Article in Molecular cancer therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
9 authors.
Mannan Nouri *Division of Medical Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-7442-9251
Andreas Varkaris *Division of Medical Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.ORCID 0000-0001-5776-8844
Susan L DalrympleDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center (SKCCC), Baltimore, Maryland.ORCID 0000-0003-1330-1964
Christopher M DennehyDivision of Medical Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.ORCID 0009-0007-5178-0915
John T IsaacsDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center (SKCCC), Baltimore, Maryland.ORCID 0000-0002-3854-4658
David J EinsteinDivision of Medical Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.ORCID 0000-0001-9163-3281
W N BrennenDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center (SKCCC), Baltimore, Maryland.ORCID 0000-0001-9807-7433
Steven P BalkDivision of Medical Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-4546-7371
Funding
Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI LODA, MASSIMO · 2002 to 2017
$36.2M
Steroid Metabolism in Castration-Resistant Prostate CancerP01CA163227 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Steven P. Balk · 2013 to 2026
$25.0M
Molecular Determinants of Response and Resistance to EZH2 and PARP inhibition in Prostate CancerP50CA272390 · NCI · DANA-FARBER CANCER INST · PI Steven P. Balk, Himisha Beltran · 2023 to 2026
$12.0M
Enhancing the Efficacy of Docetaxel in Prostate CancerR01CA266704 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Steven P. Balk, PARASKEVI GIANNAKAKOU · 2022 to 2026
$3.2M
A First-in-Class FAP-activated Protoxin to disrupt the Tumor-Stroma Parasitic Cycle fueling lethal Prostate Cancer ProgressionR01CA255259 · NCI · JOHNS HOPKINS UNIVERSITY · PI BRENNEN, WILLIAM NATHANIEL · 2021 to 2025
$2.1M
Prostate Cancer Vulnerabilities to BH3 Mimetic DrugsR01CA262536 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BALK, STEVEN P. · 2021 to 2025
$2.0M
American Society of Clinical Oncology (ASCO) 2021A010981NCI NIH HHS P01 CA163227NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA090381NCI NIH HHS P50 CA272390NCI NIH HHS R01 CA255259NCI NIH HHS R01 CA262536NCI NIH HHS R01 CA266704Prostate Cancer Foundation (PCF) Challenge AwardU.S. Department of Defense (DOD) PC200820U.S. Department of Defense (DOD) W81xwh-17-1-0350
6 · The paper itself
Abstract
Polo-like kinase 1 (PLK1) inhibitors have had limited antitumor efficacy as single agents, and focus of current efforts is on combination therapies. We initially confirmed that the PLK1-specific inhibitor onvansertib (ONV) could enhance responses to a PARP inhibitor (olaparib) in prostate cancer xenografts. To identify more effective combinations, we screened a library of bioactive compounds for efficacy in combination with ONV in LNCaP prostate cancer cells, which identified a series of compounds including multiple AKT inhibitors. We confirmed in vitro synergy between ONV and the AKT inhibitor ipatasertib (IPA) and found that the combination increased apoptosis. Mechanistic studies showed that ONV increased expression of the antiapoptotic protein SURVIVIN and that this was mitigated by IPA. Studies in three PTEN-deficient prostate cancer xenograft models showed that cotreatment with IPA and ONV led to significant tumor growth inhibition compared with monotherapies. Together, these in vitro and in vivo studies demonstrate that the efficacy of PLK1 antagonists can be enhanced by PARP or AKT inhibition and support further development of these combination therapies.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
AKT Inhibition Sensitizes to Polo-Like Kinase 1 Inhibitor Onvansertib in Prostate Cancer. · full record | OpenQuestion