidemiology,_pathogenesis,_clinical_presentation,.3.aspx
Metastases disrupt the OPG-RANKL-RANK signal transduction pathway. The balance of the interaction between OPG, RANK, and RANKL determines the nature of the lesion and its corresponding radiographic appearance, namely, osteolytic, osteoblastic, or mixed. […] Bone metastases from breast cancer are predominantly osteolytic. […] Metastatic breast cancer cells produce factors like parathyroid hormone-related peptide (PTHrP) that shares molecular similarities with parathyroid hormone (PTH) and has the same effect on osteoclasts as PTH, which is stimulation of osteoclastogenesis via RANKL. […] The presence of tumor cells in spine results in a disruption of the homeostasis between bone formation and remodeling, thereby producing osteoblastic, osteolytic, and mixed lesions. […] Understanding the molecular mechanisms involved in pathogenesis helps researchers develop new target molecules that can help reduce the tumor burden.
#63 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
The most recent development of a targeted inhibitor has been the PD-1 inhibitor nivolumab to treat patients with melanoma. […] Although improved knowledge about the molecular workings of tumors is unlikely to challenge the primacy of surgical treatment in the immediate future, a better understanding of tumor genetics may lead to better treatment for intradural spinal tumors. […] These specific differences in genetic makeup suggest a potentially different pathogenesis that necessitates consideration of specific treatment modalities. […] The application of the current knowledge gained from studies of cranial tumors will play an important role in the treatment of spinal cord tumors, despite the genetic differences between spinal tumors and their intracranial counterparts. […] Continued elucidation of the genetic features of these tumors will aid in the future design of treatment options and in clinical decision making.
#64 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
The most recent development of a targeted inhibitor has been the PD-1 inhibitor nivolumab to treat patients with melanoma. […] Although improved knowledge about the molecular workings of tumors is unlikely to challenge the primacy of surgical treatment in the immediate future, a better understanding of tumor genetics may lead to better treatment for intradural spinal tumors. […] These specific differences in genetic makeup suggest a potentially different pathogenesis that necessitates consideration of specific treatment modalities. […] The application of the current knowledge gained from studies of cranial tumors will play an important role in the treatment of spinal cord tumors, despite the genetic differences between spinal tumors and their intracranial counterparts. […] Continued elucidation of the genetic features of these tumors will aid in the future design of treatment options and in clinical decision making.
#65 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
The most recent development of a targeted inhibitor has been the PD-1 inhibitor nivolumab to treat patients with melanoma. […] Although improved knowledge about the molecular workings of tumors is unlikely to challenge the primacy of surgical treatment in the immediate future, a better understanding of tumor genetics may lead to better treatment for intradural spinal tumors. […] These specific differences in genetic makeup suggest a potentially different pathogenesis that necessitates consideration of specific treatment modalities. […] The application of the current knowledge gained from studies of cranial tumors will play an important role in the treatment of spinal cord tumors, despite the genetic differences between spinal tumors and their intracranial counterparts. […] Continued elucidation of the genetic features of these tumors will aid in the future design of treatment options and in clinical decision making.
#66 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
The most recent development of a targeted inhibitor has been the PD-1 inhibitor nivolumab to treat patients with melanoma. […] Although improved knowledge about the molecular workings of tumors is unlikely to challenge the primacy of surgical treatment in the immediate future, a better understanding of tumor genetics may lead to better treatment for intradural spinal tumors. […] These specific differences in genetic makeup suggest a potentially different pathogenesis that necessitates consideration of specific treatment modalities. […] The application of the current knowledge gained from studies of cranial tumors will play an important role in the treatment of spinal cord tumors, despite the genetic differences between spinal tumors and their intracranial counterparts. […] Continued elucidation of the genetic features of these tumors will aid in the future design of treatment options and in clinical decision making.
#67 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
The most recent development of a targeted inhibitor has been the PD-1 inhibitor nivolumab to treat patients with melanoma. […] Although improved knowledge about the molecular workings of tumors is unlikely to challenge the primacy of surgical treatment in the immediate future, a better understanding of tumor genetics may lead to better treatment for intradural spinal tumors. […] These specific differences in genetic makeup suggest a potentially different pathogenesis that necessitates consideration of specific treatment modalities. […] The application of the current knowledge gained from studies of cranial tumors will play an important role in the treatment of spinal cord tumors, despite the genetic differences between spinal tumors and their intracranial counterparts. […] Continued elucidation of the genetic features of these tumors will aid in the future design of treatment options and in clinical decision making.
