Seminoma component of mixed testicular germ cell tumor shows a higher incidence of loss of heterozygosity than pure-type seminoma.

Abstract:

:Using analysis of allelic loss (loss of heterozygosity [LOH]), we previously reported a putative progression pathway from germ cell neoplasia in situ (GCNIS) to seminoma and then to embryonal carcinoma in mixed-type testicular germ cell tumors. To identify the genetic backgrounds related to the progression of nonseminomatous germ cell tumor, patterns of LOH were studied in seminoma components in mixed tumors (18 cases), pure seminomas (20 cases), and coexisting GCNIS lesions. Each tumor was assessed for LOH at 22 polymorphic loci located on 12 chromosomal arms: 3q, 5q, 6p, 9p, 10q, 11p, 12p, 12q, 13q, 17p, 17q, and 18q. For all informative loci, the frequency of LOH in seminoma components in mixed tumors was significantly higher than that in pure seminomas (32% [96/302 loci] versus 19% [60/323 loci], P < .0001). The frequency of LOH in GCNIS lesions was not significantly different between the 2 tumor groups. The frequencies of LOH at chromosomes 6p and 10q were significantly higher in seminoma components in mixed tumors than in pure seminomas (P = .020 and P = .0041, respectively). Immunohistochemical analysis demonstrated a close association between the allelic status of the 10q23 locus and levels of phosphatase and tensin homolog deleted from chromosome 10 protein expression in seminoma (P = .00051). These data indicate that the seminoma, which has a potential to progress to nonseminomatous germ cell tumor, already exhibits several genetic changes including allelic losses of 6p and 10q, unlike pure seminoma.

journal_name

Hum Pathol

journal_title

Human pathology

authors

Miyai K,Ito K,Nakanishi K,Tsuda H

doi

10.1016/j.humpath.2018.09.007

subject

Has Abstract

pub_date

2019-02-01 00:00:00

pages

71-80

eissn

0046-8177

issn

1532-8392

pii

S0046-8177(18)30366-6

journal_volume

84

pub_type

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