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Loss of hMSH2 expression in primary breast cancer with p53 alterations

Ilaria Spagnoletti1, Claudia Pizzi, Annamaria Galietta

  • 1Dipartimento di Endocrinologia e Oncologia Molecolare e Clinica, Università di Napoli 'Federico II', 80131 Napoli, Italy.

Oncology Reports
|March 11, 2004
PubMed

Insights

DNA mismatch repair gene hMSH2 expression is underexplored in breast cancer. Loss of hMSH2 correlated with p53 and steroidal receptor expression but not microsatellite instability.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • DNA mismatch repair (MRG) gene inactivation is a pathway for cancer development, causing genetic instability.
  • Germline mutations in MRG genes are linked to hereditary non-polyposis colorectal cancer (HNPCC) and microsatellite instability (MSI).
  • The expression of MRG genes in primary breast cancer remains largely uninvestigated.

Purpose of the Study:

  • To investigate the relationship between hMSH2 expression and clinicopathological/biological characteristics in primary invasive breast cancers.
  • To explore the association between hMSH2 expression and microsatellite instability (MSI) in breast tumors.
  • To understand the role of hMSH2 in breast cancer oncogenesis.

Main Methods:

  • Analysis of hMSH2 expression in 44 primary invasive breast cancer tissues.
  • Correlation of hMSH2 expression with clinicopathological features, including p53, p185, and steroidal receptor expression.
  • Assessment of hMSH2 expression in relation to MSI at 9 dinucleotide loci in 30 cases.

Main Results:

  • hMSH2 was not expressed in 25% (11/44) of the breast cancer cases.
  • Tumors lacking hMSH2 expression showed a higher frequency of p53 alterations (p=0.05) and trends towards increased p185 and steroidal receptor expression (p=0.07).
  • No significant correlation was found between hMSH2 expression and MSI status in the analyzed cases.

Conclusions:

  • hMSH2 deficiency in breast cancer is associated with specific molecular alterations (p53, p185, steroidal receptors), suggesting potential common pathways.
  • The lack of correlation between hMSH2 and MSI indicates that breast cancer progression may involve different oncogenetic mechanisms than HNPCC.
  • Further research is needed to elucidate the precise role of hMSH2 in breast cancer development and progression.

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