Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress 2023 EHA Congress 2023 ASCO Annual Meeting
Clinical Collections
Advances in Alzheimer’s

At a glance: The ONWARDS insulin icodec trials

A round-up of the ONWARDS phase 3 clinical trials evaluating the novel weekly insulin icodec in people with diabetes.
ADVANCED SEARCH
Log in
Top
Current Treatment Options in Oncology
Published in: Current Treatment Options in Oncology 3/2016

01-03-2016 | Gynecologic Cancers (RJ Morgan, Section Editor)

New Targeted Agents in Gynecologic Cancers: Synthetic Lethality, Homologous Recombination Deficiency, and PARP Inhibitors

Authors: Fong W. Liu, MD MPH, Krishnansu S. Tewari, MD

Published in: Current Treatment Options in Oncology | Issue 3/2016

Login to get access

Opinion statement

Inhibitors of poly (ADP-ribose) polymerase (PARP) have emerged as a new class of anti-cancer drugs, specifically for malignancies bearing aberrations of the homologous recombination pathway, like those with mutations in the BRCA 1 and BRCA 2 genes. Olaparib, a potent PARP1 and PARP2 inhibitor, has been shown to significantly increase progression-free survival (PFS) in women with recurrent ovarian cancer related to a germline BRCA mutation and is currently approved fourth-line treatment in these patients. PARP inhibitors (PARPi) target the genetic phenomenon known as synthetic lethality to exploit faulty DNA repair mechanisms. While ovarian cancer is enriched with a population of tumors with known homologous recombination defects, investigations are underway to help identify pathways in other gynecologic cancers that may demonstrate susceptibility to PARPi through synthetically lethal mechanisms. The ARIEL2 trial prospectively determined a predictive assay to identify patients with HRD. The future of cancer therapeutics will likely incorporate these HRD assays to determine the best treatment plan for patients. While the role of PARPi is less clear in non-ovarian gynecologic cancers, the discovery of a predictive assay for HRD may open the door for clinical trials in these other gynecologic cancers enriched with patients with HRD. Identification of patients with tumors deficient in homologous repair or have HRD-like behavior moves cancer treatment towards individualized therapies in order to maximize treatment effect and quality of life for women living with gynecologic cancers.
Literature
1.
2.
Bridges CB. The origin of variation. The American Naturalist. 1922:13.
3.
Lord CJ, Ashworth A. Mechanisms of resistance to therapies targeting BRCA-mutant cancers. Nat Med. 2013;19:1381–8.CrossRefPubMed
4.••
Dobzhansky T. Genetics of natural populations. Xiii. Recombination and variability in populations of drosophila pseudoobscura. Genetics. 1946;31:269–90. The first description in the literature of the concept of synthetic lethality.PubMedCentral
5.
Tischler J, Lehner B, Fraser AG. Evolutionary plasticity of genetic interaction networks. Nat Genet. 2008;40:390–1.CrossRefPubMed
6.
Hartwell LH, Szankasi P, Roberts CJ, Murray AW, Friend SH. Integrating genetic approaches into the discovery of anticancer drugs. Science. 1997;278:1064–8.CrossRefPubMed
7.
Kaelin WG. The concept of synthetic lethality in the context of anticancer therapy. Nat Rev Cancer. 2005;5:689–98.CrossRefPubMed
8.
Tewari KS, Monk BJ. The 21st century handbook of clinical ovarian cancer. Cham: Adis; 2015.
