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Metastasis02:30

Metastasis

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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
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gDNA Enrichment by a Transposase-based Technology for NGS Analysis of the Whole Sequence of BRCA1, BRCA2, and 9 Genes Involved in DNA Damage Repair
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Does serous tubal intraepithelial carcinoma (STIC) metastasize? The clonal relationship between STIC and subsequent

C B van den Berg1, S Dasgupta2, P C Ewing-Graham3

  • 1Department of Gynecologic Oncology, Erasmus MC Cancer Center, University Medical Center, Rotterdam, the Netherlands.

Gynecologic Oncology
|May 17, 2024
PubMed
Summary

Serous tubal intraepithelial carcinoma (STIC) cells can spread and cause high-grade serous carcinoma (HGSC) years later in BRCA1/2 carriers. This study confirms the metastatic potential of STIC lesions.

Keywords:
BRCA1/2ClonalityHigh-grade serous carcinomaNext-generation sequencingSerous tubal intra-epithelial carcinomaTP53

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Area of Science:

  • Gynecologic Oncology
  • Cancer Genomics
  • Pathology

Background:

  • High-grade serous carcinoma (HGSC) often originates from serous tubal intraepithelial carcinoma (STIC).
  • The natural history and metastatic potential of STIC, particularly in relation to later HGSC development, remain poorly understood.
  • Clonal relationships between temporally distant STICs and HGSCs are infrequently studied.

Purpose of the Study:

  • To investigate the clonal relationship between precursor STIC lesions and subsequent peritoneal HGSC in BRCA1/2 germline pathogenic variant (GPV) carriers.
  • To explore the hypothesis that STIC lesions can metastasize and lead to HGSC development after a significant time lag.

Main Methods:

  • Focused database searches identified BRCA1/2 GPV carriers who underwent risk-reducing salpingo-oophorectomy (RRSO) with STIC but no invasive carcinoma, and later developed peritoneal HGSC.
  • Next-generation targeted sequencing was used to compare the genetic mutational profiles of STICs and HGSCs to establish clonal relationships.

Main Results:

  • Identical pathogenic mutations and TP53 loss of heterozygosity were found in STICs and HGSCs of 71% (5/7) of the patients studied.
  • The median interval between RRSO (with STIC) and subsequent HGSC diagnosis was 59 months, with a range of 24-118 months.

Conclusions:

  • Cells from STIC can exfoliate, disseminate within the peritoneal cavity, and cause HGSC in BRCA1/2 GPV carriers after long latency periods.
  • The findings support the hypothesis that STIC lesions possess metastatic potential and can serve as the origin for later HGSC development.