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Volume 13, Problème 12 (2022)

Mini-revue

DNA Hypomethylation in Prostate Cancer is Consistent

Daniela Gerovska*

With approximately 1.4 million men diagnosed with prostate cancer each year around the world, PCa remains a terrifying threat to life and a source of devastating morbidity. Increased prostate-specific antigen screening and improved treatments have resulted in a significant decrease in age-specific PCa mortality in recent decades. Nonetheless, upcoming, enhanced PSA screening recommendations highlight an increasing disparity between the benefit and harm of current diagnosis/prognosis and application of radical treatment standards. To alleviate this tense situation, new powerful diagnostic and prognostic tools are unquestionably required. They should enable a more reliable early assessment of the impending threat, allowing for timely adjusted and personalised therapy and monitoring. We present here a basic study on an epigenetic screening method using Methylated DNA Immunoprecipitation.These can be used for early detection and may contribute to a new PCa epigenetic tumour classification system. Our findings show that we can isolate short, differentially methylated CpG-rich DNA fragments and combinations of them that are found in all tumours. Tumor cell-specific differential methylated CpG dinucleotide signatures are what we call them.

Mini-revue

Clinical, Histopathologic and Genetic Characteristics of Rhabdoid Meningiomas

Aurelio Laín*

Rhabdoid meningiomas have variable histological findings, and a wide range of chromosomal copy number alterations are linked to an unpredictable disease course. We analysed 305 RM samples from patients previously reported in the literature, as well as 33 samples from 23 patients studied in our laboratory, in this study. The most common chromosomal alteration was monosomy 22, which involved the minimal but most common recurrent region loss of the 22q11.23 chromosomal region, followed by losses of chromosomes 14,1,6, and 19, polysomies of chromosomes 17,1q, and 20, and gains of 13q14.2, 10p13, and 21q21.2 chromosomal regions. Based on their CNA profile, RM could be divided into two genetic subgroups with distinct clinicopathologic features defined by the presence of chromosomal losses only or combined losses and chromosomal instability.

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