Publications by authors named "Pelin Bulut"

Breast cancer, which is the most common type of cancer among women, is a heterogenous disease. It results from progressive accumulation of genetic and epigenetic alterations in different genes. The Dok1 protein has been identified as the major substrate of protein tyrosine kinases in hematopoietic cells.

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Transcription Elongation Factor A-like 7 (TCEAL7) was first reported as a candidate tumor suppressor gene because of its inactivation in ovarian cancer as a result of promoter methylation. Down-regulation of the TCEAL7 gene expression was also associated with other cancers such as endometrial, breast, brain, prostate, gastric cancers, glioblastoma and linked to tumor phenotypes and clinical outcomes. However, there is no report in the literature investigating the role of TCEAL7 in non-small cell lung cancer.

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Lung cancer is the leading cause of cancer deaths. The main risk factor is smoking but the risk is also associated with various genetic and epigenetic components in addition to environmental factors. Increases in the gene copy numbers due to chromosomal amplifications constitute a common mechanism for oncogene activation.

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Article Synopsis
  • Lung cancer is highly lethal, and CHD5, a tumor suppressor gene, may play a role in its progression, particularly in non-small cell lung cancer (NSCLC).
  • Researchers analyzed CHD5 expression and methylation in 59 lung cancer samples, finding that CHD5 was down-regulated in 39.5% and up-regulated in 55.8% of tumors, with no significant link to methylation status.
  • The study suggests that while CHD5 may function as a tumor suppressor in NSCLC, its exact role and relationship with Akt phosphorylation remain unclear.
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Article Synopsis
  • Different genetic and epigenetic changes are linked to head and neck squamous cell carcinoma (HNSCC), with ongoing research into the mechanisms behind its development.
  • The study focused on the WWOX gene, finding its expression is significantly reduced in advanced-stage tumors and linked to methylation of its promoter region, but not to levels of miR-134.
  • The analysis revealed multiple alterations in the WWOX gene's coding and non-coding sequences in tumor samples, indicating that its inactivation contributes to the progression of HNSCC.
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