DOCSLIB.ORG

And Salivary Gland Cancers

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
And Salivary Gland Cancers Larotrectinib is highly active in patients with advanced recurrent TRK fusion thyroid (TC) and salivary gland cancers (SGC) Wirth L, 1 Drilon A, 2 Albert CM, 3 Farago A, 1 el-Diery W, 4 Ma P, 5 Sohal D, 6 Raez L, 7 Baik C, 8 Brose MS, 9 Doebele R, 10 Cox MC, 11 Ku N, 11 Hong D 12 1Massachusetts General Hospital, Boston, MA; 2Memorial Sloan Kettering Cancer Center, New York, NY; 3Seattle Children’s Hospital, Seattle, WA; 4Fox Chase Cancer Center, Philadelphia, PA; 5West Virginia University, Morgantown, WV; 6Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, 7Memorial Cancer Institute, Pembroke Pines, FL; 8University of Washington/Seattle Cancer Care Alliance, Seattle, WA; 9University of Pennsylvania, Abramson Cancer Center, Philadelphia, PA; 10 University of Colorado, Aurora, CO; 11 Loxo Oncology, South San Francisco, CA; 12 M.D. Anderson Cancer Center, Houston, TX Abstract # 20570 Introduction Patient and disease characteristics Adverse events with larotrectinib: ≥15% in safety database (n=125) n TRK fusions, involving the genes NTRK1, NTRK2, and NTRK3 , occur in a broad range of solid Characteristic Total N=19 Treatment-emergent AEs (%) Treatment-related AEs (%) tumors and are oncogenic: Median age (range), years 59 (15 –75) Grade 1 Grade 2 Grade 3 Grade 4 Total Grade 3 Grade 4 Total – Targeted inhibition of TRK can be an effective antitumor approach Female, n 7 (37%) Fatigue 15 18 5–38 1–18 ECOG 0 –1 19 (100%) n Larotrectinib is the first selective pan-TRK inhibitor in clinical development and has demonstrated Dizziness 22 42–27 1–20 1 Tumour type/histology,* n (%) 19 (100%) Nausea 20 52–26 2–18 an overall response rate of 76% by investigator assessment Thyroid 7 (37%) Anemia 89 9 –26 3–10 n The incidence of TRK fusions in TC has been reported to be as high as 27% in pediatric patients Differentiated 6 Vomiting 18 6––24 ––13 and 12% in adult patients, especially in tumors with papillary histology 2,3 Follicular 1 Papillary 5 Increased AST 16 43–23 1–18 4 n In SGCs, TRK fusions define mammary analog secretory cancers (MASC) Anaplastic 1 Constipation 20 21–22 ––12 Salivary gland 12 (63%) n Here we provide the first report summarizing the activity and safety of TRK-directed therapy with Acinar/MASC 8 Cough 18 2––21 ––2 larotrectinib in the treatment of advanced, recurrent TRK-fusion TCs and SGCs including non- Adenoid cystic 1 Increased ALT 14 24–20 4–17 papillary and non-MASC histologies Adenocarcinoma 1 Diarrhea 14 51–20 ––6 Mucoepidermoid 1 Dyspnea 10 62–18 ––– TRK fusions are rare but recurrent oncogenic drivers Sarcomatoid 1 Disease status at enrollment • 7 (13%) of 55 patients with TRK fusion cancers required dose reductions Metastatic 18 • No discontinuations for adverse events n Beyond embryogenesis, tropomyosin receptor kinase (TRK) protein expression is primarily limited Locally advanced 1 AEs, adverse events; ALT, alanine aminotransferase; AST, aspartate aminotransferase to the nervous system 5 Median number of prior systemic therapies, n=19 1 TC, n=7 3 n 3 neurotrophin receptors encoded by 3 distinct genes that regulate specific normal functions 6-10 SGC, n=12 0.5 Durable response in ETV6-NTRK3 fusion papillary TC – NTRK1 encodes TRKA → Pain, thermoregulation Previously treated 19 (100%) Previous treatment type (n=19) 33-year-old – NTRK2 encodes TRKB → Movement, memory, mood, appetite, body weight male progressed Surgery 18 (95%) through RAI, – NTRK3 encodes TRKC → Proprioception External beam radiation 18 (95%) pazopanib, trametinib Systemic treatment 12 (63%) n Recurrent chromosomal fusion events have been identified across diverse pediatric and adult Confirmed partial TC specific therapy (n=7) response with 11-17 cancers Iodine-131 3 (43%) larotrectinib 100 mg BID; Kinase inhibitor 4 (57%) Rapid improvement in cervical lymphadenopathy NTRK1/2/3 *Local pathology results Duration of treatment Promoter 5’ partner LBD Kinase domain Study baseline Study cycle 3 day 1 Study cycle 7 day 1 >21 months and ongoing at Larotrectinib is highly effective in TRK fusion TC and SGC July 17, 2017 data cut-off Tyr Tyr ERK Investigator response Independent radiology Durable response in ETV6-NTRK3 fusion MASC of the salivary gland 5’ partner TRK kinase domain assessment (n=19) response assessment (n=19) Measurable disease at baseline Tyr Tyr Tyr Tyr AKT Yes 89.5% 89.5% No 10.5% 10.5% 5’ partner TRK kinase domain 5’ partner TRK kinase domain Best overall response for patients with 66-year-old male progressed through radiotherapy, LBD, ligand binding domain measurable disease at baseline dasatinib, GDC-0941 + erlotinib, Overall response rate 88.2% 88.2% and ABBV-399 TRK fusions are found in diverse cancer histologies Complete response 17.6% 17.6% Best response of PR with Partial response 70.6% 70.6% larotrectinib 100 mg QD* Progressive disease 11.8% 11.8% Duration of treatment >21 months and ongoing at July 17, 2017 data cut-off Larotrectinib is efficacious regardless of tumor type (INV) 40 Study baseline Study cycle 3 day 1 Study cycle 7 day 1 ) 30 * % *Patient enrolled at 100 mg BID and dose reduced to 100 mg QD on C1D2 due to transient dizziness possibly related to drug ( e 20 PR, partial response; QD, once daily; BID, twice daily; RAI, radioactive iodine z i 10 s r o 0 ** m –10 u t –20 Conclusions n i e –30 g n –40 a n h –50 TRK fusions can occur in non-papillary TC, and non-MASC SGC c –60 m n TRK inhibition with larotrectinib yields high response rates, including complete responses, u –70 m i x –80 in adolescents and adults with recurrent pre-treated TRK fusion TC and SGC a Thyroid M –90 n –100 Salivary gland Responses with larotrectinib therapy are generally durable GIST, gastrointestinal stromal tumors *Patient had a mutation at enrollment known to confer resistance to TRK inhibition due to prior TRK inhibitor therapy n Prolonged larotrectinib therapy is associated with minimal toxicity and no drug discontinuations **Patient with anaplastic TC who achieved a complete response in target lesions 2 patients with TC (not shown) had non-measurable disease at baseline for TEAEs Larotrectinib is the first and only selective pan-TRK inhibitor in INV, Investigator response assessment n Genomic profiling with assays capable of identifying TRK fusions should be strongly considered clinical development Larotrectinib efficacy regardless of NTRK fusion (INV) in patients with TC and SGC of all histologies when determining systemic treatment options, especially in the setting of recurrence TRKA/B/C 19 40 n Larotrectinib is a highly potent small-molecule inhibitor of TRKA, ) 30 * % ( References TRKB, and TRKC (5–11 nM IC 50 in cellular assays) e 20 z i 10 s n Highly selective, with little or no interaction with other kinase and r o 0 ** 1. Hyman et al. J Clin Oncol . 2017; 35 (suppl; abstr LBA2501). 11. Chen et al. Anticancer Res . 2014; 34:1595-600. 18 m –10 non-kinase targets u t 2. Prasad et al. Cancer . 2016; 122:1097-107. 12. Fujimoto et al. Proc Natl Acad Sci U S A . 1996; 93:4181-6. –20 n i 3. Greco et al. Mol Cell Endocrinol . 2010; 321:44-9. 13. Dupain et al. Mol Ther Nucleic Acids . 2017; 6:315-26. n Liquid formulation allows dosing of children as young as 1 month e –30 g n –40 4. Skalova. Head Neck Pathol . 2013; 7:S30-6. 14. Wang et al. Comput Math Methods Med . 2015; 2015:912742. of age and delivers equivalent PK to capsules a h –50 5. Vaishnavi et al. Cancer Discov . 2015; 5:25-34. 15. Tognon et al. Cancer Res . 2001; 61:8909-16. c –60 n Larotrectinib is highly active against TRK fusion cancers with m 6. Crowley et al. Cell . 1994; 76:1001-11. 16. Roccato et al. Br J Cancer . 2002; 87:645-53. 1 u –70 m ETV6-NTRK3 7. Smeyne et al. Nature . 1994; 368:246-9. 17. Ardini et al. Mol Oncol . 2014; 8:1495-507. durable responses in both children and adults i x –80 a PPL-NTRK1 8. Skaper. CNS Neurol Disord Drug Targets . 2008; 7:46-62. 18. Doebele et al. Cancer Discov . 