Breast Cancer
Preclinical studies indicate that cyclin D1-CDK4/6 may be necessary in sustaining the tumorigenic potential of breast cancer cells.4 In hormone-receptor–positive breast cancer, certain CDK4/6 alterations can cause resistance to endocrine therapy.5
Glioblastoma
In patients with GBMs, the CDK4/6-Rb-E2F pathway was disrupted in 78%. And amplification/overexpression of CDK4 was detected in up to 20%.6
Head and Neck Cancer
Human papillomavirus (HPV)-negative squamous cell carcinoma of the head and neck is driven by genetic aberrations resulting in CDK4/6 activation.7
Liposarcoma
CDK4 is amplified in >95% of patients with well-differentiated/dedifferentiated liposarcomas.8
Mantle Cell lymphoma
MCL pathogenesis are associated with cell cycle CDK-Rb pathways and are potential targets for relapsed-lymphoma therapy.9
Melanoma
Crosstalk between CDK4 and CDK6 regulate cell proliferation, viability, migration, and angiogenesis in melanoma.10 In hereditary melanoma, germline mutations in CDK4 have been noted, although it likely plays a minor role.11
Neuroblastoma
The involvement of CDK4/6 in neuroblastoma pathogenesis suggests that deregulation could be a factor in driving neuroblastoma tumorigenesis.12 CDK4/6 is highly expressed in neuroblastoma. Amplification of CDK4 is associated with poor prognosis.13
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