The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
Cisplatin Resistance Associated with PARP Hyperactivation
Published version of a preprint
Abstract
Non–small cell lung carcinoma patients are frequently treated with cisplatin (CDDP), most often yielding temporary clinical responses. Here, we show that PARP1 is highly expressed and constitutively hyperactivated in a majority of human CDDP-resistant cancer cells of distinct histologic origin. Cells manifesting elevated intracellular levels of poly(ADP-ribosyl)ated proteins (PARhigh) responded to pharmacologic PARP inhibitors as well as to PARP1-targeting siRNAs by initiating a DNA damage response that translated into cell death following the activation of the intrinsic pathway of apoptosis. Moreover, PARP1-overexpressing tumor cells and xenografts displayed elevated levels of PAR, which predicted the response to PARP inhibitors in vitro and in vivo more accurately than PARP1 expression itself. Thus, a majority of CDDP-resistant cancer cells appear to develop a dependency to PARP1, becoming susceptible to PARP inhibitor–induced apoptosis. Cancer Res; 73(7); 2271–80. ©2013 AACR.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“However, mitotic catastrophe appears to constitute a major mechanism of action of anticancer chemotherapeutics, mostly reflecting the increased resistance of neoplastic cells to the induction of intrinsic apoptosis [1004–1009].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [1005]
Citations
Cites
Jemal, A., Bray, F., Ferlay, J., Ward, E., & Forman, D. (2011) · CA A Cancer Journal for Clinicians · doi:10.3322/caac.20107 · Cited by 55,079
Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
Farmer, H., McCabe, N., Lord, C. J., Tutt, A. N. J., Johnson, D. A., Richardson, T. B., Santarosa, M., Dillon, K. J., Hickson, I., Knights, C., et al. (2005) · Nature · doi:10.1038/nature03445 · Cited by 6,683
Gefitinib or Chemotherapy for Non–Small-Cell Lung Cancer with Mutated EGFR
Maemondo, M., Inoue, A., Kobayashi, K., Sugawara, S., Oizumi, S., Isobe, H., Gemma, A., Harada, M., Yoshizawa, H., Kinoshita, I., et al. (2010) · New England Journal of Medicine · doi:10.1056/nejmoa0909530 · Cited by 5,525
Inhibition of Poly(ADP-Ribose) Polymerase in Tumors from BRCA Mutation Carriers
Fong, P. C., Boss, D. S., Yap, T. A., Tutt, A., Wu, P., Mergui-Roelvink, M., Mortimer, P., Swaisland, H., Lau, A., O'Connor, M. J., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0900212 · Cited by 3,634
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Self-citationMolecular mechanisms of cisplatin resistance
Galluzzi, L., Senovilla, L., Vitale, I., Michels, J., Martins, I., Kepp, O., Castedo, M., & Kroemer, G. (2012) · Oncogene · doi:10.1038/onc.2011.384 · Cited by 2,760
Self-citationGalluzzi, L., Vitale, I., Abrams, J. M., Alnemri, E. S., Baehrecke, E. H., Blagosklonny, M. V., Dawson, T. M., Dawson, V. L., El-Deiry, W. S., Fulda, S., et al. (2012) · Cell Death & Differentiation · doi:10.1038/cdd.2011.96 · Cited by 2,421
Self-citationAudeh, M. W., Carmichael, J., Penson, R. T., Friedlander, M., Powell, B., Bell-McGuinn, K. M., Scott, C., Weitzel, J. N., Oaknin, A., Loman, N., et al. (2010) · The Lancet · doi:10.1016/s0140-6736(10)60893-8 · Cited by 2,279
Poly(ADP-ribosyl)ation reactions in the regulation of nuclear functions
D’Amours, D., Desnoyers, S., D’Silva, I., & Poirier, G. G. (1999) · Biochemical Journal · doi:10.1042/bj3420249 · Cited by 1,819
Principles of cancer therapy: oncogene and non-oncogene addiction
Luo, J., Solimini, N. L., & Elledge, S. J. (2009) · Cell · doi:10.1016/j.cell.2009.02.024 · Cited by 1,765
