27 results on '"Jankowitz R"'
Search Results
2. Prevention of bone loss with risedronate in breast cancer survivors: a randomized, controlled clinical trial
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Greenspan, S. L., Vujevich, K. T., Brufsky, A., Lembersky, B. C., van Londen, G. J., Jankowitz, R. C., Puhalla, S. L., Rastogi, P., and Perera, S.
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- 2015
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3. A phase II prospective open-label escalating dose trial of recombinant interleukin-11 in mild von Willebrand disease
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RAGNI, M. V., JANKOWITZ, R. C., CHAPMAN, H. L., MERRICKS, E. P., KLOOS, M. T., DILLOW, A. M., and NICHOLS, T. C.
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- 2008
4. Abstract P2-09-05: LCCC 1525: A phase II study of a priming dose of cyclophosphamide prior to pembrolizumab to treat metastatic triple negative breast cancer (mTNBC)
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Anders, CK, primary, Moore, D, additional, Sambade, M, additional, Cuaboy, L, additional, Garrett, A, additional, Woodcock, M, additional, McKinnon, K, additional, Cowens, K, additional, Bortone, D, additional, Calhoun, B, additional, Carey, L, additional, Dees, C, additional, Jolly, T, additional, Muss, H, additional, Reeder-Hayes, K, additional, Kaltman, R, additional, Jankowitz, R, additional, Gudena, V, additional, Olajide, O, additional, Perou, C, additional, Vincent, B, additional, and Serody, J, additional
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- 2019
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5. Prediction of Breast and Prostate Cancer Risks in Male BRCA1 and BRCA2 Mutation Carriers Using Polygenic Risk Scores
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Lecarpentier, J., Kuchenbaecker, K. B., Barrowdale, D., Dennis, J., Mcguffog, L., Leslie, G., Lee, A., Al Olama, A. A., Tyrer, J. P., Frost, D., Ellis, S., Easton, D. F., Antoniou, A. C., Tischkowitz, M., Evans, D. G., Henderson, A., Brewer, C., Eccles, D., Cook, J., Ong, K. -R., Walker, L., Side, L. E., Hodgson, S., Izatt, L., Eeles, R., Orr, N., Porteous, M. E., Davidson, R., Adlard, J., Silvestri, V., Rizzolo, P., Navazio, A. S., Valentini, V., Zelli, V., Ottini, L., Toss, A., Medici, V., Cortesi, L., Zanna, I., Palli, D., Radice, P., Manoukian, S., Peissel, B., Azzollini, J., Peterlongo, P., Viel, A., Cini, G., Damante, G., Tommasi, S., Alducci, E., Tognazzo, S., Montagna, M., Caligo, M. A., Soucy, P., Simard, J., Mulligan, A. M., Andrulis, I. L., Glendon, G., Southey, M., Campbell, I., James, P., Mitchell, G., Spurdle, A. B., Holland, H., Chenevix-Trench, G., John, E. M., Steele, L., Ding, Y. C., Neuhausen, S. L., Weitzel, J. N., Conner, T. A., Buys, S. S., Goldgar, D. E., Godwin, A. K., Sharma, P., Rebbeck, T. R., Vijai, J., Robson, M., Lincoln, A., Musinsky, J., Gaddam, P., Offit, K., Loud, J. T., Greene, M. H., Toland, A. E., Senter, L., Huo, D., Nielsen, S. M., Olopade, O. I., Nathanson, K. L., Domchek, S. M., Lorenchick, C., Jankowitz, R. C., Couch, F. J., Janavicius, R., Hansen, T. V. O., Bojesen, A., Nielsen, H. R., Skytte, A. -B., Sunde, L., Jensen, U. B., Pedersen, I. S., Krogh, L., Kruse, T. A., Thomassen, M., Osorio, A., De La Hoya, M., Garcia-Barberan, V., Caldes, T., Segura, P. P., Balmana, J., Gutierrez-Enriquez, S., Diez, O., Teule, A., Del Valle, J., Feliubadalo, L., Pujana, M. A., Lazaro, C., Izquierdo, A., Darder, E., Brunet, J., Fostira, F., Hamann, U., Sutter, C., Meindl, A., Ditsch, N., Gehrig, A., Dworniczak, B., Engel, C., Wand, D., Niederacher, D., Steinemann, D., Hahnen, E., Hauke, J., Rhiem, K., Wappenschmidt, B., Schmutzler, R. K., Kast, K., Arnold, N., Wang-Gohrke, S., Lasset, C., Damiola, F., Barjhoux, L., Mazoyer, S., Stoppa-Lyonnet, D., Belotti, M., Van Heetvelde, M., Poppe, B., De Leeneer, K., Claes, K. B. M., Kiiski, J. I., Khan, S., Nevanlinna, H., Aittomaki, K., Vvan Asperen, C. J., Vaszko, T., Kasler, M., Olah, E., Arason, A., Agnarsson, B. A., Johannsson, O. Th., Barkardottir, R. B., Teixeira, M. R., Pinto, P., Lee, J. W., Lee, M. H., Lee, J., Kim, S. -W., Kang, E., Park, S. K., Kim, Z., Tan, Y. Y., Berger, A., Singer, C. F., Yoon, S. -Y., Teo, S. -H., Von Wachenfeldt, A., Italian Association for Cancer Research, Ministère de Économie, Innovation et Exportation (Canadá), Canadian Institutes of Health Research, United States of Department of Health & Human Services, Cancer Research UK (Reino Unido), National Cancer Center. National R&D Program for Cancer Control (República de Corea), German Cancer Aid, Fondation ARC pour la recherche sur le cancer, Lietuvos Mokslo Taryba (Lituania), Asociación Española Contra el Cáncer, Fundación Mutua Madrileña, University of Kansas. Cancer Center (Estados Unidos), Ministerio de Economía y Competitividad (España), Finlands Akademi (Finlandia), Instituto de Salud Carlos III, Dutch Research Council (Holanda), Pink Ribbons Project, Biobanking and BioMolecular resources Research Infrastructure (Países Bajos), Transcan grant, Government of Catalonia (España), Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF), Ministry of Health and Welfare (Corea del Sur), Ministry of Science, Technology and Innovation (Malasia), Victorian Cancer Agency, and Ministry of Higher Education (Malasia)
