Oncology Presentation
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Identification of Recurrent Mutational Events in Anorectal Melanoma
Modern Pathology (2017) 30, 286–296 286 © 2017 USCAP, Inc All rights reserved 0893-3952/17 $32.00 Identification of recurrent mutational events in anorectal melanoma Hui Min Yang1,2,6, Susan J Hsiao1,6, David F Schaeffer2, Chi Lai3, Helen E Remotti1, David Horst4, Mahesh M Mansukhani1 and Basil A Horst1,5 1Department of Pathology & Cell Biology, Columbia University Medical Center, New York, NY, USA; 2Department of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; 3Department of Pathology and Laboratory Medicine, University of Ottawa, Ottawa, ON, Canada; 4Pathologisches Institut, Ludwig-Maximilians-Universitaet, Muenchen, Germany and 5Department of Dermatology, Columbia University Medical Center, New York, NY, USA Anorectal melanoma is a rare disease that carries a poor prognosis. To date, limited genetic analyses confirmed KIT mutations as a recurrent genetic event similar to other mucosal melanomas, occurring in up to 30% of anorectal melanomas. Importantly, a subset of tumors harboring activating KIT mutations have been found to respond to c-Kit inhibitor-based therapy, with improved patient survival at advanced tumor stages. We performed comprehensive targeted exon sequencing analysis of 467 cancer-related genes in a larger series of 15 anorectal melanomas, focusing on potentially actionable variants based on gain- and loss-of-function mutations. We report the identification of oncogenic driver events in the majority (93%) of anorectal melanomas. These included variants in canonical MAPK pathway effectors rarely observed in cutaneous melanomas (including an HRAS mutation, as well as a BRAF mutation resulting in duplication of threonine 599), and recurrent mutations in the tumor suppressor NF1 in 20% of cases, which represented the second-most frequently mutated gene after KIT in our series. -
Mutant Cancers 2 3 Heinz Hammerlindl1*, Dinoop Ravindran Menon1*, Sabrina Hammerlindl1, Abdullah Al
Author Manuscript Published OnlineFirst on December 1, 2017; DOI: 10.1158/1078-0432.CCR-16-2118 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Hammerlindl et. al 1 Acetylsalicylic Acid Governs the Effect of Sorafenib in RAS Mutant Cancers 2 3 Heinz Hammerlindl1*, Dinoop Ravindran Menon1*, Sabrina Hammerlindl1, Abdullah Al 4 Emran1, Joachim Torrano1, Katrin Sproesser3, Divya Thakkar1, Min Xiao3, Victoria G. 5 Atkinson5, Brian Gabrielli4, Nikolas K. Haass2, Meenhard Herlyn3, Clemens Krepler3, Helmut 6 Schaider1,2† 7 8 1Dermatology Research Centre, The University of Queensland, The University of 9 Queensland Diamantina Institute, Translational Research Institute, Brisbane, Australia; 10 2The University of Queensland, The University of Queensland Diamantina Institute, 11 Translational Research Institute, Brisbane, Australia; 12 3The Wistar Institute, Philadelphia, PA, U.S.A.; 13 4Mater Medical Research Institute, The University of Queensland, Translational Research 14 Institute, Brisbane, Australia; 15 5Division of Cancer Services, Princess Alexandra Hospital, Brisbane, Australia; 16 *These authors contributed equally to the study 17 18 Running title: 19 Combined aspirin and sorafenib for RAS-mutant cancer therapy 20 21 Key words: 22 Melanoma, Lung Cancer, NRAS, Sorafenib, Aspirin, RAS, ERK, AMPK 23 24 25 26 27 28 1 Downloaded from clincancerres.aacrjournals.org on September 24, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on December 1, 2017; DOI: 10.1158/1078-0432.CCR-16-2118 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Hammerlindl et. al 1 2 Grant Support 3 This work was funded by the Epiderm Foundation (H.S.), the Princess Alexandra Hospital 4 Research Foundation (PARSS2016_NearMiss) (H.S.), NIH grants PO1 CA114046, P50 5 CA174523, and the Dr. -
FOI Reference: FOI 414 - 2021