9.
Amé JC, Rolli V, Schreiber V, Niedergang C, Apiou F, Decker P, et al. PARP-2, a novel mammalian DNA damage-dependent poly(ADP-ribose) polymerase. J Biol Chem. 1999;274:17860–8.CrossRefPubMed
10.
Dantzer F, Schreiber V, Niedergang C, Trucco C, Flatter E, De La Rubia G, et al. Involvement of poly(ADP-ribose) polymerase in base excision repair. Biochimie. 1999;81:69–75.CrossRefPubMed
11.
Gibson BA, Kraus WL. New insights into the molecular and cellular functions of poly(ADP-ribose) and PARPs.
12.
13.
Isabelle M, Moreel X, Gagné JP, Rouleau M, Ethier C, Gagné P, et al. Investigation of PARP-1, PARP-2, and PARG interactomes by affinity-purification mass spectrometry. Proteome Sci. 2010;8:22.CrossRefPubMedPubMedCentral
14.
Wang M, Wu W, Rosidi B, Zhang L, Wang H, Iliakis G. PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways. Nucleic Acids Res. 2006;34:6170–82.CrossRefPubMedPubMedCentral
15.
Haince JF, McDonald D, Rodrigue A, Déry U, Masson JY, Hendzel MJ, et al. PARP1-dependent kinetics of recruitment of MRE11 and NBS1 proteins to multiple DNA damage sites. J Biol Chem. 2008;283:1197–208.CrossRefPubMed
16.
17.
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. 2003;31:4959–64.CrossRefPubMedPubMedCentral
18.
Farmer H, McCabe N, Lord CJ, Tutt AN, Johnson DA, Richardson TB, et al. Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. Nature. 2005;434:917–21.CrossRefPubMed
19.
Bryant HE, Schultz N, Thomas HD, Parker KM, Flower D, Lopez E, et al. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase. Nature. 2005;434:913–7.CrossRefPubMed
20.••
McNeish IA, Oza AM, Coleman RL, Scott CL, Konecny GE, Tinker A, et al. Results of ARIEL2: A Phase 2 trial to prospectively identify ovarian cancer patients likely to respond to rucaparib using tumor genetic analysis. ASCO Annual Meeting. Chicago, Illinois: J Clin Oncol 33, 2015 (suppl; abstr 5508); 2015. The first prospectively determined HRD assay in a PARPi clinical trial and confirmed with tumor reponse to rucaparib.
21.
Stambolic V, Suzuki A, de la Pompa JL, Brothers GM, Mirtsos C, Sasaki T, et al. Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN. Cell. 1998;95:29–39.CrossRefPubMed
22.
Wu X, Senechal K, Neshat MS, Whang YE, Sawyers CL. The PTEN/MMAC1 tumor suppressor phosphatase functions as a negative regulator of the phosphoinositide 3-kinase/Akt pathway. Proc Natl Acad Sci U S A. 1998;95:15587–91.CrossRefPubMedPubMedCentral
23.
Shen WH, Balajee AS, Wang J, Wu H, Eng C, Pandolfi PP, et al. Essential role for nuclear PTEN in maintaining chromosomal integrity. Cell. 2007;128:157–70.CrossRefPubMed
24.
Mendes-Pereira AM, Martin SA, Brough R, McCarthy A, Taylor JR, Kim JS, et al. Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors. EMBO Mol Med. 2009;1:315–22.CrossRefPubMedPubMedCentral
25.
Dedes KJ, Wetterskog D, Mendes-Pereira AM, Natrajan R, Lambros MB, Geyer FC, et al. PTEN deficiency in endometrioid endometrial adenocarcinomas predicts sensitivity to PARP inhibitors. Sci Transl Med. 2010;2:53ra75.CrossRefPubMed
26.
Hegan DC, Lu Y, Stachelek GC, Crosby ME, Bindra RS, Glazer PM. Inhibition of poly(ADP-ribose) polymerase down-regulates BRCA1 and RAD51 in a pathway mediated by E2F4 and p130. Proc Natl Acad Sci U S A. 2010;107:2201–6.CrossRefPubMedPubMedCentral
27.