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Adult ,Male ,Cancer Research ,Heterozygote ,Multifactorial Inheritance ,Genes, BRCA2 ,Genes, BRCA1 ,Breast Neoplasms ,Polymorphism, Single Nucleotide ,Risk Assessment ,Breast Neoplasms, Male ,Age Factors ,Aged ,Aged, 80 and over ,Case-Control Studies ,Genetic Predisposition to Disease ,Genetic Testing ,Genome-Wide Association Study ,Humans ,Middle Aged ,Prostatic Neoplasms ,Mutation ,Oncology ,80 and over ,Polymorphism ,skin and connective tissue diseases ,Single Nucleotide ,BRCA1 ,BRCA2 ,Genes - Abstract
Purpose BRCA1/2 mutations increase the risk of breast and prostate cancer in men. Common genetic variants modify cancer risks for female carriers of BRCA1/2 mutations. We investigated-for the first time to our knowledge-associations of common genetic variants with breast and prostate cancer risks for male carriers of BRCA1/ 2 mutations and implications for cancer risk prediction. Materials and Methods We genotyped 1,802 male carriers of BRCA1/2 mutations from the Consortium of Investigators of Modifiers of BRCA1/2 by using the custom Illumina OncoArray. We investigated the combined effects of established breast and prostate cancer susceptibility variants on cancer risks for male carriers of BRCA1/2 mutations by constructing weighted polygenic risk scores (PRSs) using published effect estimates as weights. Results In male carriers of BRCA1/2 mutations, PRS that was based on 88 female breast cancer susceptibility variants was associated with breast cancer risk (odds ratio per standard deviation of PRS, 1.36; 95% CI, 1.19 to 1.56; P = 8.6 × 10-6). Similarly, PRS that was based on 103 prostate cancer susceptibility variants was associated with prostate cancer risk (odds ratio per SD of PRS, 1.56; 95% CI, 1.35 to 1.81; P = 3.2 × 10-9). Large differences in absolute cancer risks were observed at the extremes of the PRS distribution. For example, prostate cancer risk by age 80 years at the 5th and 95th percentiles of the PRS varies from 7% to 26% for carriers of BRCA1 mutations and from 19% to 61% for carriers of BRCA2 mutations, respectively. Conclusion PRSs may provide informative cancer risk stratification for male carriers of BRCA1/2 mutations that might enable these men and their physicians to make informed decisions on the type and timing of breast and prostate cancer risk management. We thank Sue Healey for her contribution to CIMBA, in particular, for taking on the task of mutation classification with Olga Sinilnikova. BCFR Australia: We acknowledge Maggie Angelakos, Judi Maskiell, Gillian Dite, Helen Tsimiklis. BCFR Ontario: We thank members and participants in the Ontario Familial Breast Cancer Registry for their contributions to the study. BFBOCC-LT (Baltic Familial Breast Ovarian Cancer Consortium Lithuanian section): We acknowledge Vilius Rudaitis and Laimonas Griˇskeviˇcius. CBCS (Copenhagen Breast Cancer Study, Rigshospitalet): We thank Bent Ejlertsen Ejlertsen and Anne-Marie Gerdes for the recruitment and genetic counseling of participants. CNIO (Spanish National Cancer Centre): We thank Alicia Barroso, Rosario Alonso, and Guillermo Pita for their assistance. COH-CCGCRN (City of Hope Clinical Cancer Genomics Community Research Network): Patients were recruited for study from the City of Hope Clinical Cancer Genomics Community Research Network. CONSIT TEAM:We acknowledge Daniela Zaffaroni of the Fondazione IRCCS Istituto Nazionale Tumori (INT), Milan, Italy; Brunella Pilato of the Istituto Nazionale Tumori “Giovanni Paolo II”, Bari, Italy; and the personnel of the Cogentech Cancer Genetic Test Laboratory, Milan, Italy. FCCC (Fox Chase Cancer Center):We thank Jo EllenWeaver and Betsy Bove, MD, for their technical support. GEMO (GeneticModifiers of cancer risk in BRCA1/2 mutation carriers):We pay a tribute to Olga M. Sinilnikova, who with Dominique Stoppa-Lyonnet, initiated and coordinated GEMO until she died on June 30, 2014, and we thank all the GEMO collaborating groups for their contribution to this study. GEMO Collaborating Centers are: Coordinating Centres, Unit´e Mixte de G´en´etique Constitutionnelle des Cancers Fr´equents, Hospices Civils de Lyon–Centre L´eon B´erard, Equipe G´en´etique du cancer du sein, Centre de Rechercheen Canc´erologie de Lyon: Olga Sinilnikova (deceased), Sylvie Mazoyer, Francesca Damiola, Laure Barjhoux, Carole Verny-Pierre, M´elanie L´eone, Nadia Boutry-Kryza, Alain Calender, Sophie Giraud; and Service de G´en´etique Oncologique, Institut Curie, Paris: Dominique Stoppa-Lyonnet, Marion Gauthier-Villars, Bruno Buecher, Claude Houdayer, Etienne Rouleau, Lisa Golmard, Agn`es Collet, Virginie Moncoutier, Muriel Belotti, Antoine de Pauw, Camille Elan, Catherine Nogues, Emmanuelle Fourme, Anne-Marie Birot; Institut Gustave Roussy, Villejuif: Brigitte Bressac-de-Paillerets, Olivier Caron, Marine Guillaud- Bataille; Centre Jean Perrin, Clermont–Ferrand: Yves-Jean Bignon, Nancy Uhrhammer; Centre L´eon B´erard, Lyon: Christine Lasset, Val´erie Bonadona, Sandrine Handallou; Centre François Baclesse, Caen: Agn`es Hardouin, Pascaline Berthet, Dominique