#68 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
Neurological deficits may become apparent at the time of presentation and include motor weakness or paraplegia, dermatomal sensory loss, saddle anesthesia, neuropathic pain, and urinary/fecal incontinence. […] Patients with previously stable back pain who present with new pain escalation should trigger both suspicion of SCC and prompt acquisition of imaging within 24 h of presentation to show whether it is present. […] MRI is the imaging method of choice for the diagnosis of SCC with a sensitivity of 93% and specificity of 97%. […] The total dosage and number of fractions used both vary widely in the literature. […] The concept of spinal stability rests on the anatomical and functional complexity of the spinal structure. […] The clinical presentation of spinal instability is nuanced when caused by a neoplasm, each of which proceeds with its own array of bony and ligamentous involvement, neurological symptoms, bone quality, and prospect for effective repair.
#69 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
Neurological deficits may become apparent at the time of presentation and include motor weakness or paraplegia, dermatomal sensory loss, saddle anesthesia, neuropathic pain, and urinary/fecal incontinence. […] Patients with previously stable back pain who present with new pain escalation should trigger both suspicion of SCC and prompt acquisition of imaging within 24 h of presentation to show whether it is present. […] MRI is the imaging method of choice for the diagnosis of SCC with a sensitivity of 93% and specificity of 97%. […] The total dosage and number of fractions used both vary widely in the literature. […] The concept of spinal stability rests on the anatomical and functional complexity of the spinal structure. […] The clinical presentation of spinal instability is nuanced when caused by a neoplasm, each of which proceeds with its own array of bony and ligamentous involvement, neurological symptoms, bone quality, and prospect for effective repair.
#70 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The risk of burst fracture also increases with tumor size. […] Historically, surgery in the form of a simple posterior laminectomy (removal of the dorsal elements of the vertebral column) without instrumentation was performed to decompress the spinal cord. […] However, several studies showed that laminectomy alone or in combination with radiotherapy did not add any advantage. […] In fact, laminectomy is not the best option in many patients with metastatic SCC whose spinal metastases infiltrate the vertebral body anteriorly. […] Another surgical technique was thus developed consisting of an anterior approach for tumor removal with immediate posterior decompression by laminectomy, followed by spinal instrumentation for renewed stability. […] Today, the role of surgery is well established in patients with spinal metastatic disease with a neurological deficit or a high-grade SCC without deficits.
#71 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The risk of burst fracture also increases with tumor size. […] Historically, surgery in the form of a simple posterior laminectomy (removal of the dorsal elements of the vertebral column) without instrumentation was performed to decompress the spinal cord. […] However, several studies showed that laminectomy alone or in combination with radiotherapy did not add any advantage. […] In fact, laminectomy is not the best option in many patients with metastatic SCC whose spinal metastases infiltrate the vertebral body anteriorly. […] Another surgical technique was thus developed consisting of an anterior approach for tumor removal with immediate posterior decompression by laminectomy, followed by spinal instrumentation for renewed stability. […] Today, the role of surgery is well established in patients with spinal metastatic disease with a neurological deficit or a high-grade SCC without deficits.
#72 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The risk of burst fracture also increases with tumor size. […] Historically, surgery in the form of a simple posterior laminectomy (removal of the dorsal elements of the vertebral column) without instrumentation was performed to decompress the spinal cord. […] However, several studies showed that laminectomy alone or in combination with radiotherapy did not add any advantage. […] In fact, laminectomy is not the best option in many patients with metastatic SCC whose spinal metastases infiltrate the vertebral body anteriorly. […] Another surgical technique was thus developed consisting of an anterior approach for tumor removal with immediate posterior decompression by laminectomy, followed by spinal instrumentation for renewed stability. […] Today, the role of surgery is well established in patients with spinal metastatic disease with a neurological deficit or a high-grade SCC without deficits.
#73 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The risk of burst fracture also increases with tumor size. […] Historically, surgery in the form of a simple posterior laminectomy (removal of the dorsal elements of the vertebral column) without instrumentation was performed to decompress the spinal cord. […] However, several studies showed that laminectomy alone or in combination with radiotherapy did not add any advantage. […] In fact, laminectomy is not the best option in many patients with metastatic SCC whose spinal metastases infiltrate the vertebral body anteriorly. […] Another surgical technique was thus developed consisting of an anterior approach for tumor removal with immediate posterior decompression by laminectomy, followed by spinal instrumentation for renewed stability. […] Today, the role of surgery is well established in patients with spinal metastatic disease with a neurological deficit or a high-grade SCC without deficits.