Hassumi-Fukasawa MK, Miranda-Camargo FA, Zanetti BR, Galano DF, Ribeiro-Silva A, Soares EG. Expression of BAG-1 and PARP-1 in precursor lesions and invasive cervical cancer associated with human papillomavirus (HPV). Pathol Oncol Res. 2012;18:929–37.CrossRefPubMed
28.
Weaver AN, Cooper TS, Rodriguez M, Trummell HQ, Bonner JA, Rosenthal EL, et al. DNA double strand break repair defect and sensitivity to poly ADP-ribose polymerase (PARP) inhibition in human papillomavirus 16-positive head and neck squamous cell carcinoma. Oncotarget. 2015;6:26995–7007.CrossRefPubMedPubMedCentral
29.•
Fong PC, Boss DS, Yap TA, Tutt A, Wu P, Mergui-Roelvink M, et al. Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. N Engl J Med. 2009;361:123–34. Original phase I trial that determined MTD of olaparib 400mg twice daily and confirmed that its clinical benefit rate was associated with platinum sensitivity.CrossRefPubMed
30.
Fong PC, Yap TA, Boss DS, Carden CP, Mergui-Roelvink M, Gourley C, et al. Poly(ADP)-ribose polymerase inhibition: frequent durable responses in BRCA carrier ovarian cancer correlating with platinum-free interval. J Clin Oncol. 2010;28:2512–9.CrossRefPubMed
31.
Tutt A, Robson M, Garber JE, Domchek SM, Audeh MW, Weitzel JN, 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. 2010;376:235–44.CrossRefPubMed
32.
Audeh MW, Carmichael J, Penson RT, Friedlander M, Powell B, Bell-McGuinn KM, 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. 2010;376:245–51.CrossRefPubMed
33.
Yang D, Khan S, Sun Y, Hess K, Shmulevich I, Sood AK, et al. Association of BRCA1 and BRCA2 mutations with survival, chemotherapy sensitivity, and gene mutator phenotype in patients with ovarian cancer. JAMA. 2011;306:1557–65.CrossRefPubMedPubMedCentral
34.
Ledermann J, Harter P, Gourley C, Friedlander M, Vergote I, Rustin G, et al. Olaparib maintenance therapy in platinum-sensitive relapsed ovarian cancer. N Engl J Med. 2012;366:1382–92.CrossRefPubMed
35.
Kaye SB, Lubinski J, Matulonis U, Ang JE, Gourley C, Karlan BY, et al. Phase II, open-label, randomized, multicenter study comparing the efficacy and safety of olaparib, a poly (ADP-ribose) polymerase inhibitor, and pegylated liposomal doxorubicin in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer. J Clin Oncol. 2012;30:372–9.CrossRefPubMed
36.••
Ledermann J, Harter P, Gourley C, Friedlander M, Vergote I, Rustin G, et al. Olaparib maintenance therapy in patients with platinum-sensitive relapsed serous ovarian cancer: a preplanned retrospective analysis of outcomes by BRCA status in a randomised phase 2 trial. Lancet Oncol. 2014;15:852–61. Randomized phase II trial, known as Study 19, demonstrated the PFS benefit of olaparib in the maintenance setting, especially in BRCA mutation carriers. It serves as the precursor for the SOLO-1 trial.CrossRefPubMed
37.••
Kaufman B, Shapira-Frommer R, Schmutzler RK, Audeh MW, Friedlander M, Balmaña J, et al. Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation. J Clin Oncol. 2015;33:244–50. Multicenter phase II trial, known as Study 42, that lead to the FDA approval of olaparib as fourth line therapy for women with BRCA-related ovarian cancer.CrossRefPubMed
38.
39.
Rottenberg S, Jaspers JE, Kersbergen A, van der Burg E, Nygren AO, Zander SA, et al. High sensitivity of BRCA1-deficient mammary tumors to the PARP inhibitor AZD2281 alone and in combination with platinum drugs. Proc Natl Acad Sci U S A. 2008;105:17079–84.CrossRefPubMedPubMedCentral
40.