Vaur, Laurent Castera; Institut Paoli Calmettes, Marseille: Hagay Sobol, Violaine Bourdon, Tetsuro Noguchi, Audrey Remenieras, François Eisinger; CHUArnaud-de-Villeneuve,Montpellier: Isabelle Coupier, Pascal Pujol; Centre Oscar Lambret, Lille: Jean-Philippe Peyrat, Jo¨elle Fournier, Françoise R´evillion, Philippe Vennin (deceased), Claude Adenis; Centre Paul Strauss, Strasbourg: Dani`ele Muller, Jean-Pierre Fricker; Institut Bergoni´e, Bordeaux: Emmanuelle Barouk-Simonet, Françoise Bonnet, Virginie Bubien, Nicolas Sevenet, Michel Longy; Institut Claudius Regaud, Toulouse: Christine Toulas, Rosine Guimbaud, Laurence Gladieff, Viviane Feillel; CHU Grenoble: Dominique Leroux, H´el`ene Dreyfus, Christine Rebischung, Magalie Peysselon; CHU Dijon: Fanny Coron, Laurence Faivre; CHU St-Etienne: Fabienne Prieur, Marine Lebrun, Caroline Kientz; HˆotelDieu Centre Hospitalier, Chamb´ery: Sandra Fert Ferrer; Centre Antoine Lacassagne, Nice: Marc Fr´enay; CHU Limoges: Laurence V´enat-Bouvet; CHU Nantes: Capucine Delnatte; CHU Bretonneau, Tours: Isabelle Mortemousque; Groupe Hospitalier Piti´e-Salp´etri`ere, Paris: Florence Coulet, Chrystelle Colas, Florent Soubrier, MathildeWarcoin; CHU Vandoeuvre-les- Nancy: Johanna Sokolowska, Myriam Bronner; CHU Besançon: Marie-Agn`es Collonge-Rame, Alexandre Damette; Creighton University, Omaha, NE: Henry T. Lynch, Carrie L. Snyder. G-FAST (Ghent University Hospital): B.P. is a senior clinical investigator of FWO. We acknowledge the technical support of Ilse Coeneen Brecht Crombez. HCSC (Hospital Clinico San Carlos): We acknowledge Alicia Tosar and Paula Diaque for their technical assistance. HEBCS (Helsinki Breast Cancer Study):We thank Taru A. Muranen, Carl Blomqvist, MD, Kirsimari Aaltonen, MD, Irja Erkkil¨a, RN, and Virpi Palola, RN, for their help with the HEBCS data and samples. Hereditary Breast and Ovarian Cancer Research Group Netherlands (HEBON): HEBON consists of the following collaborating centers: Coordinating center: Netherlands Cancer Institute, Amsterdam: M.A. Rookus, F.B.L. Hogervorst, F.E. van Leeuwen, S. Verhoef, M.K. Schmidt, N.S. Russell, J.L. de Lange, R. Wijnands; Erasmus Medical Center: J.M. Coll´ee, A.M.W. van den Ouweland, M.J. Hooning, C. Seynaeve, C.H.M. van Deurzen, I.M. Obdeijn; Leiden University Medical Center: C.J. van Asperen, J.T. Wijnen, R.A.E.M. Tollenaar, P. Devilee, T.C.T.E.F. van Cronenburg; Radboud University NijmegenMedical Center: C.M. Kets, A.R.Mensenkamp; UniversityMedical Center Utrecht: M.G.E.M. Ausems, R.B. van der Luijt, C.C. van der Pol; Amsterdam Medical Center: C.M. Aalfs, T.A.M. van Os; Vrije Universiteit Medical Center: J.J.P. Gille, Q.Waisfisz, H.E.J. Meijers-Heijboer; University Hospital Maastricht: E.B. G´omez-Garcia, M.J. Blok; University Medical Center Groningen: J.C. Oosterwijk, A.H. van der Hout, M.J.Mourits, G.H. de Bock; The Netherlands Foundation for the Detection of Hereditary Tumours, Leiden: H.F. Vasen; The Netherlands Comprehensive Cancer Organization (IKNL): S. Siesling, J. Verloop; The Dutch Pathology Registry (PALGA): L.I.H. Overbeek. HEBON thanks the registration teams of IKNL and PALGA for part of the data collection. HUNBOCS (Molecular Genetic Studies of Breast- and Ovarian Cancer in Hungary):We thank the Hungarian Breast and Ovarian Cancer Study Group members (Janos Papp, Aniko Bozsik, Judit Franko, Maria Balogh, Gabriella Domokos, Judit Ferenczi, Department of Molecular Genetics, National Institute of Oncology, Budapest, Hungary) and the clinicians and patients for their contributions to this study. HVH (University Hospital Vall d’Hebron): We thank the Cellex Foundation for providing research facilities and equipment. ICO (Institut Catal`a d’Oncologia): We thank the ICO Hereditary Cancer Program team led by Gabriel Capella, MD. INHERIT (INterdisciplinary HEalth Research Internal Team BReast CAncer susceptibility):We thank Martine Dumont, MD, Martine Tranchant and St´ephane Dubois for QC, sample management and skillful assistance. J.S. is Chair holder of the Canada Research Chair in Oncogenetics. J.S. and P.S. were part of the QC and Genotyping coordinating group of iCOGS and Oncoarray (BCAC and CIMBA). IPOBCS (Portuguese Oncology Institute-Porto jco.org © 2017 by American Society of Clinical Oncology Polygenic Risk Scores in Male BRCA1 and BRCA2 Mutation Carriers Downloaded from ascopubs.org by CNIO-FUND on September 27, 2019 from 193.147.150.201 Copyright © 2019 American Society of Clinical Oncology. All rights reserved. Breast Cancer Study): We thank Catarina Santos, MD, for her skillful contribution to the study. kConFab (Kathleen Cuningham Consortium for Research into Familial Breast Cancer): We thank Heather Thorne, Eveline Niedermayr, all the kConFab research nurses and staff, the heads and staff of the Family Cancer Clinics, and the Clinical Follow Up Study for their contributions to this resource, and the many families who contribute to kConFab.Memorial Sloan Kettering Cancer Center:We acknowledge Lauren Jacobs, MD. OCGN (Ontario Cancer Genetics Network): We thank members and participants in the Ontario Cancer Genetics Network for their contributions to the study. OSUCCG (The Ohio State University Comprehensive Cancer Center): Kevin