CDK4 (Cyclin-dependent kinase 4)

These results suggest that PPI exerts antitumor effects against BxPC-3 cells by inhibiting STAT3 phosphorylation.

In this cohort, using a careful methodology, BRCA1/2 and PALB2 mutation carriers had reduced PFS with first-line ET + CDK4/6i compared to wild-type patients.

Aromatase inhibitor plus CDK4/6i as first-line treatment followed by fulvestrant as second-line treatment (CDK4/6i first-line group) vs aromatase inhibitor as first-line treatment followed by fulvestrant plus CDK4/6i as second-line treatment (CDK4/6i second-line group)...Post hoc analysis suggests an OS benefit with first-line use in premenopausal patients. ClinicalTrials.gov Identifier: NCT03425838.

P=N/A, N=204, Completed, AstraZeneca | Recruiting --> Completed

Treatment with FAM117A or pharmacological inhibition of CDK4/6 reduced the in vitro and in vivo tumor growth. Thus, FAM117A links intrinsic cell cycle regulation with the extrinsic immune microenvironment, providing a rationale for combined therapies that address macrophage-tumor and cell cycle regulatory events in LUAD.

Melanoma-dominant syndromes, such as CDKN2A , CDK4 , and POT1 , and melanoma-subordinate syndromes are described herein. Knowledge of these conditions will enable surgeons to incorporate these genetic insights into clinical practice and offer more personalised and effective care to patients with melanoma.

The uptake level of cascade test can be acceptable. Hospitals need to maintain contact with the young untested relatives until they have achieved sufficient growth to undertake cascade test.

P1/2, N=230, Recruiting, Exscientia AI Ltd., a wholly owned subsidiary of Recursion Pharmaceuticals, Inc. | N=165 --> 230

Collectively, these factorial results provide compelling evidence that propranolol may interact with core oncogenic kinase cluster and potential modulation of the critical signaling cascades implicated in HCC pathogenesis. Collectively, these computational findings support the hypothesis that propranolol possesses the molecular characteristics of a viable therapeutic candidate for HCC, thereby substantiating the need for rigorous experimental and translational investigation to validate its clinical potential.

Thus, our data support a model in which cyclin D1/D2-CDK4 promotes phosphorylation of Smad3, leading to upregulation of integrin subunits, activation of FAK and Rac1, and consequent lamellipodia formation and cell migration. These findings provide direct evidence that CDK4 regulates actin cytoskeletal reorganization during cell migration and suggest that CDK4/6 inhibitors may dampen cytoskeleton-dependent tumor invasion, in addition to their antiproliferative effects.

Background: Evidence on the efficacy of alpelisib in combination with fulvestrant after progression on CKD4/6 inhibitors (CDK4/6i) is derived from a single non-comparative prospective study. Our results regarding the efficacy of alpelisib plus ET were inferior to those reported in the current literature. Conversely, outcomes of everolimus plus exemestane were consistent with the current literature, denoting that the combination is an acceptable treatment option for patients with PIK3CA-mutant metastatic BC.

These findings suggest that NogoA regulates both tumour behaviour and immune remodelling in TNBC by enhancing NK cell-mediated cytotoxicity, promoting apoptosis and suppressing immune evasion pathways. Targeting the NgR1/NogoA axis may therefore represent a promising approach to strengthen NK cell-based immunotherapy, offering a novel therapeutic avenue in TNBC.