Results 181 to 190 of about 3,443,356 (396)

The Combination of the PARP Inhibitor Olaparib and the WEE1 Inhibitor AZD1775 as a New Therapeutic Option for Small Cell Lung Cancer

open access: yesClinical Cancer Research, 2018
Purpose: Introduced in 1987, platinum-based chemotherapy remains standard of care for small cell lung cancer (SCLC), a most aggressive, recalcitrant tumor.
A. Lallo   +20 more
semanticscholar   +1 more source

Vorinostat Potentiates Chemoimmunotherapy in Immune‐Enriched Pancreatic Cancer

open access: yesAdvanced Science, EarlyView.
Immune‐enriched pancreatic cancer does not confer a significant survival advantage. SAHA sensitizes these “hot” tumors to chemoimmunotherapy by disrupting a FASN/PARP9‐driven “metabolic trap” and enhancing CD8+ T cell function. A CD8high/FASNhigh/PARP9high signature identifies patients who are most likely to benefit from the “gemcitabine‐nivolumab‐SAHA”
Chen Chen   +13 more
wiley   +1 more source

Phase I, Dose-Escalation, Two-Part Trial of the PARP Inhibitor Talazoparib in Patients with Advanced Germline BRCA1/2 Mutations and Selected Sporadic Cancers

open access: yesCancer Discovery, 2017
Talazoparib inhibits PARP catalytic activity, trapping PARP1 on damaged DNA and causing cell death in BRCA1/2-mutated cells. We evaluated talazoparib therapy in this two-part, phase I, first-in-human trial.
J. D. de Bono   +15 more
semanticscholar   +1 more source

Detachment‐Induced FAK‐STAT3‐NNMT Inhibits CTCs Anoikis to Promote Breast Cancer Metastasis by Enhancing Fatty Acid Oxidation

open access: yesAdvanced Science, EarlyView.
The FAK‐STAT3‐NNMT axis drives anoikis resistance in circulating tumor cells by reprogramming fatty acid oxidation. Targeting this metabolic vulnerability suppresses metastasis, untangling a key mechanism of breast cancer progression and revealing NNMT as a promising therapeutic target.
Qingchao Tong   +13 more
wiley   +1 more source

Supplementary Figure Legends from The CHK1 Inhibitor Prexasertib Exhibits Monotherapy Activity in High-Grade Serous Ovarian Cancer Models and Sensitizes to PARP Inhibition

open access: gold, 2023
Kalindi Parmar   +18 more
openalex   +1 more source

Disruption of the SNRPF–DDX24–E2F4 Feedback Loop Uncouples Splicing and Transcriptional Regulation to Suppress Ovarian Cancer Progression

open access: yesAdvanced Science, EarlyView.
This study identifies SNRPF as a critical oncogenic driver in ovarian cancer. By regulating a self‐sustaining SNRPF–DDX24–E2F4 feedback loop through intron retention and nonsense‐mediated decay, SNRPF couples RNA splicing with transcriptional regulation to promote tumor progression.
Yingwei Li   +4 more
wiley   +1 more source

Exploring the radiochemistry of PARP inhibitors: a new era in therapy and imaging

open access: yesEJNMMI Radiopharmacy and Chemistry
Background Poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as a promising class of therapeutics, particularly in the treatment of cancers with defective DNA repair mechanisms, such as those with breast cancer genes (BRCA) mutations.
Gianluca Destro   +4 more
doaj   +1 more source

Data from <i>BRCA</i> Reversion Mutations in Circulating Tumor DNA Predict Primary and Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma

open access: gold, 2023
Kevin Lin   +24 more
openalex   +1 more source

The Polymers of Life: Exploring Cellular Function Through Polymer Concepts

open access: yesAdvanced Science, EarlyView.
Biomolecular phase separation reveals that a hidden layer of cellular organization is governed by the principles of polymer science. This review bridges polymer physics and cell biology, offering a primer on fundamental concepts, proposing a framework for interrogating cellular function, and synthesizing biophysical methods for decoding macromolecular ...
Mark Chen, Ashutosh Chilkoti
wiley   +1 more source

Supplementary Figures and Tables from ATF6-Mediated Signaling Contributes to PARP Inhibitor Resistance in Ovarian Cancer

open access: gold, 2023
Alexandra McMellen   +13 more
openalex   +1 more source

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