Improving Breast Cancer Therapy With CDK4/6 Inhibitors

Jaganathan, Hamsa; Overstreet, Karen; Reed, Elizabeth

doi:10.1016/j.clbc.2014.10.001

Cited by 3 publications

(3 citation statements)

References 6 publications

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“…Verification of variation of CDK2/CDC25C and JAK/STAT pathways According to previous reports, CDK2/CDK4/CDC25C played an important role in the regulation of cell cycle [17][18][19]. In many tumors, proliferation could be inhibited by the inhibitors of these cell cycle relative proteins [20][21][22]. And JAK2/STAT demonstrated the adjustment effect of proliferation, differentiation, apoptosis migration and immunity in cells according to previous researches [23][24][25][26].…”

Section: Identification Of Vtcn1 Associated Genes By Gene Set Enrichmmentioning

confidence: 81%

Effect of VTCN1 on progression and metastasis of ovarian carcinoma in vitro and vivo

Gao

Zhang

Chen

et al. 2015

Biomedicine & Pharmacotherapy

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Section: Identification Of Vtcn1 Associated Genes By Gene Set Enrichmmentioning

confidence: 81%

Effect of VTCN1 on progression and metastasis of ovarian carcinoma in vitro and vivo

Gao

Zhang

Chen

et al. 2015

Biomedicine & Pharmacotherapy

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“…In particular, CDK4/6 inhibitors seem to present suitable targets in a majority of patients with advanced cancer [ 25 , 26 ]. Besides CDK4/6 inhibitors palbociclib and LY2835219, which have shown high activity in breast cancer, a host similar drugs are under development, and fascaplysin and derivatives share the same target [ 27 ]. Proteins in this cell proliferative pathway include p16, an endogenous suppressor of CDK4/6, cyclin D1, the regulatory subunit of CDK4/6, and retinoblastoma (Rb) protein, a tumor suppressor [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Anticancer Activity of Fascaplysin against Lung Cancer Cell and Small Cell Lung Cancer Circulating Tumor Cell Lines

et al. 2018

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Lung cancer is a leading cause of tumor-associated mortality. Fascaplysin, a bis-indole of a marine sponge, exhibit broad anticancer activity as specific CDK4 inhibitor among several other mechanisms, and is investigated as a drug to overcome chemoresistance after the failure of targeted agents or immunotherapy. The cytotoxic activity of fascaplysin was studied using lung cancer cell lines, primary Non-Small Cell Lung Cancer (NSCLC) and Small Cell Lung Cancer (SCLC) cells, as well as SCLC circulating tumor cell lines (CTCs). This compound exhibited high activity against SCLC cell lines (mean IC50 0.89 µM), as well as SCLC CTCs as single cells and in the form of tumorospheres (mean IC50 0.57 µM). NSCLC lines showed a mean IC50 of 1.15 µM for fascaplysin. Analysis of signal transduction mediators point to an ATM-triggered signaling cascade provoked by drug-induced DNA damage. Fascaplysin reveals at least an additive cytotoxic effect with cisplatin, which is the mainstay of lung cancer chemotherapy. In conclusion, fascaplysin shows high activity against lung cancer cell lines and spheroids of SCLC CTCs which are linked to the dismal prognosis of this tumor type. Derivatives of fascaplysin may constitute valuable new agents for the treatment of lung cancer.

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“…91 In addition, the combination therapies have also exhibited improved anticancer activity compared to the single inhibitors of CDK9. The combination of AZD-4573 (16) with acalabrutinib, an inhibitor of bruton tyrosine kinase (BTK), resulted in enhanced antitumor activity in BTK inhibitor-sensitive in vivo models. 138 A combination of BAY-1143572 (7) with 5-fluorouracil exhibited synergistic antitumorigenic effects against esophageal adenocarcinoma.…”

Section: Summary and Perspectivesmentioning

confidence: 99%

Recent Developments in the Biology and Medicinal Chemistry of CDK9 Inhibitors: An Update

Qin

Tian

et al. 2020

J. Med. Chem.

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Cyclin-dependent kinase 9 (CDK9), which regulates transcriptional elongation, is an attractive therapeutic target for many cancers, especially for cancers driven by transcriptional dysregulation. In particular, CDK9 promotes RNA polymerase II pause/release, a rate-limiting step in normal transcriptional regulation that is frequently dysregulated in cancers. Emerging evidence indicates that selective CDK9 inhibition or degradation may provide a therapeutic benefit against certain cancers. Indeed, the development of CDK9 modulators (inhibitors and degraders) has attracted great attention, with several molecules currently under clinical development. This review provides an overview of recent advances in CDK9 modulators in general, with special emphasis on compounds under clinical evaluation and new emerging strategies, such as proteolysis targeting chimeras (PROTACs).

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Improving Breast Cancer Therapy With CDK4/6 Inhibitors

Cited by 3 publications

References 6 publications

Effect of VTCN1 on progression and metastasis of ovarian carcinoma in vitro and vivo

Effect of VTCN1 on progression and metastasis of ovarian carcinoma in vitro and vivo

Anticancer Activity of Fascaplysin against Lung Cancer Cell and Small Cell Lung Cancer Circulating Tumor Cell Lines

Recent Developments in the Biology and Medicinal Chemistry of CDK9 Inhibitors: An Update

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