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Mitochondrial genome analysis in penile carcinoma.

L F Araujo1,2, A T Terra3, C T G Sares3

  • 1Department of Genetics at Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.

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|June 28, 2018
PubMed
Summary

Mitochondrial genome instability, characterized by increased variants and heteroplasmy, is observed in penile carcinoma (PeCa). These alterations suggest a role for mitochondrial DNA in PeCa development and potential therapeutic strategies.

Keywords:
HeteroplasmyMitochondrial genomeMtDNA copy numberMutationPenile carcinoma

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Area of Science:

  • Oncology
  • Genetics
  • Mitochondrial Biology

Background:

  • Penile carcinoma (PeCa) is a rare cancer with potential links to socio-economic factors.
  • Mitochondrial genome alterations are implicated in tumorigenesis across various cancer types.
  • Understanding mitochondrial involvement in PeCa is crucial for novel therapeutic approaches.

Purpose of the Study:

  • To investigate mitochondrial genome alterations in penile carcinoma.
  • To evaluate heteroplasmy, mutational load, and mtDNA content in PeCa tissues.
  • To identify potential roles of mitochondrial DNA in PeCa pathogenesis.

Main Methods:

  • Next-generation sequencing (NGS) of the mitochondrial genome in 13 penile tumors and 12 non-neoplastic samples.
  • Assessment of heteroplasmy and mtDNA variants using bioinformatics tools.
  • Evaluation of variant pathogenicity with Mutpred software and mtDNA content via quantitative PCR.

Main Results:

  • Increased non-synonymous variants and higher heteroplasmy frequency in penile tumor tissues.
  • Significant depletion of mitochondrial DNA (mtDNA) content in penile tumors compared to normal tissues.
  • Identification of five novel mitochondrial variants exclusively in tumoral tissues, indicating increased mitochondrial instability.

Conclusions:

  • Penile tumors exhibit heightened mitochondrial genome instability.
  • Mitochondrial DNA copy number and variants may jointly disrupt mitochondrial function in PeCa.
  • Further research into mitochondrial biology could unveil new therapeutic avenues for PeCa.