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ROS1 gene rearrangement is associated with Non-Small-cell Lung Cancer.
Females were often inflicted by the EGFR mutations, especially for the exon 19 deletion and L858R mutation. There were significantly more ALK/ROS1 fusions in females compared to that in males and significantly more ALK/ROS1 fusions in patients <60 years old compared to patients older than 60 years of age. Exon 21 L858R and L861Q dominantly occurred in patients >/=60 years and exon 19 deletion in patients <60 years
ROS1 gene Rearrangement is associated with Metastatic Colorectal Cancer.
in 14 ROS1+ lung adenocarcinoma cases, 9 rearrangements detected (gene partner: CD74 in 8 cases and SLC34A2 in 1)
CEP72-ROS1 is a novel ROS1 fusion variant in non-small cell lung cancer (NSCLC) discovered by next-generation sequencing and could be included in ROS1 detection assay, such as reverse transcription PCR.
The upstream breakpoint lies in the same region as the breakpoint of a fused gene SLC34A2-ROS1, which encodes a constitutive kinase in the lung cancer cell line HCC78 and nonsmall-cell lung cancer (NSCLC), suggesting that the deletion in this family is a hot spot for recombination, not only in cancer samples with somatic mutation, but also in PAM patients with germline genetic defects of SLC34A2.
Although rare, patients with ovarian serous carcinoma or serous borderline tumor may exhibit ROS1 gene rearrangement and ROS1 protein expression
Study based on 47 tissue samples from spitzoid tumors revealed 2 BAP1-inactived cases. The absence of anomalous expression of translocation-related proteins ALK and ROS1 in this series, composed predominantly of low-grade/low-risk tumors, indicates that translocated spitzoid lesions may not be as prevalent as initially suggested, at least in some populations.
None of the genitourinary pseudosarcomatous myofibroblastic proliferations was found to harbour USP6 (0/12), ROS1 (0/8) or ETV6 (0/7) rearrangements
the results from three transcriptome-based platforms (Nanostring Elements, Agena LungFusion panel and ThermoFisher NGS fusion panel) were compared to those obtained from ALK, ROS1 and RET Fluorescence In Situ Hybridization on 51 clinical specimens.
lung adenocarcinoma in Asian patients aged =50 years had a higher gene mutation rate than in those aged >50 years, especially EML4-ALK and ROS1 fusion. Mutation analysis may be helpful in determining targeted therapy for the majority of these patients
The frequencies of ALK, ROS1 and RET rearrangements are low in non-adenocarcinoma NSCLC patients. And their clinical characteristics are similar to those in lung adenocarcinoma. Fusions of the above 3 genes are not prognostic factor for non-adnocarcinoma NSCLC patients.
Compared with ROS1-negative advanced NSCLCs,ROS1-rearranged advanced NSCLCs were associated with a younger age at presentation. ROS1 rearrangements were not significantly associated with sex, smoking history, drinking history and metastatic sites.
ROS1 rearrangement was detected in 1.1% of CCA patients. Although rare, conduct of clinical trials using ROS1 inhibitors in these genetically unique patients is warranted.
For intra-hepatic cholangiocarcinomas (IHCC)patients, ROS1, ALK and c-MET expression levels have prognostic significance on clinical outcomes. Although this finding may require further validation, it has led to proposal of a new stratification or enriched biomarker for future phase III trial of anti-EGFR therapy in IHCC
Polymorphisms rs1333049 and rs10757278 are associated with SCD in men and rs499818 in the women aged over 50 years.
Overcome crizotinib resistance in a ROS1-rearranged cancer.
The ROS1 S1986Y/F and ALK C1156Y mutations are homologous and displayed similar sensitivity patterns to ALK/ROS1 TKIs.
Given the results from the ROS1 cohort of the clinical trial PROFILE 1001, crizotinib represents a new treatment option and the first approved therapy for patients with metastatic non-small cell lung cancer whose tumors are ROS1 positive. Crizotinib demonstrated efficacy irrespective of prior treatment status.
ROS1 rearrangements rarely overlap with alterations in EGFR, KRAS, ALK, or other targetable oncogenes in NSCLC.
GPX1-dependent alterations in oxido-reductive stress promote ROS1 activation and mediate vascular remodeling.
Foretinib is a potent inhibitor of oncogenic ROS1 fusion proteins.
c-ros and its ligand may be necessary for differentiation of epithelia I and II in mouse.
This proto-oncogene, highly-expressed in a variety of tumor cell lines, belongs to the sevenless subfamily of tyrosine kinase insulin receptor genes. The protein encoded by this gene is a type I integral membrane protein with tyrosine kinase activity. The protein may function as a growth or differentiation factor receptor.
c-Ros receptor tyrosine kinase
, proto-oncogene c-Ros
, proto-oncogene c-Ros-1
, proto-oncogene tyrosine-protein kinase ROS
, receptor tyrosine kinase c-ros oncogene 1
, transmembrane tyrosine-specific protein kinase
, v-ros UR2 sarcoma virus oncogene homolog 1
, v-ros avian UR2 sarcoma virus oncogene homolog 1
, Ros1 proto-oncogene
, heart - derived c - ros - 1 proto - oncogene
, proto-oncogene c-ros