Farmer, H. et al. Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. Nature 434, 917–921 (2005).
Bryant, H. E. et al. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase. Nature 434, 913–917 (2005). Together with Farmer et al. (2005), this study describes the discovery of the BRCA1/2 versus PARPi synthetic lethal effects.
Weinstein, I. B. Cancer. Addiction to oncogenes — the Achilles heal of cancer. Science 297, 63–64 (2002).
Hartwell, L. H., Szankasi, P., Roberts, C. J., Murray, A. W. & Friend, S. H. Integrating genetic approaches into the discovery of anticancer drugs. Science 278, 1064–1068 (1997).
Kaelin, W. G. Jr. The concept of synthetic lethality in the context of anticancer therapy. Nat. Rev. Cancer 5, 689–698 (2005).
Brummelkamp, T. R. & Bernards, R. New tools for functional mammalian cancer genetics. Nat. Rev. Cancer 3, 781–789 (2003).
McCabe, N. et al. Deficiency in the repair of DNA damage by homologous recombination and sensitivity to poly(ADP-ribose) polymerase inhibition. Cancer Res. 66, 8109–8115 (2006).
Schultz, N., Lopez, E., Saleh-Gohari, N. & Helleday, T. Poly(ADP-ribose) polymerase (PARP-1) has a controlling role in homologous recombination. Nucleic Acids Res. 31, 4959–4964 (2003).
Moynahan, M. E., Cui, T. Y. & Jasin, M. Homology-directed DNA repair, mitomycin-c resistance, and chromosome stability is restored with correction of a Brca1 mutation. Cancer Res. 61, 4842–4850 (2001).
Bhattacharyya, A., Ear, U. S., Koller, B. H., Weichselbaum, R. R. & Bishop, D. K. The breast cancer susceptibility gene BRCA1 is required for subnuclear assembly of Rad51 and survival following treatment with the DNA cross-linking agent cisplatin. J. Biol. Chem. 275, 23899–23903 (2000).
Howlett, N. G. et al. Biallelic inactivation of BRCA2 in Fanconi anemia. Science 297, 606–609 (2002).
Kraakman-van der Zwet, M. et al. Brca2 (XRCC11) deficiency results in radioresistant DNA synthesis and a higher frequency of spontaneous deletions. Mol. Cell. Biol. 22, 669–679 (2002).
Fong, P. C. et al. Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. N. Engl. J. Med. 361, 123–134 (2009).
Plummer, R. et al. Phase I study of the poly(ADP-ribose) polymerase inhibitor, AG014699, in combination with temozolomide in patients with advanced solid tumors. Clin. Cancer Res. 14, 7917–7923 (2008). Fong et al. (2009) describes the phase 1 clinical trial of the PARPi olaparib and the sustained antitumour responses to a PARPi in patients with cancer with either BRCA1 or BRCA2 mutations, and Plummer et al. (2008) reports the first-in-human clinical trial of any PARPi.
Lau, A. et al. A pharmacodynamic (PD) evaluation of the PARP inhibitor olaparib (AZD2281) in a first-in-human phase I trial of patients with advanced solid tumours. Cancer Res. 69, 3601 (2009).
Audeh, M. W. et al. Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer: a proof-of-concept trial. Lancet 376, 245–251 (2010).
Tutt, A. et al. Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: a proof-of-concept trial. Lancet 376, 235–244 (2010).
Mateo, J., Ong, M., Tan, D. S., Gonzalez, M. A. & de Bono, J. S. Appraising iniparib, the PARP inhibitor that never was — what must we learn? Nat. Rev. Clin. Oncol. 10, 688–696 (2013).
Balmana, J., Domchek, S. M., Tutt, A. & Garber, J. E. Stumbling blocks on the path to personalized medicine in breast cancer: the case of PARP inhibitors for BRCA1/2-associated cancers. Cancer Discov. 1, 29–34 (2011).
Gelmon, K. A. et al. Olaparib in patients with recurrent high-grade serous or poorly differentiated ovarian carcinoma or triple-negative breast cancer: a phase 2, multicentre, open-label, non-randomised study. Lancet Oncol. 12, 852–861 (2011).