Sweet, Caroline Craven, Julia Cooper, Leigha Senter, and Michelle O’Conor were instrumental in accrual of study participants, ascertainment of medical records, and database management. SEABASS (South East Asian Breast Cancer Association Study): We thank Yip Cheng Har, Nur Aishah Mohd Taib, Phuah Sze Yee, Norhashimah Hassan, and all the research nurses, research assistants, and doctors involved in the MyBrCa Study for assistance in patient recruitment, data collection, and sample preparation. In addition, we thank Philip Iau, Sng Jen-Hwei, and Sharifah Nor Akmal for contributing samples from the Singapore Breast Cancer Study and the HUKM-HKL Study, respectively. SWE-BRCA (Swedish Breast Cancer Study): Swedish scientists participating as SWE-BRCA collaborators are: from Lund University and University Hospital: A° ke Borg, H°akan Olsson, Helena Jernstr¨om, Karin Henriksson, Katja Harbst, Maria Soller, Ulf Kristoffersson; from Gothenburg Sahlgrenska University Hospital: Anna O¨ fverholm, Margareta Nordling, Per Karlsson, Zakaria Einbeigi; from Stockholm and Karolinska University Hospital: Anna vonWachenfeldt, Annelie Liljegren, Annika Lindblom, Brita Arver, Gisela Barbany Bustinza, Johanna Rantala; from Ume°a University Hospital: Beatrice Melin, Christina Edwinsdotter Ardnor, Monica Emanuelsson; from Uppsala University: Hans Ehrencrona, Maritta Hellstr¨om Pigg, Richard Rosenquist; from Link¨oping University Hospital: Marie Stenmark-Askmalm, Sigrun Liedgren. University of Chicago: O.I.O. is an ACS Clinical Research Professor. We thank Cecilia Zvocec, Qun Niu, physicians, genetic counsellors, research nurses, and staff of the Cancer Risk Clinic for their contributions to this resource, and the many families who contribute to our program. VFCTG (Victorian Familial Cancer Trials Group):We acknowledge Geoffrey Lindeman, Marion Harris, Martin Delatycki of the Victorian Familial Cancer Trials Group.We thank Sarah Sawyer and Rebecca Driessen for assembling these data and Ella Thompson for performing all DNA amplification. © 2017 by American Society of Clinical Oncology JOURNAL OF CLINICAL ONCOLOGY Sí
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- 2017
6. Abstract P5-06-03: Generation and characterization of a novel invasive lobular breast carcinoma cell line WCRC-25
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Kota, K, primary, Bossart, E, additional, Basudan, A, additional, Minteer, T, additional, Meier, C, additional, Brown, D, additional, Gurda, GT, additional, Miller, L, additional, Dabbs, DJ, additional, Lee, A, additional, Puhalla, S, additional, Jankowitz, R, additional, McAuliffe, P, additional, Lucas, P, additional, and Oesterreich, S, additional
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- 2018
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7. Abstract P5-16-01: Documenting and sharing breast cancer knowledge from National Cancer Institute designated comprehensive cancer centers (NCI-CCCs) with community oncologists
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Kalra, M, primary, Karuturi, M, additional, Tripathy, D, additional, Jankowitz, R, additional, McCann, K, additional, Brufsky, A, additional, Hurvitz, S, additional, Bogler, O, additional, Housri, S, additional, and Housri, N, additional
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- 2018
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8. Abstract P6-09-14: Prognostic significance of a modified residual disease in breast and nodes (mRDBN) algorithm after neoadjuvant therapy for breast cancer
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Farrugia, DJ, primary, Landmann, A, additional, McAuliffe, PF, additional, Diego, EJ, additional, Johnson, R, additional, Bonaventura, M, additional, Soran, A, additional, Dabbs, DJ, additional, Clark, B, additional, Lembersky, BC, additional, Puhalla, SL, additional, Brufsky, A, additional, Jankowitz, R, additional, Davidson, NE, additional, Ahrendt, GM, additional, and Bhargava, R, additional
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- 2017
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9. Abstract P6-07-02: Prediction of oncotype DX® recurrence score using pathology generated equations
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Bhargava, R, primary, Klein, ME, additional, Shuai, Y, additional, Brufsky, AM, additional, Puhalla, SL, additional, Jankowitz, R, additional, and Dabbs, DJ, additional
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- 2012
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10. Biomarkers of Phenethyl Isothiocyanate-Mediated Mammary Cancer Chemoprevention in a Clinically Relevant Mouse Model
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Singh, S. V., primary, Kim, S.-H., additional, Sehrawat, A., additional, Arlotti, J. A., additional, Hahm, E.-R., additional, Sakao, K., additional, Beumer, J. H., additional, Jankowitz, R. C., additional, Chandra-Kuntal, K., additional, Lee, J., additional, Powolny, A. A., additional, and Dhir, R., additional
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- 2012
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11. Adjuvant Endocrine Therapy for Breast Cancer: Don't Ditch the Switch!
