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Low hypoxia inducible factor-1? (HIF-1?) expression in testicular germ cell tumors - a major reason for enhanced chemosensitivity?


ABSTRACT: The molecular basis for enhanced chemosensitivity of testicular germ cell tumors (GCT) has been an area of great interest, as it could potentially give us therapeutic leads in other resistant malignancies. Thus far, however, the increased sensitivity of GCT has been variously attributed to multiple factors - an inability to detoxify cisplatin, a lack of export pumps, an inability to repair the DNA damage, an intact apoptotic cascade and lack of p53 mutation; but a unifying underlying etiology leading to the aforementioned processes and having a translational implication has so far been elusive. Herein, we offer evidence to support a potential significant role for the previously demonstrated low hypoxia inducible factor-1? (HIF-1?) expression in mediating the general exquisite chemosensitivity of testicular GCT, through the aforementioned processes. This molecular mechanism based hypothesis could have a significant translational implication in platinum refractory GCT as well as other platinum resistant malignancies.

SUBMITTER: Shenoy N 

PROVIDER: S-EPMC5592826 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature

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Low hypoxia inducible factor-1α (HIF-1α) expression in testicular germ cell tumors - a major reason for enhanced chemosensitivity?

Shenoy Niraj N   Dronca Roxana R   Quevedo Fernando F   Boorjian Stephen A SA   Cheville John J   Costello Brian B   Kohli Manish M   Witzig Thomas T   Pagliaro Lance L  

Chinese journal of cancer research = Chung-kuo yen cheng yen chiu 20170801 4


The molecular basis for enhanced chemosensitivity of testicular germ cell tumors (GCT) has been an area of great interest, as it could potentially give us therapeutic leads in other resistant malignancies. Thus far, however, the increased sensitivity of GCT has been variously attributed to multiple factors - an inability to detoxify cisplatin, a lack of export pumps, an inability to repair the DNA damage, an intact apoptotic cascade and lack of p53 mutation; but a unifying underlying etiology le  ...[more]

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