FOI Reference: FOI 414 - 2021 Title: Researching the Incidence and Treatment of Melanoma and Breast Cancer Date: February 2021 FOI Category: Pharmacy FOI Request: 1. How many patients are currently (in the past 3 months) undergoing treatment for melanoma, and how many of these are BRAF+? 2. In the past 3 months, how many melanoma patients (any stage) were treated with the following: • Cobimetinib • Dabrafenib • Dabrafenib AND Trametinib • Encorafenib AND Binimetinib • Ipilimumab • Ipilimumab AND Nivolumab • Nivolumab • Pembrolizumab • Trametinib • Vemurafenib • Vemurafenib AND Cobimetinib • Other active systemic anti-cancer therapy • Palliative care only 3. If possible, could you please provide the patients treated in the past 3 months with the following therapies for metastatic melanoma ONLY: • Ipilimumab • Ipilimumab AND Nivolumab • Nivolumab • Pembrolizumab • Any other therapies 4. In the past 3 months how many patients were treated with the following for breast cancer? • Abemaciclib + Anastrozole/Exemestane/Letrozole • Abemaciclib + Fulvestrant • Alpelisib + Fulvestrant • Atezolizumab • Bevacizumab [Type text] • Eribulin • Everolimus + Exemestane • Fulvestrant as a single agent • Gemcitabine + Paclitaxel • Lapatinib • Neratinib • Olaparib • Palbociclib + Anastrozole/Exemestane/Letrozole • Palbociclib + Fulvestrant • Pertuzumab + Trastuzumab + Docetaxel • Ribociclib + Anastrozole/Exemestane/Letrozole • Ribociclib + Fulvestrant • Talazoparib • Transtuzumab + Paclitaxel • Transtuzumab as a single agent • Trastuzumab emtansine • Any other -
Targeting ALK: Precision Medicine Takes on Drug Resistance
Published OnlineFirst January 25, 2017; DOI: 10.1158/2159-8290.CD-16-1123 REVIEW Targeting ALK: Precision Medicine Takes on Drug Resistance Jessica J. Lin 1 , Gregory J. Riely 2 , and Alice T. Shaw 1 ABSTRACT Anaplastic lymphoma kinase (ALK) is a validated molecular target in several ALK - rearranged malignancies, including non–small cell lung cancer. However, the clinical benefi t of targeting ALK using tyrosine kinase inhibitors (TKI) is almost universally limited by the emergence of drug resistance. Diverse mechanisms of resistance to ALK TKIs have now been discov- ered, and these basic mechanisms are informing the development of novel therapeutic strategies to overcome resistance in the clinic. In this review, we summarize the current successes and challenges of targeting ALK. Signifi cance: Effective long-term treatment of ALK -rearranged cancers requires a mechanistic under- standing of resistance to ALK TKIs so that rational therapies can be selected to combat resistance. This review underscores the importance of serial biopsies in capturing the dynamic therapeutic vulnerabili- ties within a patient’s tumor and offers a perspective into the complexity of on-target and off-target ALK TKI resistance mechanisms. Therapeutic strategies that can successfully overcome, and poten- tially prevent, these resistance mechanisms will have the greatest impact on patient outcome. Cancer Discov; 7(2); 137–55. ©2017 AACR. INTRODUCTION trials demonstrating remarkable responses in this patient population ( 3–8 ). Yet, as with any targeted therapy, tumor The discovery of anaplastic lymphoma kinase ( ALK ) dates cells evolve and invariably acquire resistance to ALK TKIs, back to 1994 when a chromosomal rearrangement t(2;5), leading to clinical relapse. -
Tyrosine Kinase Inhibitors Or ALK Inhibitors for the First Line Treatment of Non-Small Cell Lung Cancer
Tyrosine kinase inhibitors or ALK inhibitors for the first line treatment of Non-small cell lung cancer This application seeks the addition of tyrosine kinase inhibitor erlotinib (representative of class) and gefitinib and afatinib (alternatives) as well as ALK-inhibitor crizotinib to the list of the Essential Medicines List for the treatment of non-small cell lung cancer. Introduction In 2013, there were approximately 1.8 million incident lung cancer cases diagnosed worldwide and approximately 1.6 million deaths from the disease (1). Lung cancer had the second highest absolute incidence globally after breast cancer, and in 93 countries was the leading cause of death from malignant disease, accounting for one fifth of the total global burden of disability- adjusted life years from cancer. Men were more likely to develop lung cancer than women, with 1 in 18 men and 1 in 51 women being diagnosed between birth