Ledermann, J. et al. Olaparib maintenance therapy in platinum-sensitive relapsed ovarian cancer. N. Engl. J. Med. 366, 1382–1392 (2012).
Ledermann, J. A. et al. Overall survival in patients with platinum-sensitive recurrent serous ovarian cancer receiving olaparib maintenance monotherapy: an updated analysis from a randomised, placebo-controlled, double-blind, phase 2 trial. Lancet Oncol. 17, 1579–1589 (2016). This study, together with Ledermann et al. (2012), reports Study 19, the phase 2 clinical trial in ovarian cancer that led to the regulatory approval of a PARPi: olaparib.
Deeks, E. D. Olaparib: first global approval. Drugs 75, 231–240 (2015).
Kim, G. et al. FDA approval summary: olaparib monotherapy in patients with deleterious germline BRCA-mutated advanced ovarian cancer treated with three or more lines of chemotherapy. Clin. Cancer Res. 21, 4257–4261 (2015).
Moore, K. et al. Maintenance olaparib in patients with newly diagnosed advanced ovarian cancer. N. Engl. J. Med. 379, 2495–2505 (2018).
DiSilvestro, P. et al. Overall survival with maintenance olaparib at a 7-year follow-up in patients with newly diagnosed advanced ovarian cancer and a BRCA mutation: the SOLO1/GOG 3004 trial. J. Clin. Oncol. 41, 609–617 (2023).
Swisher, E. M. et al. Rucaparib in relapsed, platinum-sensitive high-grade ovarian carcinoma (ARIEL2 part 1): an international, multicentre, open-label, phase 2 trial. Lancet Oncol. 18, 75–87 (2017).
Ledermann, J. A. et al. Rucaparib for patients with platinum-sensitive, recurrent ovarian carcinoma (ARIEL3): post-progression outcomes and updated safety results from a randomised, placebo-controlled, phase 3 trial. Lancet Oncol. 21, 710–722 (2020).
Mirza, M. R. et al. Niraparib maintenance therapy in platinum-sensitive, recurrent ovarian cancer. N. Engl. J. Med. 375, 2154–2164 (2016).
González-Martín, A. et al. Niraparib in patients with newly diagnosed advanced ovarian cancer. N. Engl. J. Med. 381, 2391–2402 (2019).
Walsh, C. Genetic implications for cancer management: the changing landscape of poly (ADP-ribose) polymerase inhibitor indications in the treatment of ovarian cancer. Clin. Obstet. Gynecol. 67, 711–719 (2024).
Robson, M. et al. Olaparib for metastatic breast cancer in patients with a germline BRCA mutation. N. Engl. J. Med. 377, 523–533 (2017).
Litton, J. K. et al. Talazoparib in patients with advanced breast cancer and a germline BRCA mutation. N. Engl. J. Med. 379, 753–763 (2018).
Mateo, J. et al. DNA-repair defects and olaparib in metastatic prostate cancer. N. Engl. J. Med. 373, 1697–1708 (2015).This study shows that somatic BRCA2 mutations in men with metastatic, castration-resistant prostate cancer were associated with antitumour responses to the PARPi olaparib, opening the way for phase 3 trials in this disease and the eventual routine use of PARPi in the treatment of prostate cancer.
de Bono, J. et al. Olaparib for metastatic castration-resistant prostate cancer. N. Engl. J. Med. 382, 2091–2102 (2020).
Abida, W. et al. Rucaparib in men with metastatic castration-resistant prostate cancer harboring a BRCA1 or BRCA2 gene alteration. J. Clin. Oncol. 38, 3763–3772 (2020).
Golan, T. et al. Maintenance olaparib for germline BRCA-mutated metastatic pancreatic cancer. N. Engl. J. Med. 381, 317–327 (2019). This study describes the phase 3 clincial trial that led to the routine use of a PARPi in the treatment of pancreatic cancer.
Garber, J. In San Antonio Breast Cancer Conference.
Tutt, A. N. J. et al. Adjuvant olaparib for patients with BRCA1- or BRCA2-mutated breast cancer. N. Engl. J. Med. 384, 2394–2405 (2021). Together with Robson et al. (2017) and Litton et al. (2018), this study describe the phase 3 clinical trials that led to the first approvals of PARPi in either advanced (Robson et al.; Litton et al.) or early (Tutt et al.) breast cancer.
