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Jiang Yio 2021-05-10 11:49:31 -04:00
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prostate.adoc
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@ -39,7 +39,7 @@ Guidelines for referral to genetic counseling are frequently changing, but at mi
*NCCN recommends germline testing for:*
* any patient with metastatic, regional, or high-risk localized prostate cancer, regardless of family history.
* patients with low- to intermediate-risk prostate cancer with intraductal histology (new in NCCN 2019 guidelines) or a ``strong family history'' of prostate cancer, meaning:
* patients with low- to intermediate-risk prostate cancer with intraductal histology (new in NCCN 2019 guidelines) or a "`strong family history`" of prostate cancer, meaning:
** a brother or father or multiple family members diagnosed with prostate cancer at age < 60 years
** known family history of high-risk germline alterations
** two or more relatives with breast, ovarian, or pancreatic cancer (suggesting BRCA2 alteration)
@ -90,15 +90,15 @@ Prostate cancer can be characterized by its typical IHC profile: cytokeratin 7/2
As treatment resistance occurs, different phenotypes may emerge. Most CRPC is still driven by AR signaling, even after developing resistance to subsequent AR-directed therapies.
Some advanced CRPC may become ``androgen indifferent,'' often harboring alterations in Rb1 and p53. These may be admixed with AR-driven tumors. A subset of these cases may have neuroendocrine features, with the most extreme exhibiting small-cell morphology.
Some advanced CRPC may become "`androgen indifferent,`" often harboring alterations in Rb1 and p53. These may be admixed with AR-driven tumors. A subset of these cases may have neuroendocrine features, with the most extreme exhibiting small-cell morphology.
Small-cell prostate cancer is a rare subset and classically occurs with rapid visceral spread in the absence of increase in serum PSA level after a period of hormonal therapy for highgrade initial disease (de novo small-cell prostate cancer is extremely rare). It is characterized primarily by morphology, but it can also be positive on synaptophysin and/or chromogranin A staining.
* During treatment of advanced prostate cancer, multiple genomic and transcriptomatic alterations could occur as mechanisms of treatment resistance
** Most prostate cancers remain dependent on AR signaling
** A subset may become ``androgen indifferent'' and are generally characterized by alterations in RB1 and p53
** A subset may become "`androgen indifferent`" and are generally characterized by alterations in RB1 and p53
** Some, but not all, of these tumors may exhibit neuroendocrine differentiation, with positive synaptophysin and/or chromogranin A staining
*** The extreme of neuroendocrine differentiation is ``small cell'' morphology, histologically similar to small cell carcinoma of the lung or other extrapulmonary sites
*** The extreme of neuroendocrine differentiation is "`small cell`" morphology, histologically similar to small cell carcinoma of the lung or other extrapulmonary sites
*** Neuroendocrine prostate cancer is associated with amplification of AURKA and MYCN, offering the opportunity for targeted therapy
*** Clinically, emergence of neuroendocrine differentiation and small cell transformation should be considered in men who develop castration-resistant disease after ADT for high-grade cancers, especially when visceral involvement is diagnosed and radiographic progression occurs in the absence of an increase in PSA