2015; 5:1049-57. M –90 9. Ammendrup-Johnsen et al. J Neurosci . 2015; 35:12425-31. 19. Chartier et al. PeerJ . 2013; 1:e126. –100 IRF2BP2-NTRK1 *Patient had a mutation at enrollment known to confer resistance to TRK inhibition due to prior TRK inhibitor therapy 10. Huang and Reichardt. Annu Rev Neurosci . 2001; 24:677-736. PK, pharmacokinetics **Patient with anaplastic TC who achieved a complete response in target lesions 2 patients with TC (not shown) had non-measurable disease at baseline INV, Investigator response assessment Acknowledgments TRK fusion TC and SGC enrolled to 3 separate clinical trials Larotrectinib responses occur early and are durable (INV) n We thank the patients and their families, many of whom traveled long distances to participate in these studies n These studies are funded by Loxo Oncology, Inc • TRK fusion status determined by local CLIA-certified Adult phase I (or similarly accredited) laboratories • Age ≥18 years • Histology determined by local lab • Advanced solid tumors n=4 • Dosing – 18 patients received the dose SCOUT: pediatric phase I/II 19 patients with equivalent of 100 mg BID on a • Age ≤21 years TRK fusion continuous 28-day schedule • Advanced solid tumors n=2 TC and SGC * – One patient received 150 mg BID * Thyroid on the same schedule Salivary gland NAVIGATE: adult/adolescent Treatment ongoing phase II ‘basket’ trial • Response assessed by investigators Time to first response • Age ≥12 years n=13 and by independent radiology review Treatment after progression • Advanced solid tumors according to RECIST v1.1 • TRK fusion positive • 17 patients had measurable disease 0 3 6 9 12 15 18 21 24 27 (5 with TC and 12 with SGC) Median time Data cut-off: July 17, 2017 to response Overall treatment duration (months) 1.84 months BID, twice daily; CLIA, clinical laboratory improvement amendments; RECIST, Response Evaluation Criteria In Solid Tumors *Patient enrolled with non-measurable disease, assessed as non-CR/non-PD INV, Investigator response assessment Copyright 2018.
Load more

Recommended publications
  • Australian Public Assessment Report for Larotrectinib
    Australian Public Assessment Report for Larotrectinib Proprietary Product Name: Vitrakvi Sponsor: Bayer Australia Limited December 2020 Therapeutic Goods Administration About the Therapeutic Goods Administration (TGA) • The Therapeutic Goods Administration (TGA) is part of the Australian Government Department of Health and is responsible for regulating medicines and medical devices. • The TGA administers the Therapeutic Goods Act 1989 (the Act), applying a risk management approach designed to ensure therapeutic goods supplied in Australia meet acceptable standards of quality, safety and efficacy (performance) when necessary. • The work of the TGA is based on applying scientific and clinical expertise to decision- making, to ensure that the benefits to consumers outweigh any risks associated with the use of medicines and medical devices. • The TGA relies on the public, healthcare professionals and industry to report problems with medicines or medical devices. TGA investigates reports received by it to determine any necessary regulatory action. • To report a problem with a medicine or medical device, please see the information on the TGA website <https://www.tga.gov.au>. About AusPARs • An Australian Public Assessment Report (AusPAR) provides information about the evaluation of a prescription medicine and the considerations that led the TGA to approve or not approve a prescription medicine submission. • AusPARs are prepared and published by the TGA. • An AusPAR is prepared for submissions that relate to new chemical entities, generic medicines, major variations and extensions of indications. • An AusPAR is a static document; it provides information that relates to a submission at a particular point in time. • A new AusPAR will be developed to reflect changes to indications and/or major variations to a prescription medicine subject to evaluation by the TGA.
