Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ERCC2 and ERCC1 are important in DNA nucleotide excision repair and lie on chromosome 19q13.3 near a putative glioma suppressor region. We genotyped constitutive variants ERCC1 C8092A and ERCC2 K751Q and R156R in approximately 450 adults with glioma and 500 controls from two independent population-based series, uniformly reviewed patients' tumors to determine histopathologic category, and determined a variety of tumor markers among astrocytic tumors. Odds ratios (ORs) for glioblastoma for those carrying two ERCC1 A alleles versus none or one were 1.67 in series 1 and 1.64 in series 2, which yielded a combined OR of 1.67 (95% CI, 0.93-3.02; P = 0.09), adjusted for age, gender, ethnicity, and series. Odds ratios for the ERCC2 variants were not consistently elevated or reduced for the two series in all cases versus controls. However, among whites, for those with ERCC2 K751Q genotype QQ versus QK/KK, the OR for nonglioblastoma histologies versus controls was 1.82 (95% CI, 0.97-3.44; P = 0.06). Also, among whites, glioma patients were significantly more likely than controls to be homozygous for variants in both ERCC1 C8092A and ERCC2 K751Q (OR, 3.2; 95% CI, 1.1-9.3). Given the numbers of comparisons made, these findings could be due to chance. However, the results might warrant clarification in additional series in conjunction with the nearby putative glioma suppressor genes (GLTSCR1 and GLTSCR2).
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PMID:ERCC1 and ERCC2 polymorphisms and adult glioma. 1621 14

Tumor hypoxia may be an indicator of poor survival in cancer patients. Thus, an understanding of the molecular mechanism responsible for hypoxic tumor selection is essential to gain further insight into tumor biology. Our aim in this study was to investigate whether hypoxia-responsive GLTSCR2 contributes to death resistance and increased invasiveness of hypoxia-selected glioblastoma cells. We found that repeated hypoxia downregulates p53-upstream regulator, GLTSCR2, which resulted in increased death resistance and invasive potential of glioblastoma cells. Restoration of GLTSCR2 expression suppressed the malignant potential of hypoxia-selected cells. Our results indicate that GLTSCR2 participates in hypoxia-induced malignant potential.
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PMID:GLTSCR2 contributes to the death resistance and invasiveness of hypoxia-selected cancer cells. 2285 Jan 12