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Puhalla, S., primary, Jankowitz, R. C., additional, and Davidson, N. E., additional
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- 2011
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12. Incidence of febrile neutropenia with docetaxel plus cyclophosphamide in a university-based breast oncology clinic.
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Soni, A., primary, Brufsky, A., additional, Jankowitz, R. C., additional, Rastogi, P., additional, Vogel, V. G., additional, and Puhalla, S., additional
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- 2011
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13. Phase II study of short course CHOP-rituximab followed by 90-y ibritumomab tiuxetan as first-line treatment for follicular lymphoma: Extended follow-up and predictors of relapse.
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Mehta, D. R., primary, Jankowitz, R. C., additional, Lenzner, D. E., additional, Land, S. R., additional, and Jacobs, S. A., additional
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- 2010
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14. Predictive value of the Theros Breast Cancer Index (TBCI) for distant recurrence and overall survival (OS) in comparison to Adjuvant! Online and clinicopathologic characteristics in women with lymph node (LN)-negative, ER-positive breast cancer (BCa).
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Jankowitz, R. C., primary, Chivukula, M., additional, Ma, X., additional, Erlander, M. G., additional, Mock, L. L., additional, Mazur, L. S., additional, Li, H., additional, Salunga, R., additional, Sereika, S., additional, and Brufsky, A., additional
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- 2010
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15. Phase II study of short course CHOP-rituximab (R) followed by ibritumomab tiuxetan (IT) as first-line treatment for follicular lymphoma (FL)
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Jankowitz, R. C., primary, Foon, K. A., additional, DeMonaco, N. A., additional, Osborn, J., additional, Wu, M., additional, Evans, T., additional, Swerdlow, S. H., additional, Joyce, J., additional, Land, S., additional, and Jacobs, S. A., additional
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- 2007
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16. Trastuzumab treatment improves brain metastasis outcomes through control and durable prolongation of systemic extracranial disease in HER2-overexpressing breast cancer patients.
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Jankowitz, R. C. and Brufsky, A. M.
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TRASTUZUMAB ,PHARMACODYNAMICS ,METASTASIS ,BRAIN cancer ,BREAST cancer patients ,HER2 gene ,CENTRAL nervous system - Abstract
The article discusses research on the effect of trastuzumab on brain metastasis (BM) outcomes in patients with HER2-overexpressing metastatic breast cancer (MBC). It references the study "Trastuzumab Treatment Improves Brain Metastasis Outcomes Through Control and Durable Prolongation of Systemic Extracranial Disease in HER2-Overexpressing Breast Cancer Patients," by Y. H. Park and colleagues, published in a 2009 issue of "British Journal of Cancer." It is said that trastuzumab imposes a delaying effect on the involvement of the central nervous system.
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- 2010
17. Investigating cortactin as a genetic driver of disease progression in invasive lobular carcinoma
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Tasdemir, N., Sikora, M. J., Zhu, L., Levine, K. M., Scott, J., Basudan, A., Sflomos, G., Sreekumar, S., Bossart, E. A., Elishaev, E., Chandran, U. R., Tseng, G. C., Jankowitz, R. C., Dabbs, D. J., McAuliffe, P. F., Brisken, C., and Davidson, N. E.
18. Morphologic and Immunohistochemistry (IHC) Profile of Luminal A Subtype Breast Cancer Patients with Recurrence and Non-Recurrence: A Single Institution Retrospective Review Study with 10 Year Follow-Up
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Hooda, S., Carter, G., Adam Brufsky, Jankowitz, R., Badve, P., and Chivukula, M.
19. Epigenetics in breast cancer: what's new?
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Huang Y, Nayak S, Jankowitz R, Davidson NE, Oesterreich S, Huang, Yi, Nayak, Shweta, Jankowitz, Rachel, Davidson, Nancy E, and Oesterreich, Steffi
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Epigenetic changes are critical for development and progression of cancers, including breast cancer. Significant progress has been made in the basic understanding of how various epigenetic changes such as DNA methylation, histone modification, miRNA expression, and higher order chromatin structure affect gene expression. The present review will focus on methylation and demethylation of histones. While the acetylation of histones has been at the forefront of well-characterized post-translational modifications of histones, including the development of inhibitors targeting de-acetylating enzymes, the past few years have witnessed a dramatic increase in knowledge regarding the role of histone methylation/demethylation. This is an exciting and rapidly evolving area of research, with much promise for potential clinical intervention in several cancers including breast cancer. We also summarize efforts to identity DNA methylation signatures that could be prognostic and/or predictive markers in breast cancer, focusing on recent studies using genome-wide approaches. Finally, we briefly review the efforts made by both the National Institutes of Health Epigenome Project and The Cancer Genome Atlas, especially highlighting the study of breast cancer epigenetics, exciting technological advances, potential roadblocks, and future directions. [ABSTRACT FROM AUTHOR]
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- 2011
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20. Prediction of oncotype DX® recurrence score using pathology generated equations.
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Bhargava, R., Klein, M. E., Shuai, Y., Brufsky, A. M., Puhalla, S. L., Jankowitz, R., and Dabbs, D. J.
