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Review
. 2022 Jan 14;14(2):416.
doi: 10.3390/cancers14020416.

The Evolution of Ovarian Carcinoma Subclassification (VSports手机版)

Martin Köbel  1 , Eun Young Kang  1
Affiliations
Review

The Evolution of Ovarian Carcinoma Subclassification

Martin Köbel et al. Cancers (Basel). .

VSports app下载 - Abstract

The phenotypically informed histotype classification remains the mainstay of ovarian carcinoma subclassification. Histotypes of ovarian epithelial neoplasms have evolved with each edition of the WHO Classification of Female Genital Tumours. The current fifth edition (2020) lists five principal histotypes: high-grade serous carcinoma (HGSC), low-grade serous carcinoma (LGSC), mucinous carcinoma (MC), endometrioid carcinoma (EC) and clear cell carcinoma (CCC). Since histotypes arise from different cells of origin, cell lineage-specific diagnostic immunohistochemical markers and histotype-specific oncogenic alterations can confirm the morphological diagnosis. A four-marker immunohistochemical panel (WT1/p53/napsin A/PR) can distinguish the five principal histotypes with high accuracy, and additional immunohistochemical markers can be used depending on the diagnostic considerations. Histotypes are further stratified into molecular subtypes and assessed with predictive biomarker tests. HGSCs have recently been subclassified based on mechanisms of chromosomal instability, mRNA expression profiles or individual candidate biomarkers. ECs are composed of the same molecular subtypes (POLE-mutated/mismatch repair-deficient/no specific molecular profile/p53-abnormal) with the same prognostic stratification as their endometrial counterparts. Although methylation analyses and gene expression and sequencing showed at least two clusters, the molecular subtypes of CCCs remain largely elusive to date. Mutational and immunohistochemical data on LGSC have suggested five molecular subtypes with prognostic differences. While our understanding of the molecular composition of ovarian carcinomas has significantly advanced and continues to evolve, the need for treatment options suitable for these alterations is becoming more obvious. Further preclinical studies using histotype-defined and molecular subtype-characterized model systems are needed to expand the therapeutic spectrum for women diagnosed with ovarian carcinomas VSports手机版. .

Keywords: histotype; immunohistochemistry; molecular subtype; ovarian cancer; subclassification. V体育安卓版.

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"V体育ios版" Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Stratification of (tubo-)ovarian high-grade serous, low-grade serous, endometrioid, clear cell and mucinous carcinoma histotypes into molecular subtypes. NAPSA = napsin A; HRD = homologous repair deficiency; Dup = BRCA1-associated tandem duplications; Del = BRCA2-associated interstitial deletions; FBI = fold-back inversions; TD = tandem duplications; CDKN2Aalt = CDKN2A alterations; MAPKmut = MAPK pathway mutations; USP9Xmut = USP9X mutations; NSMP = no specific molecular profile; POLEmut = POLE mutated; MMRd = mismatch repair deficient; p53abn = p53 abnormal; p53wt = p53 normal/wild type.
Figure 2
Figure 2
Four-marker immunohistochemical panel to distinguish the five principal histotypes of ovarian carcinomas: high-grade serous, low-grade serous, endometrioid, clear cell and mucinous carcinomas. PAX8 may be added as generic Mullerian marker, although there is limited sensitivity for endometrioid and mucinous carcinomas and limitations with specificity toward renal and thyroid primaries. NAPSA = napsin A.
See this image and copyright information in PMC

References

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