In conclusion, the <i>MDR1</i> gene and P-glycoprotein have a positive correlation with the occurrence of gastrointestinal tumors, and a negative correlation between the <i>MDR1</i> gene and P-glycoprotein with resistance of chemotherapeutic drugs.
Two 8-bp polyadenine tracts of the ACVR2 gene are targets for inactivating frameshift mutations in gastrointestinal neoplasms having microsatellite instability (MSI).
Differences were apparent in gastrointestinal tumors and smooth muscle cells where monoclonal antibodies (mAbs) to the first epidermal growth factor (EGF) domain (CD97(EGF)) showed a more restricted staining pattern than mAbs to the stalk region (CD97(stalk)).
Differences were apparent in gastrointestinal tumors and smooth muscle cells where monoclonal antibodies (mAbs) to the first epidermal growth factor (EGF) domain (CD97(EGF)) showed a more restricted staining pattern than mAbs to the stalk region (CD97(stalk)).
To investigate the role of ADM in gastrointestinal tumor progression, we determined the expression levels of ADM in 72 cases of stomach cancer and 84 cases of colon cancer and determined whether there was an association between the ADM expression levels and pathological parameters or clinical survival rates.
Reference intervals for gastrointestinal tumor markers (AFP, CEA, CA199 and CA724) in healthy adults of Han nationality in Chongqing by Roche ECLIA system.
There was no correlation between this resistance phenotype and the presence or absence of constitutive mitogen-activated protein kinase (MAPK) and/or AKT pathway activation, commonly observed in gastrointestinal tumors.
Examples of these molecularly targeted biomarker therapies are: tyrosine kinase inhibitors in chronic myeloid leukemia and gastrointestinal tumors; anaplastic lymphoma kinase (ALK) inhibitors in lung cancer with EML4-ALk fusion; HER2/neu blockage in HER2/neu-positive breast cancer; and epidermal growth factor receptors (EGFR) inhibition in EGFR-mutated lung cancer.
Because genetic and epigenetic alterations of the adenomatous polyposis coli (APC) gene are common events in gastrointestinal tumor development, we sought to investigate the frequency and level of aberrant APC promoter methylation in primary tumors and paired preoperative serum or plasma samples of lung cancer patients by semiquantitative methylation-specific fluorogenic real-time PCR.
The mutated genes with positive or negative roles in cell growth or survival in aneuploid gastrointestinal cancer (e.g., APC, K-ras, and p53) are less frequently mutated in near-diploid MMP gastrointestinal tumors.
Established MSH6-null mice present a frequent occurrence of gastrointestinal tumors without microsatellite instability (MI), suggesting the possibility of the APC gene being a mutational target.
Apobec-1 messenger RNA (mRNA) undergoes alternative splicing, generating a catalytically inactive peptide, apobec-T. We have examined apobec-1 gene expression in human gastrointestinal tumors and in colon cancer-derived cell lines.
Our results demonstrate a novel mechanism for activation of beta-catenin in gastrointestinal tumors and support the concept that overexpression of p73 isoforms can play an important role in tumorigenesis.
Interestingly, while the AC-mRNA is expressed in all segments of the normal gastrointestinal tract, none of the gastrointestinal tumor tissues had any AC-mRNA expression.
Frameshifts in short mononucleotide tracts (SMT) in genes, such as TGFbetaRII and BAX, are common in gastrointestinal tumors of the microsatellite mutator phenotype (MMP).
Mutational studies of 57 sporadic gastrointestinal tumor DNAs revealed the presence of length variations in three of them: (a) BLM; (b) CBL; and (c) HOXA1.