Mucin-producing tumors of the prostate include both primary and secondary tumors with mucinous differentiation or features involving the prostate gland. These tumors are relatively rare and have variable prognostic and therapeutic implications. Primary mucinous (colloid) adenocarcinoma of the prostate is defined as prostatic adenocarcinoma with mucinous differentiation involving 25% or more of the entire tumor. Another primary tumor of the prostate that may have mucinous features is primary mucin-producing urothelial-type adenocarcinoma of the prostate (mucinous prostatic urethral adenocarcinoma). Primary mucin-producing urothelial-type adenocarcinoma of the prostate is a distinct entity that typically arises from the prostatic urethra possibly from urethritis glandularis or glandular metaplasia with malignant transformation, and it is analogous to adenocarcinoma with mucinous differentiation arising from the urinary bladder. Signet ring cell tumors of the prostate, though rare, may also have mucinous features. Secondary tumors with mucinous differentiation that may involve the prostate include adenocarcinomas of the urinary bladder and colorectum. Pathologists should also be aware of mucin-producing tumor-like lesions involving the prostate, including mucinous metaplasia, and benign Cowper glands that may mimic malignancy. Herein we present an updated and comprehensive review of the clinicopathologic, immunohistochemical, molecular, and prognostic features of mucinous tumors and tumor-like lesions involving the prostate gland, with emphasis on mucinous prostatic adenocarcinoma and its mimickers, including potential diagnostic pitfalls.

Abstract-Although genetic determinants protecting against the development of elevated blood pressure (BP) are well investigated, less is known regarding their impact on longevity. We concomitantly assessed genomic regions of rat chromosomes 3 and 7 (RNO3 and RNO7) carrying genetic determinants of BP without known epistasis, for their independent and combinatorial effects on BP and the presence of genetic determinants of survival using Dahl salt-sensitive (S) strains carrying congenic segments from Dahl salt-resistant (R) rats. Although congenic and bicongenic S.R strains carried independent BP quantitative trait loci within the RNO3 and RNO7 congenic regions, only the RNO3 allele(s) independently affected survival. The bicongenic S.R strain showed epistasis between R-rat RNO3 and RNO7 alleles for BP under salt-loading conditions, with less-than-additive effects observed on a 2% NaCl diet and greater-than-additive effects observed after prolonged feeding on a 4% NaCl diet. These RNO3 and RNO7 congenic region alleles had more-than-additive effects on survival. Increased survival of bicongenic compared with RNO3 congenic rats was attributable, in part, to maintaining lower BP despite chronic exposure to an increased dietary salt (4% NaCl) intake, with both strains showing delays in reaching highest BP. R-rat RNO3 alleles were also associated with superior systolic function, with the S.R bicongenic strain showing epistasis between R-rat RNO3 and RNO7 alleles leading to compensatory hypertrophy. Whether these alleles affect survival by additional actions within other BP-regulating tissues/organs remains unexplored. This is the first report of simultaneous detection of independent and epistatic loci dictating, in part, longevity in a hypertensive rat strain. M ost human morbidity and mortality stem from complex diseases and disorders, of which phenotypes result from interactions of multiple genes with environmental factors. Hypertension is such a disorder, an independent predisposing factor in the development of several diseases responsible for adult morbidity and mortality, including atherosclerosis, coronary heart disease, peripheral artery disease, heart failure, renal failure, and stroke. 1 Little is known regarding the relationships between genetic determinants of blood pressure (BP) with genetic determinants of these diseases or overall mortality. We hypothesized that genetic factors contribute to the extended survival of some hypertensive subjects but not others. The obvious difficulty of using death as an end point in studying life span in human hypertensive subjects suggests that hypertension-survival relationships are better studied using animal models.Inbred Dahl salt-sensitive (SS/Jr or S) and Dahl salt-resistant (SR/Jr or R) rat strains 2 are contrasting models of high and relatively normal BP, respectively, selectively bred from outbred Sprague-Dawley rats under salt-loading conditions. 3 Supplemental dietary NaCl increases BP in S rats, with little or no effect on BP in R rats. Segregating populations a...

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