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POLYMERASE chain reaction , *ESTROGEN receptors , *BREAST cancer , *CANCER , *DISEASE relapse - Abstract
BACKGROUND: Oncotype DX® is a quantitative reverse transcription polymerase chain reaction based assay that has been shown to have prognostic and predictive value in estrogen receptor (ER) positive breast cancers. The result is reported as a recurrence score (RS) ranging from 0-100, divided into low risk (<18), intermediate risk (18-30), and high risk (^:31) categories. Prior studies have shown that RS is influenced by ER and progesterone receptor (PR) expression, HER2 status, proliferation index, and tumor grade. Our pilot study showed that RS can be predicted by an equation incorporating standard morpho-immunohistologic variables (referred to as Original Magee Equation; Mod Pathol. 2008;21:1255-1261). METHODS: Using a dataset of 817 cases, we formulated three additional equations to predict the RS category for an independent set of 255 cases. Three models were built based on different hypotheses and data availability and are represented below. New Maqee Equation 1 (nMED: RS = 15.31385 + Nottingham score-1.4055+ ER H-score-(-0.01924) + PR H-score-(-0.02925) + (0 for HER2 negative, 0.77681 for equivocal, 11.58134 for HER2 positive) + Tumor size-0.78677 + KI67 index-0.13269. New Maqee Equation 2 (nME2): RS = 18.8042+ Nottingham score-2.34123 + ER H-score-(-0.03749) + PR H-score-(-0.03065) + (0 for HER2 negative, 1.82921 for equivocal, 11.51378 for HER2 positive) + Tumor size-0.04267. New Maqee Equation 3 (nME3): RS = 24.30812+ ER H-score-(-0.02177) + PR H-score-(-0.02884) + (0 for HER2 negative, 1.46495 for equivocal, 12.75525 for HER2 positive) + Kl-67-0.18649. RESULTS: The concordance between the risk category of oncofype DX® and our equations was 55.8%, 59.4%, and 54.4% for nME1, nME2, and nME3 respectively. With exclusion of the intermediate risk categories for both the actual RS and estimated RS, the concordance for each equation increased to more than 95%, reflecting the very low two step discordance (100% {76/76}, 98.6% {75/76}, and 98.7% {79/80} for nME1, nME2, and nME3 respectively). Even when the estimated RS fell in the intermediate category with any of the equations, the actual RS was either intermediate or low in more than 85% of the cases. The Pearson correlation coefficient between estimated and actual RS was similar for each of the equations (0.61661, 0.60386 and 0.59407 for nME1, nME2 and nME3, respectively). CONCLUSIONS: Any of the 3 equations can be used to estimate the RS depending on available data. If the estimated RS is clearly high or low, the oncologists should not expect a dramatically different result from oncofype DX®, and the oncofype DX® test may not be needed. Conversely, an oncofype DX® result that is dramatically different from what is expected based on standard morpho-immunohistologic variables should be thoroughly investigated. [ABSTRACT FROM AUTHOR]
- Published
- 2012
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21. Estrogen regulation and functional role of FGFR4 in estrogen receptor positive breast cancer.
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Ding K, Chen L, Levine K, Sikora M, Tasdemir N, Dabbs D, Jankowitz R, Hazan R, Shah OS, Atkinson JM, Lee AV, and Oesterreich S
- Abstract
Background: Resistance to endocrine therapy is a major challenge of managing estrogen receptor positive (ER+) breast cancer. We previously reported frequent overexpression of FGFR4 in endocrine resistant cell lines and breast cancers that recurred and metastasized following endocrine therapy, suggesting FGFR4 as a potential driver of endocrine resistance. In this study, we investigated the role of FGFR4 in mediating endocrine resistance and explored the therapeutic potential of targeting FGFR4 in advanced breast cancer., Methods: A gene expression signature of FGFR4 activity was examined in ER+ breast cancer pre- and post-neoadjuvant endocrine therapy and the association between FGFR4 expression and patient survival was examined. A correlation analysis was used to uncover potential regulators of FGFR4 overexpression. To investigate if FGFR4 is necessary to drive endocrine resistance, we tested response to FGFR4 inhibition in long term estrogen deprived (LTED) cells and their paired parental cells. Doxycycline inducible FGFR4 overexpression and knockdown cell models were generated to examine if FGFR4 was sufficient to confer endocrine resistance. Finally, we examined response to FGFR4 monotherapy or combination therapy with fulvestrant in breast cancer cell lines to explore the potential of FGFR4 targeted therapy for advanced breast cancer and assessed the importance of PAM50 subtype in response to FGFR4 inhibition., Results: A FGFR4 activity gene signature was significantly upregulated post neoadjuvant aromatase inhibitor treatment, and high FGFR4 expression predicted poorer survival in patients with ER+ breast cancer. Gene expression association analysis using TCGA, METABRIC and SCAN-B datasets uncovered ER as the most significant gene negatively correlated with FGFR4 expression. ER negatively regulates FGFR4 expression at both the mRNA and protein level across multiple ER+ breast cancer cell lines. Despite robust overexpression of FGFR4, LTED cells did not show enhanced responses to FGFR4 inhibition compared to parental cells. Similarly, FGFR4 overexpression, knockdown or hotspot mutations did not significantly alter response to endocrine treatment in ER+ cell lines, nor did FGFR4 and fulvestrant combination treatment show synergistic effects. The HER2-like subtype of breast cancer showed elevated expression of FGFR4 and an increased response to FGFR4 inhibition relative to other breast cancer subtypes., Conclusions: Despite ER-mediated upregulation of FGFR4 post endocrine therapy, our study does not support a general role of FGFR4 in mediating endocrine resistance in ER+ breast cancer. Our data suggests that specific genomic backgrounds such as HER2 expression may be required for FGFR4 function in breast cancer and should be further explored.
