Progression of malignant tumors is largely due to clonal evolution of the primary tumor, clones acquiring different sets of molecular genetic lesions. Lesions can confer a selective advantage in proliferation rate or metastasis on the tumor cell population, especially if developing resistance to anticancer therapy.
The biologic and prognostic value of focal neuroendocrine differentiation (NED) in conventional prostate adenocarcinoma (PC) patients who undergo radical prostatectomy (RP) remains controversial. In this systematic review and meta-analysis, we assessed the association of focal NED in conventional PC with oncological outcomes after RP.
Although prostate cancer is common in the western world and is associated with favorable overall survival, neuroendocrine prostate cancer is difficult to detect and is known to aggressively metastasize throughout the body.
Small cell neuroendocrine (NE) carcinomas of the prostate classically lose androgen receptor (AR) expression, may harbor loss of the RB1, TP53, and PTEN tumor suppressor genes, and are associated with a poor prognosis.
To evaluate the value of the serum neuroendocrine differentiation (NED) markers in helping to select the best treatment sequence of abiraterone acetate (AA) and docetaxel-prednisone (DP) in mCRPC.
Eighty-eight mCRPC patients were identified (42 in the DP-to-AA group and 46 in the AA-to-DP group).
Neuroendocrine neoplasms of the prostate represent a multifarious group of tumors that exist both in pure forms and associated with prostatic adenocarcinoma. Morphologically, neuroendocrine cells in prostate neoplasms can range from being indistinguishable from surrounding prostate adenocarcinoma cells to having high-grade neuroendocrine appearances similar to neuroendocrine malignancies of other organs.
Neuroendocrine-like trans-differentiation of prostate cancer adenocarcinomas correlates with serum levels of Chromogranin A (CgA) and drives treatment resistance. Aim of this work was to evaluate whether CgA could serve as a response predictor for 177Lu-PSMA617 radio-ligand therapy (PSMA-RLT) in comparison to the established tumor markers.
Prostate cancer (PCa) with neuroendocrine differentiation (NED) is tightly associated with hormone refractory PCa (HRPC), an aggressive form of cancer that is nearly impossible to treat. Determining the mechanism of the development of NED may yield novel therapeutic strategies for HRPC.
The grading and prognosis of prostatic adenocarcinoma with Paneth cell-like differentiation (PanEC) of the prostate is controversial with limited available data. We identified 80 cases, not previously published, of PanEC first identified on biopsy (n=69), transurethral resection (TURP)(n=1) and radical prostatectomy (RP) (n=10).
Critical issues in prostate cancer (PC) are a. identification of molecular drivers of the highly aggressive neuroendocrine differentiation (NED) in adenocarcinoma, and b. early assessment of disease progression.
Loss of tumor suppressor proteins, such as the retinoblastoma protein (Rb), results in tumor progression and metastasis. Metastasis is facilitated by low oxygen availability within the tumor that is detected by hypoxia inducible factors (HIFs).
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