    [Show full text]
  • Cogent Biosciences Announces Creation of Cogent Research Team
    Cogent Biosciences Announces Creation of Cogent Research Team April 6, 2021 Names industry veteran John Robinson, PhD as Chief Scientific Officer New Boulder-based team with exceptional track record of drug discovery and development focused on creating novel small molecule therapies for rare, genetically driven diseases Strong year-end cash position of $242.2 million supports company goals into 2024, including three CGT9486 clinical trials on-track to start this year, beginning with ASM in 1H21 BOULDER, Colo. and CAMBRIDGE, Mass., April 6, 2021 /PRNewswire/ -- Cogent Biosciences, Inc. (Nasdaq: COGT), a biotechnology company focused on developing precision therapies for genetically defined diseases, today announced the formation of the Cogent Research Team led by newly appointed Chief Scientific Officer, John Robinson, PhD. "Today marks an important step forward for Cogent Biosciences as we announce the formation of the Cogent Research Team with a focus on discovering and developing new small molecule therapies for patients fighting rare, genetically driven diseases," said Andrew Robbins, President and Chief Executive Officer of Cogent Biosciences. "I am thrilled to welcome John onboard as Cogent Biosciences' Chief Scientific Officer. John's expertise and seasoned leadership make him ideally suited to lead this new team of world class scientists. Given the team's impressive experience and accomplishments, we are excited for Cogent Biosciences' future and the opportunity to expand our pipeline and deliver novel precision therapies for patients." With an exceptional track record of innovation, the Cogent Research Team will focus on pioneering best-in-class, small molecule therapeutics to both improve upon existing drugs with clear limitations, as well as create new breakthroughs for diseases where others have been unable to find solutions.
    [Show full text]
  • Phase II Study of Selumetinib, an Orally Active Inhibitor of MEK1 and MEK2 Kinases, in KRASG12R-Mutant Pancreatic Ductal Adenocarcinoma
    UC Davis UC Davis Previously Published Works Title Phase II study of selumetinib, an orally active inhibitor of MEK1 and MEK2 kinases, in KRASG12R-mutant pancreatic ductal adenocarcinoma. Permalink https://escholarship.org/uc/item/3520819s Journal Investigational new drugs, 39(3) ISSN 0167-6997 Authors Kenney, Cara Kunst, Tricia Webb, Santhana et al. Publication Date 2021-06-01 DOI 10.1007/s10637-020-01044-8 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Investigational New Drugs (2021) 39:821–828 https://doi.org/10.1007/s10637-020-01044-8 SHORT REPORT Phase II study of selumetinib, an orally active inhibitor of MEK1 and MEK2 kinases, in KRASG12R-mutant pancreatic ductal adenocarcinoma Cara Kenney1 & Tricia Kunst1 & Santhana Webb1 & Devisser Christina Jr2 & Christy Arrowood3 & Seth M. Steinberg4 & Niharika B. Mettu3 & Edward J. Kim2 & Udo Rudloff1,5 Received: 5 November 2020 /Accepted: 3 December 2020 / Published online: 6 January 2021 # This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2020 Summary Background Preclinical evidence has suggested that a subset of pancreatic cancers with the G12R mutational isoform of the KRAS oncogene is more sensitive to MAPK pathway blockade than pancreatic tumors with other KRAS isoforms. We con- ducted a biomarker-driven trial of selumetinib (KOSELUGO™; ARRY-142886), an orally active, allosteric mitogen-activated protein kinase 1 and 2 (MEK1/2) inhibitor, in pancreas cancer patients with somatic KRASG12R mutations. Methods In this two- stage, phase II study (NCT03040986) patients with advanced pancreas cancer harboring somatic KRASG12R variants who had received at least one standard-of-care systemic therapy regimen received 75 mg selumetinib orally twice a day until disease progression or unacceptable toxicity occurred.
    [Show full text]
  • Patient Group Input Submissions
    CBCN’s 2012 Metastatic Breast Cancer Patient and Caregiver Survey Report: An online survey was distributed to patients living with metastatic breast cancer and their caregivers. No patients surveyed had experience with the treatment under review. Survey questions comprised of a combination of scoring options and free form commentary. Patients were contacted through the membership databases of CBCN and other patient organizations. -71 patients participated in the survey -16 caregivers participated in the survey Printed sources: A review was conducted of current studies and grey literature to identify issues and experiences that are commonly shared among many women living with metastatic breast cancer. 3. Disease Experience Metastatic breast cancer is the spread of cancerous cell growth to areas of the body other than where the cancer first formed. It is most commonly spread to the bones, but can include the lungs, liver, brain and skin. Triple-negative breast cancer (TNBC) is breast cancer that is estrogen-receptor-negative, progesterone-receptor-negative and HER2-negative. Accounting for 12-17% of breast cancers, TNBC’s have been shown to be relatively aggressive and display a high risk of metastasis and death within 5 years after diagnosis. TNBC is considered to be vastly heterogeneous and is often used as an umbrella term, encompassing a wide spectrum of entities with marked genetic, transcriptional, histological, and clinical differences. 1 A rare cancer that is more commonly associated with TNBC, is secretory breast carcinomas- a cancer that occurs due to an over secretion of mucin in the tumor. It is considered a subtype of invasive ductal carcinoma but is prone to metastasis and local recurrence.