and age 79 years (1). Non-small cell lung cancer (NSCLC) is the most common form of the disease, accounting for 85–90% of all lung cancers (2)(43). For patients with resectable disease, adjuvant chemotherapy improves the absolute 5-year survival rates in Stage II and III NSCLC (9,13,65,44-47). Acceptable adjuvant chemotherapy options include etoposide/cisplatin, docetaxel/cisplatin, gemcitabine/cisplatin, pemetrexed/cisplatin, and carboplatin/paclitaxel for patients with comorbidities or unable to tolerate cisplatin. In patients with non-metastatic but inoperable NSCLC or Stage III disease, concurrent chemoradiotherapy has been shown to improve overall survival (OS) and median survival (47-53). However, most patients with NSCLC present with advanced stage disease – stage IV in particular – and half of all patients treated initially for potentially curable early-stage disease will experience recurrences with metastatic disease (3). -
Crc Research
JUNE 2020 COLORECTAL CANCER RESEARCH & PRACTICE UPDATES Colorectal Cancer Canada curates monthly Research & Practice Updates to inform clinicians, patients and their loved ones of new innovations in colorectal cancer care. The following updates extend from June 1st 2020 to June 30th, 2020 inclusive and are intended for informational purposes only JUNE 2020 PREVIEW DRUGS & SYSTEMIC THERAPIES ........................................................................................................... 2 Practice-changing GI Cancer Highlights from Virtual ASCO 2020 ................................................................................................ 2 Updated BEACON: Doublet as good as triplet in metastatic CRC ................................................................................................ 2 Pembrolizumab doubles progression-free survival in MSI-H/dMMR metastatic colorectal cancer ............................................ 2 Updated findings from the CheckMate-142 trial in mCRC .......................................................................................................... 2 DRUGS & SYSTEMIC THERAPIES 1 Practice-changing GI cancer highlights from virtual ASCO 2020 12 June 2020 The American Society of Clinical Oncology (ASCO) held its annual meeting at the end of last month online and presented various findings which are likely to have a positive impact on colorectal cancer (CRC) treatment in the near future. One study looked at the treatment of locally-advanced rectal cancer with a high-dose of FOLFIRINOX -
Tumor Resistance Against ALK Targeted Therapy-Where It Comes from and Where It Goes
cancers Review Tumor Resistance against ALK Targeted Therapy-Where It Comes From and Where It Goes Geeta Geeta Sharma 1,† ID , Ines Mota 2,†, Luca Mologni 1,3 ID , Enrico Patrucco 2, Carlo Gambacorti-Passerini 1,3,4,† and Roberto Chiarle 2,5,†,* 1 Department of Medicine and Surgery, University of Milano-Bicocca, Monza 20900, Italy; [email protected] (G.G.S.); [email protected] (L.M.); [email protected] (C.G.-P.) 2 Department of Molecular Biotechnology and Health Sciences, University of Turin, Turin 10124, Italy; [email protected] (I.M.); [email protected] (E.P.) 3 Galkem Srl, Monza 20900, Italy 4 Hematology and Clinical Research Unit, San Gerardo Hospital, Monza 20900, Italy 5 Department of Pathology, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, USA * Correspondence: [email protected] † These authors contributed equally to this work. Received: 1 February 2018; Accepted: 26 February 2018; Published: 28 February 2018 Abstract: Anaplastic lymphoma kinase (ALK) is a validated molecular target in several ALK-rearranged malignancies, particularly in non-small-cell lung cancer (NSCLC), which has generated considerable interest and effort in developing ALK tyrosine kinase inhibitors (TKI). Crizotinib was the first ALK inhibitor to receive FDA approval for ALK-positive NSCLC patients treatment. However, the clinical benefit observed in targeting ALK in NSCLC is almost universally limited by the emergence of drug resistance with a median of occurrence of approximately 10 months after the initiation of therapy. Thus, to overcome crizotinib resistance, second/third-generation ALK inhibitors have been developed and received, or are close to receiving, FDA approval. -