Geyer, C. E. Jr. et al. Overall survival in the OlympiA phase III trial of adjuvant olaparib in patients with germline pathogenic variants in BRCA1/2 and high-risk, early breast cancer. Ann. Oncol. 33, 1250–1268 (2022).
Bedrosian, I. et al. Germline testing in patients with breast cancer: ASCO-Society of Surgical Oncology Guideline. J. Clin. Oncol. 42, 584–604 (2024).
Murai, J. et al. Trapping of PARP1 and PARP2 by clinical PARP inhibitors. Cancer Res. 72, 5588–5599 (2012).
Zandarashvili, L. et al. Structural basis for allosteric PARP-1 retention on DNA breaks. Science 368, eaax6367 (2020). Together with Murai et al. (2012), this study shows that PARP inhibition induces synthetic lethality not only by inhibiting the catalytic activity of PARP1, but also by trapping PARP1 in chromatin.
Vaitsiankova, A. et al. PARP inhibition impedes the maturation of nascent DNA strands during DNA replication. Nat. Struct. Mol. Biol. 29, 329–338 (2022).
Petropoulos, M. et al. Transcription-replication conflicts underlie sensitivity to PARP inhibitors. Nature 628, 433–441 (2024).
Shen, Y. et al. BMN 673, a novel and highly potent PARP1/2 inhibitor for the treatment of human cancers with DNA repair deficiency. Clin. Cancer Res. 19, 5003–5015 (2013).
Lowery, M. A. et al. Phase II trial of veliparib in patients with previously treated BRCA-mutated pancreas ductal adenocarcinoma. Eur. J. Cancer 89, 19–26 (2018).
Coleman, R. L. et al. A phase II evaluation of the potent, highly selective PARP inhibitor veliparib in the treatment of persistent or recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer in patients who carry a germline BRCA1 or BRCA2 mutation — an NRG Oncology/Gynecologic Oncology Group study. Gynecol. Oncol. 137, 386–391 (2015).
Coleman, R. L. et al. Veliparib with first-line chemotherapy and as maintenance therapy in ovarian cancer. N. Engl. J. Med. 381, 2403–2415 (2019).
Han, H. S. et al. Veliparib monotherapy following carboplatin/paclitaxel plus veliparib combination therapy in patients with germline BRCA-associated advanced breast cancer: results of exploratory analyses from the phase III BROCADE3 trial. Ann. Oncol. 33, 299–309 (2022).
Diéras, V. et al. Veliparib with carboplatin and paclitaxel in BRCA-mutated advanced breast cancer (BROCADE3): final overall survival results from a randomized phase 3 trial. Eur. J. Cancer 200, 113580 (2024).
Lin, X. et al. Inactive Parp2 causes Tp53-dependent lethal anemia by blocking replication-associated nick ligation in erythroblasts. Mol. Cell 84, 3916–3931.e7 (2024).
Illuzzi, G. et al. Preclinical characterization of AZD5305, a next-generation, highly selective PARP1 inhibitor and trapper. Clin. Cancer Res. 28, 4724–4736 (2022).
Khalizieva, A., Moser, S. C., Bouwman, P. & Jonkers, J. BRCA1 and BRCA2: from cancer susceptibility to synthetic lethality. Genes Dev. 39, 86–108 (2025).
Cong, K. et al. Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency. Mol. Cell 81, 3128–3144.e7 (2021).
Lim, P. X., Zaman, M. Feng, W. & Jasin, M. BRCA2 promotes genomic integrity and therapy resistance primarily through its role in homology-directed repair. Mol. Cell 84, 447–462 (2024).
Lahiri, S. et al. BRCA2 prevents PARPi-mediated PARP1 retention to protect RAD51 filaments. Nature 640, 1103–1111 (2025).
Bajrami, I. et al. Genome-wide profiling of genetic synthetic lethality identifies CDK12 as a novel determinant of PARP1/2 inhibitor sensitivity. Cancer Res. 74, 287–297 (2014).