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- 2024
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22. Evaluating the efficacy of a priming dose of cyclophosphamide prior to pembrolizumab to treat metastatic triple negative breast cancer.
- Author
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Anders CK, Woodcock MG, Van Swearingen AED, Moore DT, Sambade MJ, Laurie S, Robeson A, Kolupaev O, Cuaboy LA, Garrett AL, McKinnon K, Cowens K, Bortone D, Calhoun BC, Wilkinson AD, Carey L, Jolly T, Muss H, Reeder-Hayes K, Kaltman R, Jankowitz R, Gudena V, Olajide O, Perou C, Dees EC, Vincent BG, and Serody JS
- Subjects
- Adult, Aged, Aged, 80 and over, Antibodies, Monoclonal, Humanized pharmacology, Antineoplastic Combined Chemotherapy Protocols pharmacology, Cyclophosphamide pharmacology, Female, Humans, Middle Aged, Neoplasm Metastasis, Antibodies, Monoclonal, Humanized therapeutic use, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Cyclophosphamide therapeutic use, Immunotherapy methods, Triple Negative Breast Neoplasms drug therapy
- Abstract
Purpose: Triple negative breast cancer (TNBC) is characterized by the presence of immune cells in the tumor microenvironment, however, the response to single-agent immune checkpoint inhibitor (ICI) therapy is modest. Preclinical models have demonstrated that intratumoral regulatory T cells (T
regs ) dampen the antitumor response to ICI. We performed a single-arm phase II trial to evaluate the efficacy of a single low dose of cyclophosphamide (Cy) to deplete Tregs administered before initiating pembrolizumab., Patients and Methods: 40 patients with pretreated metastatic TNBC were enrolled. The primary endpoints were progression-free survival (PFS) and change in peripheral blood Tregs after Cy. Secondary endpoints included overall response rate (ORR), duration of response, overall survival, treatment-related adverse events (AEs), and correlative evaluations., Results: Median PFS was 1.8 months, and the ORR was 21%. Tregs were not significantly decreased after Cy prior to ICI (-3.3%, p=0.19), and increased significantly after the first cycle of therapy (+21% between cycles 1 and 2, p=0.005). Immune-related AEs were similar to historical pembrolizumab monotherapy, and were associated with response to therapy (p=0.02). Patients with pretreatment tumors harboring increased expression of B cell metagene signatures and increased circulating B cell receptor repertoire diversity were associated with clinical response and immune-related toxicity (IRT)., Conclusions: Among patients with heavily pretreated TNBC, Cy prior to pembrolizumab did not significantly deplete Tregs , and in those with decreased numbers there was rapid recovery following therapy. Increased B cell gene expression in baseline samples was associated with clinical response and IRT., Competing Interests: Competing interests: CKA receives research funding from PUMA, Lilly, MSD, Seattle Genetics, Nektar, Tesaro, and G1 Therapeutics, ZION, Novartis, Pfizer; compensation for consulting from Genentech, Eisai, IPSEN, Seattle Genetics, AstraZeneca, Novartis; and royalties from UpToDate and Jones and Bartlett. BV holds equity in GeneCentric Therapeutics. CP is an equity stockholder and consultant of BioClassifier, and an equity stock holder, consultant, and Board of Directors member of GeneCentric Therapeutics. CP is also listed as an inventor on patent applications for the Breast PAM50 assay. JS receives funding from MSD, GSK, and Carisma, is a scientific consultant for PIQUE Therapeutics and has filed IP for the use of STING agonists to enhance CAR T cell for breast cancer. The other authors have no conflicts requiring disclosure., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)- Published
- 2022
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23. Correction to: Effectiveness of a Short Duration of Neoadjuvant Endocrine Therapy in Patients with HR+ Breast Cancer-An NCDB Analysis (2004-2016).
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Goldbach MM, Burkbauer L, Bharani T, Williams AD, Keele L, Rothman J, Jankowitz R, and Tchou JC
- Published
- 2021
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24. Effectiveness of a Short Duration of Neoadjuvant Endocrine Therapy in Patients with HR+ Breast Cancer-An NCDB Analysis (2004-2016).
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Goldbach MM, Burkbauer L, Bharani T, Williams AD, Keele L, Rothman J, Jankowitz R, and Tchou JC
- Subjects
- Aged, Chemotherapy, Adjuvant, Female, Humans, Neoadjuvant Therapy, Neoplasm Staging, Receptor, ErbB-2, SARS-CoV-2, Breast Neoplasms drug therapy, Breast Neoplasms pathology, COVID-19
- Abstract
Background: National medical/surgical organizations have recommended the use of neoadjuvant endocrine therapy (NET) to bridge surgery delay of weeks to months for patients with hormone receptor positive (HR+) breast cancer during the ongoing coronavirus disease 2019 (COVID-19) pandemic. The effects of NET of varying durations on pathologic response are unclear. Using the National Cancer Database (NCDB), we evaluated objective response to short (< 9 weeks), moderate (9-27 weeks), and long (> 27 weeks) duration of NET., Patients and Methods: The study cohort included female patients diagnosed with nonmetastatic invasive HR+ breast cancer, stratifying by those who received NET versus no NET between 2004 and 2016. Pathologic response was grouped into four categories (complete, downstaged, stable, upstaged) by comparing clinical and pathologic staging data. Objective response to NET included complete, downstaged, and stable pathologic response. Clinical characteristics were compared using χ
2 and analysis of variance (ANOVA) tests. Multivariable logistic regression was used to determine factors associated with NET use and objective response according to NET duration., Results: A minority (1.2%) received NET in our cohort. Factors associated with NET use included older age, non-Black patients, more advanced clinical stage, higher comorbidity score, government insurance, and lobular histology. Objective response rate (ORR) was 56.7%, 52.1%, and 49.0% after short, moderate, and long NET duration, respectively., Conclusion: Short NET duration did not result in an inferior ORR. Future study to evaluate the interaction between surgery delay and NET use on clinical outcome will provide insights into the safety of NET to bridge potential surgery delay in patients with HR+ breast cancer., (© 2021. Society of Surgical Oncology.)- Published
- 2021
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25. Prediction of the Oncotype DX recurrence score: use of pathology-generated equations derived by linear regression analysis.