Melanoma in Focus
MELANOMA IN FOCUS Current Developments in the Management of Melanoma Section Editor: John M. Kirkwood, MD Melanoma in Focus In the Pipeline: Encorafenib and Binimetinib in BRAF-Mutated Melanoma Keith Flaherty, MD Professor of Medicine Harvard Medical School Boston, Massachusetts H&O What makes the BRAF inhibitor encorafenib The FDA is currently reviewing the use of plus the MEK inhibitor binimetinib a good encorafenib/binimetinib in patients with BRAFmutant combination for use in BRAF-mutated locally advanced, unresectable, or metastatic melanoma; melanoma? Array BioPharma submitted the application in June 2017 on the basis of the results of COLUMBUS. Nothing KF Like other combinations of BRAF and MEK further will be known until the FDA has completed its inhibitors, encorafenib/binimetinib has been dem standard review. on strated to be superior to monotherapy with a BRAF inhibitor for patients who have BRAFmutated H&O Could you talk more about the design and melanoma. The phase 3 COLUMBUS trial (Study results of COLUMBUS? Comparing Combination of LGX818 Plus MEK162 Versus Vemurafenib and LGX818 Monotherapy in KF COLUMBUS, which I presented at the Society for BRAF Mutant Melanoma) showed better progression Melanoma Research 2016 Congress in November of free survival (PFS) and overall response rates (ORRs) that year, was designed to demonstrate the superiority with encorafenib/binimetinib than with the BRAF of encorafenib/binimetinib over encorafenib alone or inhibitor vemurafenib (Zelboraf, Genentech/Daiichi vemurafenib (Table). It included 921 patients who had Sankyo). locally advanced, unresectable, or metastatic melanoma Followup in this trial has not been long enough to with a BRAF V600 mutation. -
Oncology Orals Solid Tumors
Oncology Oral Medications Solid Tumors Enrollment Form Fax Referral To: 1-800-323-2445 Phone: 1-800-237-2767 Email Referral To: [email protected] Six Simple Steps to Submitting a Referral 1 PATIENT INFORMATION (Complete or include demographic sheet) Patient Name: _______________________________________ Address: ____________________________ City, State, ZIP Code: ___________________________________ Preferred Contact Methods: Phone (primary # provided below) Text (cell # provided below) Email (email provided below) Note: Carrier charges may apply. If unable to contact via text or email, Specialty Pharmacy will attempt to contact by phone. Primary Phone: ____________________________ Alternate Phone: ________________________________ Primary Language: _________________________________ DOB: __________________ Gender: Male Female Email: __________________________________ Last Four of SSN: ________ 2 PRESCRIBER INFORMATION Prescriber’s Name: _________________________________________________________________ State License #: _____________________________________ NPI #: _____________________ DEA #: _____________________ Group or Hospital: _______________________________________________________________ Address: ______________________________________________ City, State, ZIP Code: ______________________________________________________________ Phone: ______________________ Fax: ______________________ Contact Person: ________________________ Contact’s Phone: _______________________ 3 INSURANCE INFORMATION Please fax copy of prescription -
2020 VIRTUAL NF CONFERENCE JUNE 15 - 16, 2020 Keeping the NF Community Connected
