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PubMed:15849821 JSONTXT

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DisGeNET

Id Subject Object Predicate Lexical cue
T0 1629-1635 gene:771 denotes CA XII
T1 1639-1656 disease:C0009404 denotes colorectal tumors
R1 T0 T1 associated_with CA XII,colorectal tumors

DisGeNET5_gene_disease

Id Subject Object Predicate Lexical cue
15849821-9#46#51#gene768 1623-1628 gene768 denotes CA IX
15849821-9#52#58#gene771 1629-1635 gene771 denotes CA XII
15849821-9#62#79#diseaseC0009404 1639-1656 diseaseC0009404 denotes colorectal tumors
46#51#gene76862#79#diseaseC0009404 15849821-9#46#51#gene768 15849821-9#62#79#diseaseC0009404 associated_with CA IX,colorectal tumors
52#58#gene77162#79#diseaseC0009404 15849821-9#52#58#gene771 15849821-9#62#79#diseaseC0009404 associated_with CA XII,colorectal tumors

PubMed_Structured_Abstracts

Id Subject Object Predicate Lexical cue
T1 150-268 OBJECTIVE denotes To analyze possible relationships between CA IX/CA XII and pVHL expression in normal and neoplastic colorectal mucosa.
T2 278-716 METHODS denotes Immunohistochemical staining of 42 tissue specimens obtained from 17 cancer patients was performed to evaluate the distribution and semi-quantitatively assess the levels of CA IX, CA XII and pVHL. VHL mRNAs from 14 fresh-frozen tumors was amplified by RT-PCR and subjected to sequencing. CA9 and CA12 mRNA levels were analyzed by semi-quantitative RT-PCR in comparison with VEGF as an indicator of hypoxia that uncouples the pVHL control.
T3 726-1257 RESULTS denotes Tumor tissues were associated with a borderline increase of CA IX staining signal and slight but significant decrease of CA XII immunoreactivity, whereas no association was found for pVHL. Sequence analysis of RT-PCR-amplified VHL mRNAs revealed no deletions/mutations, suggesting that they were VHL-competent. We did not observe any correlation between pVHL and CA IX/CA XII proteins as well as between VEGF and CA9 mRNAs, but the tumor-associated changes in mRNA levels of VEGF and CA12 showed a significant inverse relationship.
T4 1270-1729 CONCLUSIONS denotes Our results indicate that CA9 and CA12 are regulated by different intratumoral factors and that lack of apparent relationship between the levels of CA IX/CA XII and pVHL cannot be fully assigned to uncoupling of negative regulatory function of pVHL by tumor hypoxia signified by induced VEGF transcription. The interplay between the functional pVHL and CA IX/CA XII in colorectal tumors seems rather complex and is not evident merely at the expression levels.