Cited by
Sorted by citations
Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680
Self-citationModulation of oxidative stress as an anticancer strategy
Gorrini, C., Harris, I. S., & Mak, T. W. (2013) · Nature Reviews Drug Discovery · doi:10.1038/nrd4002 · Cited by 3,579
Systems biology of cisplatin resistance: past, present and future
Galluzzi, L., Vitale, I., Michels, J., Brenner, C., Szabadkai, G., Harel-Bellan, A., Castedo, M., & Kroemer, G. (2014) · Cell Death & Disease · doi:10.1038/cddis.2013.428 · Cited by 782
Self-citationThe multifaceted role of reactive oxygen species in tumorigenesis
Kirtonia, A., Sethi, G., & Garg, M. (2020) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-020-03536-5 · Cited by 452
Cisplatin in the modern era: The backbone of first-line chemotherapy for non-small cell lung cancer
Fennell, D. A., Summers, Y., Cadranel, J. L., Benepal, T., Christoph, D. C., Lal, R., Das, M., Maxwell, F., Visseren‐Grul, C., & Ferry, D. (2016) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2016.01.003 · Cited by 382
Metadata
- Authors
- Michels, J., Vitale, I., Galluzzi, L., Adam, J., Olaussen, K. A., Kepp, O., Senovilla, L., Talhaoui, I., Guegan, J., Enot, D. P., Talbot, M., Robin, A., Girard, P., Oréar, C., Lissa, D., Sukkurwala, A. Q., Garcia, P., Behnam-Motlagh, P., Kohno, K., Wu, G. S., Brenner, C., Dessen, P., Saparbaev, M., Soria, J.-C., Castedo, M., & Kroemer, G.
- Affiliations
- Université Paris-Sud (FR)
- Authors' Affiliations: 1U848, 2U981, 3U985, INSERM; 4Institut Gustave Roussy; 5Université Paris Sud; 6UMR8200, CNRS; Plateformes de 7Bioinformatique, 8Génomique, and 9Metabolomique, Institut Gustave Roussy; Villejuif; 10Université Paris Descartes; 11Department of Thoracic Oncology, Institut Mutualiste Montsouris; 12Equipe 11 labellisée par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers; 13Pôle de Biologie, Hôpital Européen Georges Pompidou AP-HP, Paris; 14U769, INSERM-LabEx LERMIT, Université Paris-Sud, Châtenay Malabry, France; 15Department of Medical Biosciences, Clinical Chemistry, Umeå University, Umeå, Sweden; 16Department of Molecular Biology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu/Fukuoka, Japan; and 17Molecular Therapeutics Program, Karmanos Cancer Institute, Department of Oncology and Pathology, Wayne State University School of Medicine, Detroit, Michigan
- ORCID
- Venue
- Cancer Research
- Published
- 2013-04-01
- Volume
- 73
- Issue
- 7
- Pages
- 2271-2280
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2060534647
- Cited by
- 176
- References
- 47
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 10 · 2023: 10 · 2022: 11 · 2021: 15 · 2020: 14 · 2019: 12 · 2018: 13 · 2017: 15 · 2016: 17 · 2015: 19 · 2014: 18 · 2013: 8
- FWCI
- 11.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- U.S. Food and Drug Administration
- Topics
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- cisplatin resistance, PARP1, PARP inhibitors, non-small cell lung cancer, DNA damage response, mitochondrial apoptosis, poly(ADP-ribosyl)ation, siRNA knockdown, xenografts, chemoresistance
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Poly (ADP-Ribose) Polymerase-1, Animals, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Cisplatin, Female, Humans, Lung Neoplasms, Mice, Nude, Phenanthrenes, Poly(ADP-ribose) Polymerases, RNA, Messenger, Tumor Cells, Cultured, Blotting, Western, Apoptosis, Drug Resistance, Neoplasm, Reverse Transcriptase Polymerase Chain Reaction, Xenograft Model Antitumor Assays, Cell Proliferation, Mice, Real-Time Polymerase Chain Reaction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review