2020 VIRTUAL NF CONFERENCE JUNE 15 - 16, 2020 Keeping the NF community connected CONTENTS Table of Contents INFORMATION Welcome Message .................................................................................................................4 Foundation Staff .....................................................................................................................5 Advisory Boards ....................................................................................................................6 Funding Opportunities ............................................................................................................7 The Friedrich von Recklinghausen Award: NF Tradition and Progress .......................................8 Schedule at a Glance ..............................................................................................................9 Conference Co-Chairs ..........................................................................................................10 Keynote Speaker ..................................................................................................................11 Agenda ................................................................................................................................12 Acknowledgments ................................................................................................................72 Sponsor ...............................................................................................................................73 -
Braftovi, INN-Encorafenib
ANNEX I SUMMARY OF PRODUCT CHARACTERISTICS 1 This medicinal product is subject to additional monitoring. This will allow quick identification of new safety information. Healthcare professionals are asked to report any suspected adverse reactions. See section 4.8 for how to report adverse reactions. 1. NAME OF THE MEDICINAL PRODUCT Braftovi 50 mg hard capsules Braftovi 75 mg hard capsules 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Braftovi 50 mg hard capsules Each hard capsule contains 50 mg of encorafenib. Braftovi 75 mg hard capsules Each hard capsule contains 75 mg of encorafenib. For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM Hard capsule (capsule). Braftovi 50 mg hard capsules Orange opaque cap and flesh opaque body, printed with a stylised “A” on the cap and “LGX 50mg” on the body. The length of the capsule is approximately 22 mm. Braftovi 75 mg hard capsules Flesh coloured opaque cap and white opaque body, printed with a stylised “A” on the cap and “LGX 75mg” on the body. The length of the capsule is approximately 23 mm. 4. CLINICAL PARTICULARS 4.1 Therapeutic indications Encorafenib is indicated: - in combination with binimetinib for the treatment of adult patients with unresectable or metastatic melanoma with a BRAF V600 mutation (see sections 4.4 and 5.1). - in combination with cetuximab, for the treatment of adult patients with metastatic colorectal cancer (CRC) with a BRAF V600E mutation, who have received prior systemic therapy (see sections 4.4 and 5.1). 4.2 Posology and method of administration Encorafenib treatment should be initiated and supervised under the responsibility of a physician experienced in the use of anticancer medicinal products. -
ALK) Inhibitors for Treatment-Naïve ALK-Positive Lung Cancer
cancers Systematic Review Systematic Review and Network Meta-Analysis of Anaplastic Lymphoma Kinase (ALK) Inhibitors for Treatment-Naïve ALK-Positive Lung Cancer Cheng-Hao Chuang 1,† , Hsiao-Ling Chen 2,†, Hsiu-Mei Chang 2 , Yu-Chen Tsai 1, Kuan-Li Wu 1, I-Hua Chen 3, Kung-Chao Chen 3, Jui-Ying Lee 4, Yong-Chieh Chang 2, Chin-Ling Chen 5 , Yu-Kang Tu 6,7 , Jen-Yu Hung 1,5,8 , Chih-Jen Yang 1,8,9,10,* and Inn-Wen Chong 1,8,10,* 1 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan; [email protected] (C.-H.C.); [email protected] (Y.-C.T.); [email protected] (K.-L.W.); [email protected] (J.-Y.H.) 2 Department of Pharmacy, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan; [email protected] (H.-L.C.); [email protected] (H.-M.C.); [email protected] (Y.-C.C.) 3 Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan; [email protected] (I-H.C.); [email protected] (K.-C.C.) 4 Division of Chest Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan; [email protected] 5 Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan; [email protected] Citation: Chuang, C.-H.; Chen, H.-L.; 6 Institute of Epidemiology and Preventive Medicine, National Taiwan University, Taipei 100, Taiwan; Chang, H.-M.; Tsai, Y.-C.; Wu, K.-L.; [email protected] Chen, I-H.; Chen, K.-C.; Lee, J.-Y.; 7 Department of Medical Research, National Taiwan University Hospital, Taipei 100, Taiwan Chang, Y.-C.; Chen, C.-L.; et al.