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The frequencies of ALK, ROS1 and RET (show RET Proteins) 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 (show EGFR Proteins) therapy in IHCC
Polymorphisms rs1333049 and rs10757278 are associated with SCD (show SCD Proteins) 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.
Durable benefits with pemetrexed-based therapies in RET (show RET Proteins)-rearranged lung cancers are comparable with ALK- and ROS1-rearranged lung cancers. When selecting therapies for patients with RET (show RET Proteins)-rearranged lung cancers, pemetrexed-containing regimens should be considered.
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