#74 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The risk of burst fracture also increases with tumor size. […] Historically, surgery in the form of a simple posterior laminectomy (removal of the dorsal elements of the vertebral column) without instrumentation was performed to decompress the spinal cord. […] However, several studies showed that laminectomy alone or in combination with radiotherapy did not add any advantage. […] In fact, laminectomy is not the best option in many patients with metastatic SCC whose spinal metastases infiltrate the vertebral body anteriorly. […] Another surgical technique was thus developed consisting of an anterior approach for tumor removal with immediate posterior decompression by laminectomy, followed by spinal instrumentation for renewed stability. […] Today, the role of surgery is well established in patients with spinal metastatic disease with a neurological deficit or a high-grade SCC without deficits.
#75 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
The risk of burst fracture also increases with tumor size. […] Historically, surgery in the form of a simple posterior laminectomy (removal of the dorsal elements of the vertebral column) without instrumentation was performed to decompress the spinal cord. […] However, several studies showed that laminectomy alone or in combination with radiotherapy did not add any advantage. […] In fact, laminectomy is not the best option in many patients with metastatic SCC whose spinal metastases infiltrate the vertebral body anteriorly. […] Another surgical technique was thus developed consisting of an anterior approach for tumor removal with immediate posterior decompression by laminectomy, followed by spinal instrumentation for renewed stability. […] Today, the role of surgery is well established in patients with spinal metastatic disease with a neurological deficit or a high-grade SCC without deficits.
#76 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
In such cases, surgery is indicated regardless of the SINS score. […] The urgency of surgical management of SCC cannot be disputed. […] The risk factors predicting loss of ambulation following surgical decompression were preoperative ambulation loss, recurrent or persistent tumor after radiotherapy to the surgical site, a procedure other than vertebral corpectomy, and a primary tumor other than breast cancer. […] In addition, surgery within 48 h of the onset of motor deficits was shown to provide better ambulatory outcomes. […] The indications for surgical decompression in metastatic epidural SCC are summarized in Table 5.
#77 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
In such cases, surgery is indicated regardless of the SINS score. […] The urgency of surgical management of SCC cannot be disputed. […] The risk factors predicting loss of ambulation following surgical decompression were preoperative ambulation loss, recurrent or persistent tumor after radiotherapy to the surgical site, a procedure other than vertebral corpectomy, and a primary tumor other than breast cancer. […] In addition, surgery within 48 h of the onset of motor deficits was shown to provide better ambulatory outcomes. […] The indications for surgical decompression in metastatic epidural SCC are summarized in Table 5.
#78 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
In such cases, surgery is indicated regardless of the SINS score. […] The urgency of surgical management of SCC cannot be disputed. […] The risk factors predicting loss of ambulation following surgical decompression were preoperative ambulation loss, recurrent or persistent tumor after radiotherapy to the surgical site, a procedure other than vertebral corpectomy, and a primary tumor other than breast cancer. […] In addition, surgery within 48 h of the onset of motor deficits was shown to provide better ambulatory outcomes. […] The indications for surgical decompression in metastatic epidural SCC are summarized in Table 5.
#79 Neurosurgical emergencies in spinal tumors: pathophysiology and clinical management | Emergency Cancer Care | Full Text
https://emergcancercare.biomedcentral.com/articles/10.1186/s44201-024-00024-5
In such cases, surgery is indicated regardless of the SINS score. […] The urgency of surgical management of SCC cannot be disputed. […] The risk factors predicting loss of ambulation following surgical decompression were preoperative ambulation loss, recurrent or persistent tumor after radiotherapy to the surgical site, a procedure other than vertebral corpectomy, and a primary tumor other than breast cancer. […] In addition, surgery within 48 h of the onset of motor deficits was shown to provide better ambulatory outcomes. […] The indications for surgical decompression in metastatic epidural SCC are summarized in Table 5.
#80 The genetic basis of intradural spinal tumors and its impact on clinical treatment in: Neurosurgical Focus Volume 39 Issue 2 (2015) Journals
https://thejns.org/focus/view/journals/neurosurg-focus/39/2/article-pE3.xml
The most recent development of a targeted inhibitor has been the PD-1 inhibitor nivolumab to treat patients with melanoma. […] Although improved knowledge about the molecular workings of tumors is unlikely to challenge the primacy of surgical treatment in the immediate future, a better understanding of tumor genetics may lead to better treatment for intradural spinal tumors. […] These specific differences in genetic makeup suggest a potentially different pathogenesis that necessitates consideration of specific treatment modalities. […] The application of the current knowledge gained from studies of cranial tumors will play an important role in the treatment of spinal cord tumors, despite the genetic differences between spinal tumors and their intracranial counterparts. […] Continued elucidation of the genetic features of these tumors will aid in the future design of treatment options and in clinical decision making.