Evers B, Drost R, Schut E, de Bruin M, van der Burg E, Derksen PW, et al. Selective inhibition of BRCA2-deficient mammary tumor cell growth by AZD2281 and cisplatin. Clin Cancer Res. 2008;14:3916–25.CrossRefPubMed
41.
Hay T, Matthews JR, Pietzka L, Lau A, Cranston A, Nygren AO, et al. Poly(ADP-ribose) polymerase-1 inhibitor treatment regresses autochthonous Brca2/p53-mutant mammary tumors in vivo and delays tumor relapse in combination with carboplatin. Cancer Res. 2009;69:3850–5.CrossRefPubMed
42.
Joenje H, Patel KJ. The emerging genetic and molecular basis of fanconi anaemia. Nat Rev Genet. 2001;2:446–57.CrossRefPubMed
43.
44.
45.
Pothuri B. BRCA1- and BRCA2-related mutations: therapeutic implications in ovarian cancer. Ann Oncol. 2013;24 Suppl 8:viii22–7.CrossRefPubMed
46.
Del Conte G, Sessa C, von Moos R, Viganò L, Digena T, Locatelli A, et al. Phase I study of olaparib in combination with liposomal doxorubicin in patients with advanced solid tumours. Br J Cancer. 2014;111:651–9.CrossRefPubMedPubMedCentral
47.
Lee JM, Hays JL, Annunziata CM, Noonan AM, Minasian L, Zujewski JA, et al. Phase I/Ib study of olaparib and carboplatin in BRCA1 or BRCA2 mutation-associated breast or ovarian cancer with biomarker analyses. J Natl Cancer Inst. 2014;106:dju089.CrossRefPubMedPubMedCentral
48.•
Oza AM, Cibula D, Benzaquen AO, Poole C, Mathijssen RH, Sonke GS, et al. Olaparib combined with chemotherapy for recurrent platinum-sensitive ovarian cancer: a randomised phase 2 trial. Lancet Oncol. 2015;16:87–97. Randomized phase II trial, known as Study 41, that demonstrated improved PFS of olaparib with chemotherapy compared to carboplatin/paclitaxel alone.CrossRefPubMed
49.
Rivkin SE, Iriarte D, Sloan H, Wiseman C, Moon J. Phase Ib/II with expansion of patients at the MTD study of olaparib plus weekly (metronomic) carboplatin and paclitaxel in relapsed ovarian cancer patients. ASCO Annual Meeting. Chicago, IL J Clin Oncol 32:5s, 2014 (suppl; abstr 5527).
50.
Giansanti V, Donà F, Tillhon M, Scovassi AI. PARP inhibitors: new tools to protect from inflammation. Biochem Pharmacol. 2010;80:1869–77.CrossRefPubMed
51.
Khanna KK, Jackson SP. DNA double-strand breaks: signaling, repair and the cancer connection. Nat Genet. 2001;27:247–54.CrossRefPubMed
52.•
Liu JF, Tolaney SM, Birrer M, Fleming GF, Buss MK, Dahlberg SE, et al. A Phase 1 trial of the poly(ADP-ribose) polymerase inhibitor olaparib (AZD2281) in combination with the anti-angiogenic cediranib (AZD2171) in recurrent epithelial ovarian or triple-negative breast cancer. Eur J Cancer. 2013;49:2972–8. The initial phase I trial that established the MTD of olaparib to be 200mg BID in combination with cedrianib 30mg daily.CrossRefPubMedPubMedCentral
53.
Matulonis UA, Berlin S, Ivy P, Tyburski K, Krasner C, Zarwan C, et al. Cediranib, an oral inhibitor of vascular endothelial growth factor receptor kinases, is an active drug in recurrent epithelial ovarian, fallopian tube, and peritoneal cancer. J Clin Oncol. 2009;27:5601–6.CrossRefPubMedPubMedCentral
54.••
Liu JF, Barry WT, Birrer M, Lee JM, Buckanovich RJ, Fleming GF, et al. Combination cediranib and olaparib versus olaparib alone for women with recurrent platinum-sensitive ovarian cancer: a randomised phase 2 study. Lancet Oncol. 2014;15:1207–14. Randomized phase II trial demonstrating significantly improved PFS of combination cediranib and olaparib compared to olaparib alone.CrossRefPubMedPubMedCentral