- Author
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Klein ME, Dabbs DJ, Shuai Y, Brufsky AM, Jankowitz R, Puhalla SL, and Bhargava R
- Subjects
- Biomarkers, Tumor analysis, Biomarkers, Tumor genetics, Female, Gene Expression Profiling, Humans, Linear Models, Algorithms, Breast Neoplasms drug therapy, Breast Neoplasms genetics, Decision Support Techniques, Neoplasm Recurrence, Local genetics
- Abstract
Oncotype DX is a commercial assay frequently used for making chemotherapy decisions in estrogen receptor (ER)-positive breast cancers. The result is reported as a recurrence score ranging from 0 to 100, divided into low-risk (<18), intermediate-risk (18-30), and high-risk (≥31) categories. Our pilot study showed that recurrence score can be predicted by an equation incorporating standard morphoimmunohistologic variables (referred to as original Magee equation). Using a data set of 817 cases, we formulated three additional equations (referred to as new Magee equations 1, 2, and 3) to predict the recurrence score category for an independent set of 255 cases. The concordance between the risk category of Oncotype DX and our equations was 54.3%, 55.8%, 59.4%, and 54.4% for original Magee equation, new Magee equations 1, 2, and 3, respectively. When the intermediate category was eliminated, the concordance increased to 96.9%, 100%, 98.6%, and 98.7% for original Magee equation, new Magee equations 1, 2, and 3, respectively. Even when the estimated recurrence score fell in the intermediate category with any of the equations, the actual recurrence score was either intermediate or low in more than 80% of the cases. Any of the four equations can be used to estimate the recurrence score depending on available data. If the estimated recurrence score is clearly high or low, the oncologists should not expect a dramatically different result from Oncotype DX, and the Oncotype DX test may not be needed. Conversely, an Oncotype DX result that is dramatically different from what is expected based on standard morphoimmunohistologic variables should be thoroughly investigated.
- Published
- 2013
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26. Phase II trial of short-course CHOP-R followed by 90Y-ibritumomab tiuxetan and extended rituximab in previously untreated follicular lymphoma.
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Jacobs SA, Swerdlow SH, Kant J, Foon KA, Jankowitz R, Land SR, DeMonaco N, Joyce J, Osborn JL, Evans TL, Schaefer PM, and Luong TM
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- Adult, Aged, Aged, 80 and over, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Combined Chemotherapy Protocols adverse effects, Drug Administration Schedule, Female, Humans, Male, Middle Aged, Rituximab, Antibodies, Monoclonal administration & dosage, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Lymphoma, Follicular drug therapy
- Abstract
Purpose: Radioimmunotherapy has been approved for relapsed follicular lymphoma (FL), including rituximab-refractory FL. This study was designed to determine the CR rate with short-course chemoimmunotherapy with cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab (CHOP-R) followed by 90-Y ibritumomab tiuxetan (RIT) with extended rituximab as first-line treatment., Experimental Design: Between March 2004 and February 2007, 60 patients with stage II to IV symptomatic or bulky FL from a single institution supported by a large community network entered this phase II trial. Patients received CHOP-R for three treatment cycles before RIT followed by four additional weekly treatments with rituximab. Response was determined using fusion [(18) F] fluorodeoxyglucose-positron emission tomography (PET)-computed tomography (CT) imaging., Results: Of the 60 patients entering this trial, 55 patients completed all protocol therapy. The median follow up was 19.7 months (range, 0.26-35.9 months). For intent-to-treat analysis, the complete response (CR) rate after CHOP-R, as assessed by CT and PET imaging, was 40% and 46%, respectively. After RIT, the CR rate improved, as assessed by CT and PET imaging, to 82% and 89%, respectively. Ten patients have progressed, including eight from best response of CR. Seven of 18 patients who were PET positive after CHOP-R progressed compared with 3 of 37 patients who were PET negative (P=0.010)., Conclusions: In patients with previously untreated, symptomatic or bulky FL, short-course chemoimmunotherapy and consolidation RIT and extended rituximab resulted in a high CR rate. Failure to achieve an early PET CR after CHOP-R indicated high risk of relapse.
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- 2008
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27. Anaphylaxis after administration of ibritumomab tiuxetan for follicular non-hodgkin lymphoma.
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Jankowitz R, Joyce J, and Jacobs SA
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- Enzyme-Linked Immunosorbent Assay, Humans, Male, Middle Aged, Radioimmunotherapy methods, Yttrium Radioisotopes adverse effects, Anaphylaxis chemically induced, Antibodies, Monoclonal adverse effects, Lymphoma, Follicular radiotherapy
- Abstract
We report an anaphylactic reaction in a 45-year-old gentleman with an 8-year history of extensively treated, relapsing follicular lymphoma who was receiving a second treatment with ibritumomab tiuxetan. Within seconds of receiving Y-90 ibritumomab, he developed chest tightness, shallow respirations, hypotension, and incontinence. After successful resuscitation, a human antimouse antibody (HAMA) level was found to be elevated, 618 ng/mL (reference 0-188 ng/mL).
- Published
- 2008
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