    [Show full text]
  • 2020 Master Class Course Best Practices and Expanding Treatment Options in Soft Tissue Sarcomas Including GIST George D
    2020 Master Class Course Best Practices and Expanding Treatment Options in Soft Tissue Sarcomas including GIST George D. Demetri, MD FACP FASCO 1 George D. Demetri, MD Faculty Disclosure • Scientific consultant with sponsored research to Dana-Farber: Bayer, Pfizer, Novartis, Epizyme, Roche/Genentech, Epizyme, LOXO Oncology, AbbVie, GlaxoSmithKline, Janssen, PharmaMar, Daiichi-Sankyo, AdaptImmune • Scientific consultant: GlaxoSmithKline, EMD-Serono, Sanofi, ICON plc, MEDSCAPE, Mirati, WCG/Arsenal Capital, Polaris, MJ Hennessey/OncLive, C4 Therapeutics, Synlogic, McCann Health • Consultant/SAB member with minor equity holding: G1 Therapeutics, Caris Life Sciences, Erasca Pharmaceuticals, RELAY Therapeutics, Bessor Pharmaceuticals, Champions Biotechnology, Caprion/HistoGeneX • Board of Directors member and Scientific Advisory Board Consultant with minor equity holding: Blueprint Medicines, Translate BIO • Patents/Royalties: Novartis royalty to Dana-Farber for use patent of imatinib in GIST • Non-Financial Interests: AACR Science Policy and Government Affairs Committee Chair, Alexandria Real Estate Equities, Faculty of this CE activity may include discussions of products or devices that are not currently labeled for use by the FDA. The faculty have been informed of their responsibility to disclose to the audience if they will be discussing off label or investigational uses (any uses not approved by the FDA) of products or devices. 2 Soft Tissue Sarcomas: Approximate Anatomic Distribution Head and Neck 10% Upper extremities 15% Trunk 10% Retroperitoneal, pelvic and visceral Lower extremities 15% 50% (includes GIST and GYN sarcomas) Modified from Clark MA et al. NEJM 2005;353:701-11 3 Sarcomas represent an exceedingly diverse set of diseases Bone Sarcomas 10% GIST Un- differentiated Liposarcomas Leiomyo- Sarcomas 4 Ducimetiere et al.
    [Show full text]
  • Presentación De Powerpoint
    Molecular Tumor Board in Non-Small Cell Lung Cancer Jordi Remon Masip CIOCC Barcelona – HM Delfos @JordiRemon #SEOM20 Disclosure Information I do not have COI related to this specific presentation Why do we need a MTB in NSCLC? • Introduction • To understand the genomic profile from NGS reports • To prioritize the druggable genomic alteration: baseline / resistant • Increasing the detection of potential druggable genomic alterations • To include patients in basket trials • NGS is a reality but MTB and precision approach have challenges MTB is included in one equation MOLECULAR TUMOR BOARD Y MTB is included in one equation GENOMIC MOLECULAR TUMOR PROFILE BOARD X + Y MTB is included in one equation GENOMIC MOLECULAR TUMOR PERSONALISED PROFILE BOARD TREATMENT X + Y = Z Precision oncology in practice EGFR TKI Find actionable gens with ALK/ROS1 TKI approved therapy BRAF TKI Find actionable genes for RET / NTRK TKI clinical trials MET TKI Precision oncology in practice EGFR TKI Find actionable gens with ALK/ROS1 TKI approved therapy BRAF TKI Find actionable genes for RET / NTRK TKI clinical trials MET TKI Additional information about non-actionable gene mutations prognostic markers of sensitivity Two major steps in NSCLC outcome Immunotherapy Personalised treatment, ALK+: 5-y OS, KEYNOTE 024 Trial 5-y OS, ALEX trial Median OS, HR, (95%CI) 5-Year OS Rate, Median OS, HR, (95%CI) 5-Year OS Rate, mo % mo % 26.3 0.62 31.9 Not reached 0.67 63 13.4 (0.48-0.81) 16.7 57.4 (0.46-0.98) 46 Alectinib 26.4% Crizotinib Pembrolizumab Chemotherapy Brahmer – ESMO 2020 Mok – Annls of Oncology 2020 Number of oncogenes increases over time NTRK rearrangement Figure from Garrido – CTO 2019 (modified based on updated ESMO guidelines 2020 by Planchard et al.) Number of oncogenes increases over time NRG1 KRAS RET MET HER2 UN NTRK rearrangement Coming Future….