55.
Wagner LM. Profile of veliparib and its potential in the treatment of solid tumors. Oncol Targets Ther. 2015;8:1931–9.CrossRef
56.•
Coleman RL, Sill MW, Bell-McGuinn K, Aghajanian C, Gray HJ, Tewari KS, 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. 2015;137:386–91. Phase II trial demonstrating activity of veliparib in heavily pretreated patients with BRCA-related ovarian cancer.CrossRefPubMed
57.
Kummar S, Ji J, Morgan R, Lenz HJ, Puhalla SL, Belani CP, et al. A phase I study of veliparib in combination with metronomic cyclophosphamide in adults with refractory solid tumors and lymphomas. Clin Cancer Res. 2012;18:1726–34.CrossRefPubMedPubMedCentral
58.
Kummar S, Chen A, Ji J, Zhang Y, Reid JM, Ames M, et al. Phase I study of PARP inhibitor ABT-888 in combination with topotecan in adults with refractory solid tumors and lymphomas. Cancer Res. 2011;71:5626–34.CrossRefPubMedPubMedCentral
59.
Tan AR, Toppmeyer D, Stein MN, Moss RA, Gounder M, Lindquist DC, et al. Phase I trial of veliparib, (ABT-888), a poly(ADP-ribose) polymerase (PARP) inhibitor, in combination with doxorubicin and cyclophosphamide in breast cancer and other solid tumors. ASCO Annual Meeting. Chicago, Illinois: J Clin Oncol 29: (suppl; abstr 3041); 2011.
60.
Liu FW, Cripe J, Tewari KS. Anti-angiogenesis therapy in gynecologic malignancies. Oncology (Williston Park). 2015;29:350–60.
61.
Burger RA, Brady MF, Bookman MA, Fleming GF, Monk BJ, Huang H, et al. Incorporation of bevacizumab in the primary treatment of ovarian cancer. N Engl J Med. 2011;365:2473–83.CrossRefPubMed
62.
Sandhu SK, Schelman WR, Wilding G, Moreno V, Baird RD, Miranda S, et al. The poly(ADP-ribose) polymerase inhibitor niraparib (MK4827) in BRCA mutation carriers and patients with sporadic cancer: a phase 1 dose-escalation trial. Lancet Oncol. 2013;14:882–92.CrossRefPubMed
63.•
Matulonis U, Mahner S, Wenham RM, Ledermann JA, Monk BJ, Del Campo JM, et al. A phase 3 randomized double-blind trial of maintenance with niraparib versus placebo in patients with platinum-sensitive ovarian cancer (ENGOT-OV16/NOVA trial). ASCO Annual Meeting. Chicago, Illinois: J Clin Oncol 32:5s, 2014 (suppl; abstr TPS5625); 2014. A phase III double-blind, placebo-controlled, 2:1 randomized trial of maintenance niraparib versus placebo in patients with recurrent platinum sensitive high grade serous ovarian cancer or known to have a germline BRCA mutation.
64.
Moore KN, Zhang Z-Y, Agarwal S, Patel MR, Burris HA, Martell RE, et al. Food effect substudy of a phase 3 randomized double-blind trial of maintenance with niraparib (MK4827), a poly(ADP)ribose polymerase (PARP) inhibitor versus placebo in patients with platinum-sensitive ovarian cancer. ASCO Annual Meeting. Chicago, Illinois: J Clin Oncol 32: (suppl; abstr e16531), 2014.
65.
Ihnen M, zu Eulenburg C, Kolarova T, Qi JW, Manivong K, Chalukya M, et al. Therapeutic potential of the poly(ADP-ribose) polymerase inhibitor rucaparib for the treatment of sporadic human ovarian cancer. Mol Cancer Ther. 2013;12:1002–15.CrossRefPubMedPubMedCentral
66.
Shapiro G, Kristeleit R, Middleton M, Burris H, Rhoda Molife L, Jeff E, et al. Pharmacokinetics of orally administered rucaparib in patients with advanced solid tumors. Mol Cancer Ther. 2013;12:A218. Proceedings of AACR/NCI/EORTC targeted therapies meeting.CrossRef
