Mutations in the ST7/RAY1/HELG locus rarely occur in primary colorectal, gastric, and hepatocellular carcinomas

S Yoshimura1, T Yamada, S Ohwada

  • 1Second Department of Surgery, Gunma University Faculty of Medicine, 3-39-15, Showa-machi, Maebashi, Gunma 371-8511, Japan.

Insights

The ST7 gene was investigated as a potential tumor suppressor. Mutations in ST7 were found to be rare in colorectal, gastric, and hepatocellular carcinomas, suggesting it is not a major driver of these cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Loss of heterozygosity on chromosome 7q31 suggests tumor suppressor genes.
  • The ST7 gene was initially proposed as a candidate tumor suppressor based on mutations in colon and breast cancer cell lines.

Purpose of the Study:

  • To determine the frequency of ST7 gene mutations in primary colorectal, gastric, and hepatocellular carcinomas.
  • To clarify the role of ST7 as a tumor suppressor in these specific cancer types.

Main Methods:

  • Analysis of ST7 coding sequences in 144 primary tumor samples (48 colorectal, 48 gastric, 48 hepatocellular).
  • Utilized polymerase chain reaction-single-strand conformational polymorphism (PCR-SSCP) and direct sequencing.
  • Somatic mutations were identified and localized.

Main Results:

  • Only three somatic mutations in the ST7 gene were detected across all 144 samples.
  • The identified mutations were located near the exon-intron junction of intron 8.
  • The overall mutation frequency was very low in the studied primary carcinomas.

Conclusions:

  • Mutations in the ST7 gene are infrequent in primary colorectal, gastric, and hepatocellular carcinomas.
  • The ST7 gene is unlikely to be a frequently mutated tumor suppressor in these cancer types.
  • Further research may be needed to fully elucidate the role of ST7 in tumorigenesis.

Related Concept Videos

Mismatch Repair01:36

Mismatch Repair

Overview
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...