Mantle cell lymphoma diagnosed from radical prostatectomy for prostate adenocarcinoma: a case report.

We present a case of 64 - year - old man with mantle cell lymphoma (MCL) diagnosed in radical prostatectomy for adenocarcinoma. Lymphoma of the prostate, either primary or secondary, is a rare entity. The prognosis of lymphoma involving the prostate is usually poor. The most common form of leukemia/lymphoma involving the prostate is that of chronic lymphocytic leukemia/lymphoma (CLL/SLL). Mantle cell lymphoma of the prostate is an exceedingly rare entity. The association between MCL and urologic cancer was previously described, however the etiologic connection between these two conditions remains unknown. The pathologists should pay attention to all lymphoid infiltrates in the prostate, especially in cases when these are dense.

Sarcosine is a prostate epigenetic modifier that elicits aberrant methylation patterns through the SAMe-Dnmts axis.

DNA hypermethylation is one of the most common epigenetic modifications in prostate cancer (PCa). Several studies have delineated sarcosine as a PCa oncometabolite that increases the migration of malignant prostate cells while decreasing their doubling time. Here, we show that incubation of prostate cells with sarcosine elicited the upregulation of sarcosine N-demethylation enzymes, sarcosine dehydrogenase and pipecolic acid oxidase. This process was accompanied by a considerable increase in the production of the major methyl-donor S-adenosylmethionine (SAMe), together with an elevation of cellular methylation potential. Global DNA methylation analyses revealed increases in methylated CpG islands in distinct prostate cell lines incubated with sarcosine, but not in cells of nonprostate origin. This phenomenon was further associated with marked upregulation of DNA methyltransferases (Dnmts). Epigenetic changes were recapitulated through blunting of Dnmts using the hypomethylating agent 5-azacytidine, which was able to inhibit sarcosine-induced migration of prostate cells. Moreover, spatial mapping revealed concomitant increases in sarcosine, SAMe and Dnmt1 in histologically confirmed malignant prostate tissue, but not in adjacent or nonmalignant tissue, which is in line with the obtained in vitro data. In summary, we show here for the first time that sarcosine acts as an epigenetic modifier of prostate cells and that this may contribute to its oncometabolic role.