    [Show full text]
  • TRK Inhibitors: Tissue-Agnostic Anti-Cancer Drugs
    pharmaceuticals Review TRK Inhibitors: Tissue-Agnostic Anti-Cancer Drugs Sun-Young Han Research Institute of Pharmaceutical Sciences and College of Pharmacy, Gyeongsang National University, Jinju-si 52828, Korea; [email protected] Abstract: Recently, two tropomycin receptor kinase (Trk) inhibitors, larotrectinib and entrectinib, have been approved for Trk fusion-positive cancer patients. Clinical trials for larotrectinib and entrectinib were performed with patients selected based on the presence of Trk fusion, regardless of cancer type. This unique approach, called tissue-agnostic development, expedited the process of Trk inhibitor development. In the present review, the development processes of larotrectinib and entrectinib have been described, along with discussion on other Trk inhibitors currently in clinical trials. The on-target effects of Trk inhibitors in Trk signaling exhibit adverse effects on the central nervous system, such as withdrawal pain, weight gain, and dizziness. A next generation sequencing-based method has been approved for companion diagnostics of larotrectinib, which can detect various types of Trk fusions in tumor samples. With the adoption of the tissue-agnostic approach, the development of Trk inhibitors has been accelerated. Keywords: Trk; NTRK; tissue-agnostic; larotrectinib; entrectinib; Trk fusion 1. Introduction Citation: Han, S.-Y. TRK Inhibitors: Tropomyosin receptor kinases (Trk) are tyrosine kinases encoded by neurotrophic Tissue-Agnostic Anti-Cancer Drugs. tyrosine/tropomyosin receptor kinase (NTRK) genes [1]. Chromosomal rearrangement of Pharmaceuticals 2021, 14, 632. https:// NTRK genes is found in cancer tissues [2]. The resulting fusion proteins containing part of doi.org/10.3390/ph14070632 the Trk protein have a constitutively active form of kinase that transduces deregulating signals.
    [Show full text]
  • (NCCN) Breast Cancer Clinical Practice Guidelines
    NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Breast Cancer Version 5.2020 — July 15, 2020 NCCN.org NCCN Guidelines for Patients® available at www.nccn.org/patients Continue Version 5.2020, 07/15/20 © 2020 National Comprehensive Cancer Network® (NCCN®), All rights reserved. NCCN Guidelines® and this illustration may not be reproduced in any form without the express written permission of NCCN. NCCN Guidelines Index NCCN Guidelines Version 5.2020 Table of Contents Breast Cancer Discussion *William J. Gradishar, MD/Chair ‡ † Sharon H. Giordano, MD, MPH † Sameer A. Patel, MD Ÿ Robert H. Lurie Comprehensive Cancer The University of Texas Fox Chase Cancer Center Center of Northwestern University MD Anderson Cancer Center Lori J. Pierce, MD § *Benjamin O. Anderson, MD/Vice-Chair ¶ Matthew P. Goetz, MD ‡ † University of Michigan Fred Hutchinson Cancer Research Mayo Clinic Cancer Center Rogel Cancer Center Center/Seattle Cancer Care Alliance Lori J. Goldstein, MD † Hope S. Rugo, MD † Jame Abraham, MD ‡ † Fox Chase Cancer Center UCSF Helen Diller Family Case Comprehensive Cancer Center/ Comprehensive Cancer Center Steven J. Isakoff, MD, PhD † University Hospitals Seidman Cancer Center Massachusetts General Hospital Amy Sitapati, MD Þ and Cleveland Clinic Taussig Cancer Institute Cancer Center UC San Diego Moores Cancer Center Rebecca Aft, MD, PhD ¶ Jairam Krishnamurthy, MD † Karen Lisa Smith, MD, MPH † Siteman Cancer Center at Barnes- Fred & Pamela Buffet Cancer Center The Sidney Kimmel Comprehensive Jewish Hospital and Washington Cancer Center at Johns Hopkins University School of Medicine Janice Lyons, MD § Case Comprehensive Cancer Center/ Mary Lou Smith, JD, MBA ¥ Doreen Agnese, MD ¶ University Hospitals Seidman Cancer Center Research Advocacy Network The Ohio State University Comprehensive and Cleveland Clinic Taussig Cancer Institute Cancer Center - James Cancer Hospital Hatem Soliman, MD † and Solove Research Institute P.
