DNAJC9 expression in basal-like and luminal A breast cancer subtypes predicts worse survival.

Background: This study aimed to analyze the role of genetic/epigenetic alterations and the prognostic value of the DNAJC9 gene in breast cancer.

Materials And Methods: RT-PCR and Q-RT-PCR methods are used to examine DNAJC9 expression in breast cell lines. Survival ratios of breast cancer patients were evaluated by using bc-GenExMiner.

Identification of Gene Promoter Hypermethylation as a Potential Biomarker for Lung Cancer.

Background/aim: Recent studies imply the significance of promoter CpG methylation as a biomarker for various cancer types in different genes. ALX3 is one of the candidate genes with prominent promoter methylation status change. In this study, the methylation status of ALX3 gene promoter and its expression was analyzed in lung cancer cell lines and clinical samples from The Cancer Genome Atlas Program (TCGA) program.

High expression of () predicts unfavorable survival outcomes in breast cancer.

is associated with several cancers, but its biomarker potential in breast cancer is not adequately known. Q-RT-PCR, immunohistochemistry, COBRA methods and tools (KM-Plotter, UALCAN) were used to analyze the expression level, methylation status and prognostic value of in breast cancer. expression was significantly higher in clinical tumor samples compared with normal samples.

Downregulation of DNAJC10 (ERDJ5) is associated with poor survival in breast cancer.

Background: DNAJC10 (ERDJ5), a member of HSP40 family, was considered as an anti-oncogenic gene in neuroblastoma, prostate and colon cancers. But, the role and importance of DNAJC10 gene in breast cancer is currently unknown. In this study, in vitro/in vivo expression, biomarker potential and genetic/epigenetic alterations of DNAJC10 were analyzed in breast cancer.

Role of FLT3 in the proliferation and aggressiveness of hepatocellular carcinoma.

Background/aim: Previously we showed that Fms-like tyrosine kinase (FLT3) changes its cellular localization upon partial hepatectomy, suggesting a role in liver regeneration. FLT3 was also shown to play an important function in cellular proliferation and activation of PI3K and Ras. Thus, we aimed to investigate the role of FLT3 in hepatocellular tumorigenesis utilizing in vitro and in vivo models.

PTPRD is homozygously deleted and epigenetically downregulated in human hepatocellular carcinomas.

PTPRD (protein tyrosine phosphatase, receptor type, D) is a tumor suppressor gene, frequently inactivated through deletions or epigenetic mechanisms in several cancers with importance for global health. In this study, we provide new and functionally integrated evidence on genetic and epigenetic alterations of PTPRD gene in hepatocellular carcinomas (HCCs). Importantly, HCC is the sixth most common malignancy and the third most common cause of cancer-related mortality worldwide.

SIP1 is downregulated in hepatocellular carcinoma by promoter hypermethylation.

Background: Smad interacting protein-1 is a transcription factor that is implicated in transforming growth factor-β/bone morphogenetic protein signaling and a repressor of E-cadherin and human telomerase reverse transcriptase. It is also involved in epithelial-mesenchymal transition and tumorigenesis. However, genetic and epigenetic alterations of SIP1 have not been fully elucidated in cancers.

Mdm2 Snp309 G allele displays high frequency and inverse correlation with somatic P53 mutations in hepatocellular carcinoma.

Loss of function of the p53 protein, which may occur through a range of molecular events, is critical in hepatocellular carcinoma (HCC) evolution. MDM2, an oncogene, acts as a major regulator of the p53 protein. A polymorphism in the MDM2 promoter, SNP309 (T/G), has been shown to alter protein expression and may thus play a role in carcinogenesis.