From 68537a0b9573ae1e6c580425a3156cf80fe052b8 Mon Sep 17 00:00:00 2001 From: jyio Date: Mon, 10 May 2021 11:49:31 -0400 Subject: [PATCH] Curved quotes --- prostate.adoc | 8 ++++---- 1 file changed, 4 insertions(+), 4 deletions(-) diff --git a/prostate.adoc b/prostate.adoc index 5e9b08e..87a2758 100644 --- a/prostate.adoc +++ b/prostate.adoc @@ -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