    [Show full text]
  • Treating Stomach Cancer
    cancer.org | 1.800.227.2345 Treating Stomach Cancer If you've been diagnosed with stomach cancer (also known as gastric cancer), your cancer care team will discuss your treatment options with you. It's important to weigh the benefits of each treatment option against the possible risks and side effects. How is stomach cancer treated? The main treatments for stomach cancer are: ● Surgery for Stomach Cancer ● Chemotherapy for Stomach Cancer ● Targeted Drug Therapy for Stomach Cancer ● Immunotherapy for Stomach Cancer ● Radiation Therapy for Stomach Cancer Common treatment approaches Often the best approach uses 2 or more types of treatment. Your treatment options depend on many factors. The location and the stage (extent of spread) of the cancer are very important. In choosing your treatment plan, you and your cancer care team will also take your age, overall health, and personal preferences into account. ● Treatment Choices Based on the Extent of Stomach Cancer Who treats stomach cancer? Stomach cancer is often treated by a team of doctors with different specialties. Most likely, your treatment team will include: 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 ● A gastroenterologist: a doctor who specializes in treating diseases of the digestive system ● A surgical oncologist: a doctor who treats cancer with surgery ● A medical oncologist: a doctor who treats cancer with medicines such as chemotherapy, targeted therapy, and immunotherapy ● A radiation oncologist: a doctor who treats cancer with radiation therapy You might have many other health care professionals on your treatment team as well, including physician assistants (PAs), nurse practitioners (NPs), nurses, psychologists, social workers, nutrition specialists, rehabilitation specialists, and others.
    [Show full text]
  • Larotrectinib Versus Prior Therapies in Tropomyosin Receptor Kinase Fusion Cancer: an Intra-Patient Comparative Analysis
    cancers Article Larotrectinib versus Prior Therapies in Tropomyosin Receptor Kinase Fusion Cancer: An Intra-Patient Comparative Analysis 1,2, 3, 4 5 Antoine Italiano *, Shivani Nanda z, Andrew Briggs , Jesus Garcia-Foncillas , Ulrik Lassen 6 , Gilles Vassal 7, Shivaani Kummar 8,§, Cornelis M. van Tilburg 9, 10 11, 3 3 3 David S. Hong , Theodore W. Laetsch k, Karen Keating , John A. Reeves , Marc Fellous , 3 12,13, 12,13, ,¶ Barrett H. Childs , Alexander Drilon y and David M. Hyman y 1 Early Phase Trials Unit, Institut Bergonie, 33000 Bordeaux, France 2 University of Bordeaux, 33076 Bordeaux, France 3 Bayer HealthCare Pharmaceuticals, Inc., Whippany, NJ 07981, USA; [email protected] (S.N.); [email protected] (K.K.); [email protected] (J.A.R.); [email protected] (M.F.); [email protected] (B.H.C.) 4 London School of Hygiene & Tropical Medicine, Bloomsbury, London WC1E 7HT, UK; [email protected] 5 OncoHealth Institute, University Hospital Fundación Jiménez Díaz, 28040 Madrid, Spain; [email protected] 6 Department of Oncology, Rigshospitalet, 2100 Copenhagen, Denmark; [email protected] 7 Institut Gustave Roussy, 94800 Villejuif Cedex, France; [email protected] 8 Stanford Cancer Institute, Stanford University, Palo Alto, CA 94304, USA; [email protected] 9 Hopp Children’s Cancer Center Heidelberg (KiTZ), Heidelberg University Hospital and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; [email protected] 10 Investigational Cancer Therapeutics,
    [Show full text]
  • November 18 - 21, 2020
    November 18 - 21, 2020 ALL TIMES ARE EASTERN STANDARD TIME (EST) Wednesday, 18 November, 2020 8:00 am - 11:00 am TARPSWG Meeting (email: [email protected]) – Chair: Alessandro Gronchi 11:00 am - 1:00 pm Ultra Rare Sarcoma Meeting – Chair: Silvia Stacchiotti 1:00 pm - 3:00 pm SARC Meeting 3:00 pm - 5:00 pm SELNET Meeting: State of Art of Management for Localized STS in Limbs and Retroperitoneum – Chair: Javier Martin-Broto Thursday, 19 November, 2020 8:00 am - 9:00 am – Session 1 – OPENING CEREMONY INTRODUCTION TO CTOS 2020 President: Kirsten Sundby Hall Program Chairs: Silvia Stacchiotti, Margaret von Mehren, Inga-Marie Schaefer 25 YEAR RETROSPECTIVE Presenter: Shreyas Patel 9:00 am - 10:00 am – Session 2 – IMMUNOTHERAPY IN SARCOMA: ALVEOLAR SOFT PART SARCOMA, CLEAR CELL SARCOMA, SYNOVIAL SARCOMA Chair: Seth Pollack Discussant: Breelyn Wilky Panelists: Armelle Dufresne, Bob Maki, Enrico Grignani Presenters: Akira Kawai, Nadia Hindi, Sandra d'Angelo, Brian van Tine Paper #01 3421748 EFFICACY AND SAFETY OF NIVOLUMAB MONOTHERAPY IN PATIENTS WITH UNRESECTABLE CLEAR CELL SARCOMA AND ALVEOLAR SOFT PART SARCOMA (OSCAR TRIAL, NCCH1510): A MULTICENTER, PHASE 2 CLINICAL TRIAL Akira Kawai2, Tadaaki Nishikawa1, Mamiko Kawasaki3, Sawako Tomatsuri3, Nobuko Okamura3, Gakuto Ogawa3, Akihiro Hirakawa4, Taro Shibata3, Kenichi Nakamura3, Shigeki Kakunaga5, Kenji Tamura1, Masashi Ando6, Toshifumi Ozaki7, Takafumi Ueda5, Kan Yonemori1 1Breast and Medical Oncology, National Cancer Center Hospital, Tokyo, JAPAN; 2Oncology and Rehabilitation Medicine, National
    [Show full text]
  • NCCN Guidelines for Central Nervous System Cancers Cancer V.1.2021 – Annual 10/23/2020
    NCCN Guidelines for Central Nervous System Cancers Cancer v.1.2021 – Annual 10/23/2020 Guideline Page Institution Vote Panel Discussion/References and Request YES NO ABSTAIN ABSENT GLIO-1, GLIO-5 Based on a review of the data and discussion, the 0 24 0 5 External request: panel consensus did not support the addition of these specific recommendations into the Guidelines as they Submission/NX Development Corp (06/02/20): agree that this is already covered in the Guideline. For the Anaplastic Oligodendroglioma, Anaplastic Oligoastrocytoma, Anaplastic Astrocytoma, Anaplastic Gliomas and Glioblastoma (GLIO-1) workflow, under surgery, we recommend inclusion of Aminolevulinic acid hydrochloride (ALA, Brand Name Gleolan™) as an adjunct for the visualization of malignant tissue and to improve the completeness of resection during fluorescence guided glioma surgery. For the Anaplastic Oligodendroglioma, Anaplastic Oligoastrocytoma, Anaplastic Astrocytoma, Anaplastic Gliomas and Glioblastoma (GLIO-5) workflow, under recurrence resection, we recommend inclusion of Aminolevulinic acid hydrochloride (ALA, Brand Name Gleolan™) as an adjunct for the visualization of malignant tissue and to improve the completeness of resection during fluorescence guided glioma surgery. GLIO-2 The panel consensus supported the removal of 24 0 0 5 Internal request: “Standard RT + neoadjuvant or adjuvant PCV” for adjuvant treatment of anaplastic astrocytoma Consider removal of “Standard RT ÷ neoadjuvant or adjuvant PCV” for adjuvant treatment of anaplastic astrocytoma BRAIN-D (1 of 15, 2 of 15, 3 of 15) The panel consensus supported the inclusion of 24 0 0 5 Internal request: larotrectinib and entrectinib for tumors with NTRK gene fusion for recurrent or progressive disease Consider including larotrectinib and entrectinib for under useful in certain circumstances for low-grade NTRK gene fusion tumors.
    [Show full text]