Loveday, C. et al. Germline mutations in RAD51D confer susceptibility to ovarian cancer. Nat. Genet. 43, 879–882 (2011).
Sakai, W. et al. Secondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated cancers. Nature 451, 1116–1120 (2008).
Edwards, S. L. et al. Resistance to therapy caused by intragenic deletion in BRCA2. Nature 451, 1111–1115 (2008).
Pettitt, S. J. et al. Clinical BRCA1/2 reversion analysis identifies hotspot mutations and predicted neoantigens associated with therapy resistance. Cancer Discov. 10, 1475–1488 (2020).
Tobalina, L., Armenia, J., Irving, E., O’Connor, M. J. & Forment, J. V. A meta-analysis of reversion mutations in BRCA genes identifies signatures of DNA end-joining repair mechanisms driving therapy resistance. Ann. Oncol. 32, 103–112 (2021).
Harvey-Jones, E. et al. Longitudinal profiling identifies co-occurring BRCA1/2 reversions, TP53BP1, RIF1 and PAXIP1 mutations in PARP inhibitor-resistant advanced breast cancer. Ann. Oncol. 35, 364–380 (2024).
Nesic, K. et al. BRCA1 secondary splice-site mutations drive exon-skipping and PARP inhibitor resistance. Preprint at medRxiv https://doi.org/10.1101/2023.03.20.23287465 (2023).
Seed, G. et al. Elucidating acquired PARP inhibitor resistance in advanced prostate cancer. Cancer Cell 42, 2113–2123.e4 (2024).
Lin, K. K. et al. BRCA reversion mutations in circulating tumor DNA predict primary and acquired resistance to the PARP inhibitor rucaparib in high-grade ovarian carcinoma. Cancer Discov. 9, 210–219 (2019). Together with Sakai et al. (2008), this study describes the discovery of reversion mutations in BRCA1 and BRCA2 that cause PARPi and platinum salt resistance and show that these are frequently observed in patients.
Zatreanu, D. et al. Polθ inhibitors elicit BRCA-gene synthetic lethality and target PARP inhibitor resistance. Nat. Commun. 12, 3636 (2021).
Drean, A. et al. Modeling therapy resistance in BRCA1/2-mutant cancers. Mol. Cancer Ther. 16, 2022–2034 (2017).
Kim, H. et al. Combining PARP with ATR inhibition overcomes PARP inhibitor and platinum resistance in ovarian cancer models. Nat. Commun. 11, 3726 (2020).
Yap, T. A. et al. Camonsertib in DNA damage response-deficient advanced solid tumors: phase 1 trial results. Nat. Med. 29, 1400–1411 (2023).
Dias, M. P., Moser, S. C., Ganesan, S. & Jonkers, J. Understanding and overcoming resistance to PARP inhibitors in cancer therapy. Nat. Rev. Clin. Oncol. 18, 773–791 (2021).
Zhou, J. et al. A first-in-class polymerase θ inhibitor selectively targets homologous-recombination-deficient tumors. Nat. Cancer 2, 598–610 (2021).
Adam, S. et al. The CIP2A–TOPBP1 axis safeguards chromosome stability and is a synthetic lethal target for BRCA-mutated cancer. Nat. Cancer 2, 1357–1371 (2021).
Ceccaldi, R. et al. Homologous-recombination-deficient tumours are dependent on Polθ-mediated repair. Nature 518, 258–262 (2015).
Mateos-Gomez, P. A. et al. Mammalian polymerase θ promotes alternative NHEJ and suppresses recombination. Nature 518, 254–257 (2015).
Torrado, C., Ashton, N. W., D’Andrea, A. D. & Yap, T. A. USP1 inhibition: a journey from target discovery to clinical translation. Pharmacol. Ther. 271, 108865 (2025).
Pan, X. et al. FANCM, BRCA1, and BLM cooperatively resolve the replication stress at the ALT telomeres. Proc. Natl Acad. Sci. USA 114, E5940–E5949 (2017).
Martires, L. C. M. et al. LIG1 is a synthetic lethal target in BRCA1 mutant cancers. Mol. Cancer Ther. 24, 618–627 (2025).
Feng, Z. et al. Rad52 inactivation is synthetically lethal with BRCA2 deficiency. Proc. Natl Acad. Sci. USA 108, 686–691 (2011).
Haider, S. et al. The transcriptomic architecture of common cancers reflects synthetic lethal interactions. Nat. Genet. 57, 522–529 (2025).
Mengwasser, K. E. et al. Genetic screens reveal FEN1 and APEX2 as BRCA2 synthetic lethal targets. Mol. Cell 73, 885–899.e6 (2019).
Schäffer, A. A., Chung, Y., Kammula, A. V., Ruppin, E. & Lee, J. S. A systematic analysis of the landscape of synthetic lethality-driven precision oncology. Med 5, 73–89.e9 (2024).
Tsherniak, A. et al. Defining a cancer dependency map. Cell 170, 564–576.e16 (2017).
Ryan, C. J., Devakumar, L. P. S., Pettitt, S. J. & Lord, C. J. Complex synthetic lethality in cancer. Nat. Genet. 55, 2039–2048 (2023).
Ryan, C. J., Bajrami, I. & Lord, C. J. Synthetic lethality and cancer — penetrance as the major barrier. Trends Cancer 4, 671–683 (2018).
Lord, C. J., Quinn, N. & Ryan, C. J. Integrative analysis of large-scale loss-of-function screens identifies robust cancer-associated genetic interactions. eLife 9, e58925 (2020).
Downward, J. RAS synthetic lethal screens revisited: still seeking the elusive prize? Clin. Cancer Res. 21, 1802–1809 (2015).
Ashworth, A., Lord, C. J. & Reis-Filho, J. S. Genetic interactions in cancer progression and treatment. Cell 145, 30–38 (2011).
Fong, S. H. et al. A multilineage screen identifies actionable synthetic lethal interactions in human cancers. Nat. Genet. 57, 154–164 (2025).
Noordermeer, S. M. et al. The shieldin complex mediates 53BP1-dependent DNA repair. Nature 560, 117–121 (2018).
Pantelidou, C. et al. PARP inhibitor efficacy depends on CD8+ T-cell recruitment via intratumoral STING pathway activation in BRCA-deficient models of triple-negative breast cancer. Cancer Discov. 9, 722–737 (2019). This study describes the discovery that the cGAS–STING pathway and CD8+ T cells are important mediators of PARPi antitumour responses.
Li, X. et al. C5aR1 inhibition reprograms tumor associated macrophages and reverses PARP inhibitor resistance in breast cancer. Nat. Commun. 15, 4485 (2024).
Luo, Y. et al. Neoadjuvant PARPi or chemotherapy in ovarian cancer informs targeting effector Treg cells for homologous-recombination-deficient tumors. Cell 187, 4905–4925.e24 (2024).
Diéras, V. et al. Veliparib with carboplatin and paclitaxel in BRCA-mutated advanced breast cancer (BROCADE3): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Oncol. 21, 1269–1282 (2020).
Abraham, J. E. et al. Neoadjuvant PARP inhibitor scheduling in BRCA1 and BRCA2 related breast cancer: PARTNER, a randomized phase II/III trial. Nat. Commun. 16, 4269 (2025).
Fasching, P. A. et al. Neoadjuvant paclitaxel/olaparib in comparison to paclitaxel/carboplatin in patients with HER2-negative breast cancer and HRD-long-term survival of the GeparOLA study. Clin. Cancer Res. 31, 1596–1604 (2025).
Murai, J. et al. Rationale for poly(ADP-ribose) polymerase (PARP) inhibitors in combination therapy with camptothecins or temozolomide based on PARP trapping versus catalytic inhibition. J. Pharmacol. Exp. Ther. 349, 408–416 (2014).
Wethington, S. L. et al. Combination ATR (ceralasertib) and PARP (olaparib) inhibitor (CAPRI) trial in acquired PARP inhibitor-resistant homologous recombination-deficient ovarian cancer. Clin. Cancer Res. 29, 2800–2807 (2023).
Clarke, N. W. et al. Efficacy and safety of olaparib plus abiraterone versus placebo plus abiraterone in the first-line treatment of patients with asymptomatic/mildly symptomatic and symptomatic metastatic castration-resistant prostate cancer: analyses from the phase 3 PROpel trial. Eur. Urol. Oncol. 8, 394–406 (2025).
Beije, N. et al. PARP inhibitors for prostate cancer: tangled up in PROfound and PROpel (and TALAPRO-2) Blues. Eur. Urol. 84, 253–256 (2023).
Ray-Coquard, I. et al. Olaparib plus bevacizumab as first-line maintenance in ovarian cancer. N. Engl. J. Med. 381, 2416–2428 (2019). This study describes the phase 3 clinical trial that led to the routine use of a PARPi as part of a drug combination (olapaprib used in combination with bevacizumab in ovarian cancer).
Samstein, R. M. et al. Mutations in BRCA1 and BRCA2 differentially affect the tumor microenvironment and response to checkpoint blockade immunotherapy. Nat. Cancer 1, 1188–1203 (2021).
Pedretti, F. et al. Harnessing STING signaling and natural killer cells overcomes PARP inhibitor resistance in homologous recombination-deficient breast cancer. Cancer Res. 85, 1888–1908 (2025).
Chabanon, R. M. et al. PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer. J. Clin. Invest. 129, 1211–1228 (2019).
Ghanem, A. & Domchek, S. M. New therapeutic options for BRCA mutant patients. Annu. Rev. Med. 76, 175–187 (2025).
Drew, Y., Zenke, F. T. & Curtin, N. J. DNA damage response inhibitors in cancer therapy: lessons from the past, current status and future implications. Nat. Rev. Drug Discov. 24, 19–39 (2025).
Lee, J. S. et al. Synthetic lethality-mediated precision oncology via the tumor transcriptome. Cell 184, 2487–2502.e13 (2021).
Chambon, P., Weill, J. D. & Mandel, P. Nicotinamide mononucleotide activation of new DNA-dependent polyadenylic acid synthesizing nuclear enzyme. Biochem. Biophys. Res. Commun. 11, 39–43 (1963).
Hilz, H. & Stone, P. Poly(ADP-ribose) and ADP-ribosylation of proteins. Rev. Physiol. Biochem. Pharmacol. 76, 1–58 (1976).
Purnell, M. R., Stone, P. R. & Whish, W. J. ADP-ribosylation of nuclear proteins. Biochem. Soc. Trans. 8, 215–227 (1980).
Durkacz, B. W., Omidiji, O., Gray, D. A. & Shall, S. (ADP-ribose)n participates in DNA excision repair. Nature 283, 593–596 (1980).
Zahradka, P. & Ebisuzaki, K. A shuttle mechanism for DNA-protein interactions. The regulation of poly(ADP-ribose) polymerase. Eur. J. Biochem. 127, 579–585 (1982).
Purnell, M. R. & Whish, W. J. Novel inhibitors of poly(ADP-ribose) synthetase. Biochem. J. 185, 775–777 (1980).
Miki, Y. et al. A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Science 266, 66–71 (1994).
Wooster, R. et al. Identification of the breast cancer susceptibility gene BRCA2. Nature 378, 789–792 (1995).
Moynahan, M. E., Pierce, A. J. & Jasin, M. BRCA2 is required for homology-directed repair of chromosomal breaks. Mol. Cell 7, 263–272 (2001).
Connor, F. et al. Tumorigenesis and a DNA repair defect in mice with a truncating Brca2 mutation. Nat. Genet. 17, 423–430 (1997).
Tutt, A. et al. Carboplatin in BRCA1/2-mutated and triple-negative breast cancer BRCAness subgroups: the TNT trial. Nat. Med. 24, 628–637 (2018).
Turner, N., Tutt, A. & Ashworth, A. Hallmarks of ‘BRCAness’ in sporadic cancers. Nat. Rev. Cancer 4, 814–819 (2004).
Dobzhansky, T. Genetics of natural populations; recombination and variability in populations of Drosophila pseudoobscura. Genetics 31, 269–290 (1946). This article describes the synthetic lethal concept.
Gurley, K. E. & Kemp, C. J. Synthetic lethality between mutation in Atm and DNA-PKcs during murine embryogenesis. Curr. Biol. 11, 191–194 (2001).