67.
Kristeleit R, Shapira-Frommer R, Burris H, Patel MR, Lorusso P, Oza AM, et al. Phase 1/2 study of oral rucaparib: updated phase 1 and preliminary phase 2 results. Ann Oncol. 2014;25(suppl_4):iv305–26. doi:10.​1093/​annonc/​mdu338. ESMO Annual Meeting. Madrid, Spain.
68.
Swisher EM, Oza AM, Coleman RL, Scott C, Lin K, Dominy E, et al. Tumor BRCA mutation or high genomic LOH identify ovarian cancer patients likely to respond to rucaparib: interim results for ARIEL2 clinical trial. Chicago: Annual Meeting on Women’s Cancer; 2015.
69.
Shen Y, Rehman FL, Feng Y, Boshuizen J, Bajrami I, Elliott R, 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. 2013;19:5003–15.CrossRefPubMed
70.
De Bono JS, Mina LA, Gonzalez M, Curtin NJ, Wang E, Henshaw JW, et al. First-in-human trial of novel oral PARP inhibitor BMN 673 in patients with solid tumors. ASCO Annual Meeting. Chicago, Illinois: J Clin Oncol 31 (suppl; abstr 2580); 2013.
71.
Haluska P, Timms KM, AlHilli M, Wang Y, Hartman AM, Jones J, et al. Homologous recombination deficiency (HRD) score and niraparib efficacy in high grade ovarian cancer. Eur J Cancer. 2014;50(supp 6 abst 214):72. 26th EORTC–NCI–AACR Symposium on Molecular Targets and Cancer Therapies. Madrid, Spain.CrossRef
72.
Watkins JA, Irshad S, Grigoriadis A, Tutt AN. Genomic scars as biomarkers of homologous recombination deficiency and drug response in breast and ovarian cancers. Breast Cancer Res. 2014;16:211.CrossRefPubMedPubMedCentral
73.
Birkbak NJ, Wang ZC, Kim JY, Eklund AC, Li Q, Tian R, et al. Telomeric allelic imbalance indicates defective DNA repair and sensitivity to DNA-damaging agents. Cancer Discov. 2012;2:366–75.CrossRefPubMedPubMedCentral
74.
Mulligan JM, Hill LA, Deharo S, Irwin G, Boyle D, Keating KE, et al. Identification and validation of an anthracycline/cyclophosphamide-based chemotherapy response assay in breast cancer. J Natl Cancer Inst. 2014;106:djt335.CrossRefPubMedPubMedCentral
75.
Telli ML, Jensen KC, Vinayak S, Kurian AW, Lipson JA, Flaherty PJ, et al. Phase II study of gemcitabine, carboplatin, and iniparib as neoadjuvant therapy for triple-negative and BRCA1/2 mutation-associated breast cancer with assessment of a tumor-based measure of genomic instability: PrECOG 0105. J Clin Oncol. 2015;33:1895–901.CrossRefPubMed
Metadata
Title
New Targeted Agents in Gynecologic Cancers: Synthetic Lethality, Homologous Recombination Deficiency, and PARP Inhibitors
Authors
Fong W. Liu, MD MPH
Krishnansu S. Tewari, MD
Publication date
01-03-2016
Publisher
Springer US
Published in
Current Treatment Options in Oncology / Issue 3/2016
Print ISSN: 1527-2729
Electronic ISSN: 1534-6277
DOI
https://doi.org/10.1007/s11864-015-0378-9

Other articles of this Issue 3/2016

Current Treatment Options in Oncology 3/2016 Go to the issue

Gynecologic Cancers (RJ Morgan, Section Editor)

New Approaches for Immune Directed Treatment for Ovarian Cancer

Lymphoma (JW Sweetenham, Section Editor)

Waldenstrom Macroglobulinemia: Familial Predisposition and the Role of Genomics in Prognosis and Treatment Selection

Lung Cancer (HA Wakelee, Section Editor)

Medical Treatment in Elderly Patients with Non-Small Cell Lung Cancer

Genitourinary Cancers (W Oh and M Galsky, Section Editors)

Bladder Sparing Approaches for Muscle-Invasive Bladder Cancers
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits