D7- Prostate Cancer Questions - Amin

22. All of the following drugs antagonizes with androgen receptor EXCEPT a. Degarelix b. Bicalutamide c. Nilutamide d. Enzalutamide e. Flutamide

a. Degarelix

15. All of the following are true about ERG in prostate carcinogenesis EXCEPT a. Drives prostate carcinogenesis independently of androgen receptor involvement b. Primarily activated through gene fusion/chromosomal rearrangement c. Transcribes genes which are important for cell proliferation d. Transmembrane protease, serine 2 (TMPRSS2) is the most common fusion partner e. Works like a tumor suppressor gene f. Works like an oncogene

a. Drives prostate carcinogenesis e. Works like a tumor suppressor gene

28. In cell therapy, immune cells are treated with PAP-GM-CSF. What is the primary function of GM-CSF in this case? a. Increase in the proliferation of antigen presenting cells b. Increase in the antigenicity of antigen presenting cells c. Help antigen presenting cells to recognize cancer cells d. All e. None

a. Increase in the proliferation of antigen presenting cells

26. What is the mechanism of action of Abiraterone? a. Inhibition of androgen synthesis b. Inhibition of androgen receptor synthesis c. Inhibition of androgen release d. Inhibition of GnRH activity e. Inhibition of LH release by the pituitary

a. Inhibition of androgen synthesis

17. Which of the following drug will cause testosterone flare? a. Leuprolide b. Triptorelin c. Mitoxantrone d. Degarelix e. Flutamide f. Enzalutamide g. Docetaxel

a. Leuprolide b. Triptorelin

20. Which of the following drug desensitize pituitary gonadotropes by binding to GnRH receptor? a. Leuprolide b. Triptorelin c. Mitoxantrone d. Degarelix e. Flutamide f. Enzalutamide g. Docetaxel

a. Leuprolide b. Triptorelin

13. Which is true about the function of LH? a. Stimulates Leydig cells of the testes to release testosterone b. Stimulates Sertoli cells of the testes to release testosterone c. Stimulates testes to synthesize testosterone d. Regulates release of androgen binding protein to stabilize testosterone in the plasma e. Stimulates binding of testosterone with sex hormone binding globulin f. Low level of testosterone directly stimulates pituitary to produce and release LH

a. Stimulates Leydig cells of the testes to release testosterone c. Stimulates testes to synthesize testosterone f. Low level of testosterone directly stimulates pituitary to produce and release LH

7. Which of the genetic alterations are the most frequent in prostate carcinogenesis? a. TMPRSS2-Ets fusion b. SPOP mutation c. PTEN loss d. P53 mutation e. Myc amplification

a. TMPRSS2-Ets fusion

16. In prostate cancer, wild-type SPOP functions as- a. An oncogene b. A tumor suppressor gene c. A kinase d. A protease e. All of the above f. None

b. A tumor suppressor gene d. A protease

10. How does PTEN mutation contribute to prostate carcinogenesis? a. By activating EGFR b. By activating PI3-AKT c. By activating Ras-MAPK d. By activating Rho-Ras signaling e. ALL

b. By activating PI3-AKT

19. What is the mechanism of action of degarelix? a. GnRH agonism b. GnRH antagonism c. AR antagonism d. Inhibition of androgen synthesis e. AR degradation

b. GnRH antagonism

6. All of the following are true about AR-HSP complex EXCEPT- a. Functionally inactive b. Resides in the nucleus c. Resides in the cytoplasm d. Ligand binding dissociates the complex e. AR binding with HSP is required for nuclear translocation f. Important for prostate carcinogenesis

b. Resides in the nucleus e. AR binding with HSP is required for nuclear translocation f. Important for prostate carcinogenesis

8. All of the following are true about SPOP mutation in prostate carcinogenesis EXCEPT a. SPOP mutation drives a subset of prostate cancer b. SPOP mutation increases androgen receptor degradation c. SPOP mutation inactivates SPOP d. SPOP mutation increases AR level e. SPOP mutation in prostate cancer decreases AR level

b. SPOP mutation increases androgen receptor degradation e. SPOP mutation in prostate cancer decreases AR level

2. Which is the major androgen in our body? a. Progesterone b. Testosterone c. Estrogen d. All e. None

b. Testosterone

5. Majority of prostate cancers are- a. Squamous cell carcinoma b. Adenoma c. Adenocarcinoma d. Sarcoma e. Myeloma

c. Adenocarcinoma

25. All of the following are true about CYP17A1 EXCEPT a. An enzyme that boosts androgen synthesis b. Catalyzes multiple steps in androgen synthesis c. Antagonizes the synthesis of androgen d. Causes hydroxylation e. Located in endoplasmic reticulum

c. Antagonizes the synthesis of androgen

30. Which of the following activates T-cells to kill cancer cells in case of cell therapy? a. GM-CSF b. PAP-GM-CSF c. Antigen presenting cells d. PAP e. All f. None

c. Antigen presenting cells

12. Prostate cancer cell proliferation could be inhibited by all of the following ways EXCEPT- a. By blocking AR activity b. By using competitive inhibitors of GnRH c. By short term activation of GnRH receptor with GnRH agonists d. By persistent activation of GnRH receptors with GnRH agonists e. By increasing the level of androgens f. By increasing the level of AR g. By inhibiting the endogenous biosynthesis of androgen (testosterone)

c. By short term activation of GnRH receptor with GnRH agonists e. By increasing the level of androgens f. By increasing the level of AR

14. All of the following are true about androgen-androgen receptor interaction EXCEPT- a. Causes dimerization of androgen receptors b. Causes posttranslational modifications of androgen receptors c. Causes conformational change of androgen receptor which is important for cytoplasmic translocation of the receptor d. Causes conformational change of androgen receptor which is important for nuclear translocation of the receptor e. Important for the regulation of androgen receptor-dependent transcription

c. Causes conformational change of androgen receptor which is important for cytoplasmic translocation of the receptor

31. All of the following may cause resistance to androgen deprivation therapy EXCEPT a. Amplification of AR b. Mutation in AR c. Degradation of AR d. Increase SPOP activity e. Splice variants of AR f. Activation of other receptor tyrosine kinases

c. Degradation of AR d. Increase SPOP activity

9. All of the followings are true about TMPRSS2-Ets fusion in prostate cancer EXCEPT a. The most frequent genetic alterations found in prostate cancer b. Fusion increases the transcription of Ets c. Fusion increases the transcription of TMPRSS2 target genes d. Fusion increases the transcription of Ets target genes e. All of the above are true

c. Fusion increases the transcription of TMPRSS2 target genes

18. Which drug is not suitable for bone metastatic patients? a. GnRH antagonists b. CYP17A1 inhibitor c. GnRH agonists d. AR antagonists e. Docetaxel f. None

c. GnRH agonists

29. In cell therapy, immune cells are treated with PAP-GM-CSF. What is the primary function of PAP (antigen present in prostate cancer) in this case? a. Increase in the proliferation of antigen presenting cells b. Increase in the antigenicity of antigen presenting cells c. Help antigen presenting cells to recognize cancer cells d. All e. None

c. Help antigen presenting cells to recognize cancer cells

24. All of the following are true about Enzalutamide EXCEPT a. Inhibits androgen-androgen receptor interactions b. Inhibits nuclear translocation of AR c. Inhibits androgen synthesis d. Inhibits AR-DNA interaction e. All

c. Inhibits androgen synthesis

4. All of the following are true about androgen receptor EXCEPT a. Testosterone is an endogenous ligand b. A nuclear receptor c. Inactive receptor usually resides in the cytoplasm d. A transmembrane receptor e. Regulates gene transcription

d. A transmembrane receptor

23. Gynecomastia is associated with a. GnRH agonists b. GnRH antagonists c. Testosterone synthesis inhibitors d. AR antagonists e. Chemo drugs

d. AR antagonists

27. Which is the mechanism of apoptosis induced by Vaccine Therapy/Immune Therapy/cell therapy/ Sipuleucel-T? a. Activation of p53 b. Inhibition of anti-apoptotic Bcl2 c. Increase in the expression of pro-apoptotic Bcl2 d. Boosting the immune system of the patient e. Activation of extrinsic apoptotic machinery f. T-cell mediated killing/cytotoxicity

d. Boosting the immune system of the patient f. T-cell mediated killing/cytotoxicity

21. Which of the following drug inhibits LH release by binding to and inhibiting GnRH receptors? a. Leuprolide b. Triptorelin c. Mitoxantrone d. Degarelix e. Flutamide f. Enzalutamide g. Docetaxel

d. Degarelix

3. Which of the following is released by low circulating testosterone? a. LH b. FSH c. TSH d. GnRH e. None

d. GnRH

11. All of the following are true about the contribution of AR in prostate carcinogenesis EXCEPT- a. Activates genes which contribute to prostate cell proliferation (PSA, cyclin D1)) b. Activates genes which contribute to angiogenesis (VEGF) c. Activates expression of fusion genes which contribute to prostate carcinogenesis by regulating other genes (TRPSS2) d. SPOP mutation increases AR level e. ALL

e. ALL

1. All of the following cancers are somehow related to steroid hormones EXCEPT a. Thyroid b. Prostate c. Ovarian d. Breast e. Lung f. ALL

e. Lung