We identified a novel pathogenic homozygous c.948A>G (p.Ile316Met) mutation in the MET gene in one deaf Moroccan young girl carrying a total bilateral non-syndromic hearing impairment.
<b>Conclusion:</b> Our case-control study suggests that MET T1010I seems to be a risk factor for TNBC in the Caucasian Greek population, in contrast with MET rs40239, where no correlation was found.
<b>Conclusion:</b> Our case-control study suggests that MET T1010I seems to be a risk factor for TNBC in the Caucasian Greek population, in contrast with MET rs40239, where no correlation was found.
<b>Conclusion:</b> Our case-control study suggests that MET T1010I seems to be a risk factor for TNBC in the Caucasian Greek population, in contrast with MET rs40239, where no correlation was found.
<b>Conclusion:</b> Our case-control study suggests that MET T1010I seems to be a risk factor for TNBC in the Caucasian Greek population, in contrast with MET rs40239, where no correlation was found.
Two SNPs, rs147960238 in CD163 (p = 2.2 × 10<sup>-5</sup>) and rs17138945 in MET (p = 5.6 × 10<sup>-5</sup>) were significantly associated with survival of patients with lower-grade glioma.
Among them, the MET p.N375S and MLH1 p.V384D mutations, each was detected in two cases, and has rarely been found to be involved in thyroid cancer pathogenesis before.
Among them, the MET p.N375S and MLH1 p.V384D mutations, each was detected in two cases, and has rarely been found to be involved in thyroid cancer pathogenesis before.
Among them, the MET p.N375S and MLH1 p.V384D mutations, each was detected in two cases, and has rarely been found to be involved in thyroid cancer pathogenesis before.
Finally, a <i>MET</i>ex14 del mutation-positive NSCLC patient who responded to crizotinib but later relapsed, demonstrated a mixed response to glesatinib including reduction in size of a <i>MET</i> Y1230H mutation-positive liver metastasis and concurrent loss of detection of this mutation in plasma DNA.<b>Conclusions:</b> Together, these data demonstrate that glesatinib exhibits a distinct mechanism of target inhibition and can overcome resistance to type I MET inhibitors.<i></i>.
Hence, although the juxtamembrane mutations of MET do not affect its known proteolytic cleavages, the R970C MET variant favors calpain dependent proteolytic cleavage in lung cancer</span> cells.
Hence, although the juxtamembrane mutations of MET do not affect its known proteolytic cleavages, the R970C MET variant favors calpain dependent proteolytic cleavage in lung cancer</span> cells.
Hence, although the juxtamembrane mutations of MET do not affect its known proteolytic cleavages, the R970C MET variant favors calpain dependent proteolytic cleavage in lung cancer</span> cells.
Our findings have shown that the SNPs rs41281081 and rs76322625 in MET 3'UTR, through disruption of the regulatory role of miR-335 and miR-1026 in MET expression, may act as promoting factors in the pathogenesis of NSCLC.
Furthermore, the carriers of the GA and AA genotypes in rs41281081, and the CU and UU genotypes in rs76322625 presented with poor cell differentiation and large tumor size, as well as a high probability of metastasis.
Furthermore, the carriers of the GA and AA genotypes in rs41281081, and the CU and UU genotypes in rs76322625 presented with poor cell differentiation and large tumor size, as well as a high probability of metastasis.
A selective effect of MET-T1010I as compared to wild type MET on cell invasion both in-vitro and in-vivo suggests that the MET-T1010I SNP may alter tumor pathophysiology and should be considered as a potential biomarker when implementing MET targeted clinical trials.
The HGF growth factor receptor MET is potentially functionally altered due to an uncommon germline single nucleotide polymorphism (SNP), MET-T1010I, in many cancer lineages including breast cancer where the MET-T1010I SNP is present in 2% of patients with metastatic breast cancer.