Researchers from Wenzhou Medical University and affiliated organizations have published data from a study that aimed to investigate the relationship between the tumor suppressor microRNA-143 (miR-143) and RNA-binding protein Musashi homolog 2 (MSI2), the abnormal expression of which has been previously associated with cancer progression.
It was previously shown that AXL overexpression is associated with poor prognosis, metastasis, as well as drug resistance in various hematological and solid tumors, and that inhibition of AXL phosphorylation could overcome drug resistance to FLT3 inhibitors. CTS-2016 is an AXL/FLT3 inhibitor being developed by Cytosinlab Therapeutics Co. Ltd. as a novel tyrosine kinase inhibitor for cancer.
Although FMS-like tyrosine kinase 3 (FLT3) inhibitors have shown success treating FLT3-mutated acute myeloid leukemia (AML), around 30% to 50% of patients show primary resistance to both type I and type II inhibitors. Therefore, identifying therapeutic strategies to overcome this resistance and enhance the efficacy of FLT3 inhibitors remains an urgent need.
Daiichi Sankyo Co Ltd. has experienced yet another setback with its quizartinib NDA submission, as the U.S. FDA has now extended the review period by three months to July 24, 2023, to allow additional time to review requested updates to the proposed Risk Evaluation and Mitigation Strategies.
Daiichi Sankyo Co Ltd. has experienced yet another setback with its quizartinib NDA submission, as the U.S. FDA has now extended the review period by three months to July 24, 2023, to allow additional time to review requested updates to the proposed Risk Evaluation and Mitigation Strategies. No additional efficacy or safety data has been requested.
Mutations in fms-related receptor tyrosine kinase 3 (FLT3) are related to the increase of reactive oxygen species (ROS) in acute myeloid leukemia (AML). Recent studies suggest that by regulating ROS production and antioxidant expression, oncogenes such as FLT3 directly influence leukemia progression, even during anticancer therapy.
Function Oncology Inc. emerged from stealth on April 12 with the announcement of a $28 million series A financing that will continue support development of its CRISPR-enabled platform to profile cancer in patient-specific detail. The platform goes beyond next-generation sequencing to measure gene function, potentially allowing identification of new therapeutic targets and better matching of available therapies to vulnerabilities in an individual’s tumors.
Cancer treatment developer Apollomics Inc. merged with special purpose acquisition company (SPAC) Maxpro Capital Acquisition Corp., gaining a listing on Nasdaq under the ticker APLM and raising $23.65 million of private investment in public equity (PIPE).
.png?height=488&t=1670008838&width=650 "Acute myeloid leukemia")
