ArticleCell death & disease2014
Triggering necroptosis in cisplatin and IAP antagonist-resistant ovarian carcinoma.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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.
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Who cites it
31 citing papers in PubMed, 66 citations in OpenAlex.
- Birinapant enhances cisplatin sensitivity in epithelial ovarian cancer through modulation of apoptotic and survival signaling pathways.Cancer chemotherapy and pharmacology · 2026Article
- Programmed cell death in cancer: targeting necroptosis to kill tumor cell.Cell death discovery · 2026Review
- Cisplatin resistance in ovarian cancer: exploration and insights from metal ion homeostasis imbalance.Frontiers in cell and developmental biology · 2026Review
- Liquid Plasma Induces Necroptosis Without Inflammatory Responses in Head and Neck Cancer Cells.World journal of oncology · 2025Article
- Targeting mitochondria: a novel approach for treating platinum-resistant ovarian cancer.Journal of translational medicine · 2024Review
- Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024Review
- Cyclophosphamide induces ovarian granulosa cell ferroptosis via a mechanism associated with HO-1 and ROS-mediated mitochondrial dysfunction.Journal of ovarian research · 2024Article
- Ferroptosis: mechanism, immunotherapy and role in ovarian cancer.Frontiers in immunology · 2024Review
- Acetylshikonin induces necroptosis via the RIPK1/RIPK3-dependent pathway in lung cancer.Aging · 2023Article
- Necroptosis-related genes are associated with prognostic features of kidney renal clear cell carcinoma.Discover oncology · 2023Article
- A comprehensive pan-cancer analysis of necroptosis molecules in four gynecologic cancers.BMC cancer · 2022Article
- Fisetin-induced cell death in human ovarian cancer cell lines via zbp1-mediated necroptosis.Journal of ovarian research · 2022Article
- Ferroptosis, necroptosis, and pyroptosis in the occurrence and development of ovarian cancer.Frontiers in immunology · 2022Review
- Platinum drugs and taxanes: can we overcome resistance?Cell death discovery · 2021Review
- Tumor-intrinsic determinants of immunogenic cell death modalities.Oncoimmunology · 2021Review
- XIAP Knockdown in Alcohol-Associated Liver Disease Models Exhibits DivergentFrontiers in physiology · 2021Article
- IAP-1 promoted cisplatin resistance in nasopharyngeal carcinoma via inhibition of caspase-3-mediated apoptosis.American journal of cancer research · 2021Article
- Necroptosis in Cholangiocarcinoma.Cells · 2020Review
- Necroptosis in stressed ovary.Journal of biomedical science · 2019Review
- Exploiting Necroptosis for Therapy of Acute Lymphoblastic Leukemia.Frontiers in cell and developmental biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Ovarian cancer patients are typically treated with carboplatin and paclitaxel, but suffer a high rate of relapse with recalcitrant disease. This challenge has fostered the development of novel approaches to treatment, including antagonists of the 'inhibitor of apoptosis proteins' (IAPs), also called SMAC mimetics, as apoptosis-inducing agents whose action is opposed by caspase inhibitors. Surprisingly, IAP antagonist plus caspase inhibitor (IZ) treatment selectively induced a tumor necrosis factor-α (TNFα)-dependent death among several apoptosis-resistant cell lines and patient xenografts. The induction of necroptosis was common in ovarian cancer, with expression of catalytically active receptor-interacting protein kinase-3 (RIPK3) necessary for death, and in fact sufficient to compromise survival of RIPK3-negative, necroptosis-resistant ovarian cancer cells. The formation of a necrosome-like complex with a second critical effector, receptor-interacting serine-threonine kinase-1 (RIPK1), was observed. RIPK1, RIPK3 and TNFα were required for the induction of death, as agents that inhibit the function of any of these targets prevented cell death. Abundant RIPK3 transcript is common in serous ovarian cancers, suggesting that further evaluation and targeting of this RIPK3-dependent pathway may be of clinical benefit.
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Registered trials
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.