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CD38 Overexpressed Monocytes Play a Critical Role in the Fibrogenesis in Myeloproliferative Neoplasms and Can be Used As a Therapeutic Target to Ameliorate Fibrosis

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Blood 2024年 144卷 874-874页

作者： Yiru Yan Jinqin Liu Lin Yang Gang Huang Xiaofan Zhu Raajit Rampal Zhijian Xiao Bing Li State Key Laboratory of Experimental Hematology National Clinical Research Center for Blood Diseases Haihe Laboratory of Cell Ecosystem Institute of Hematology & Blood Diseases Hospital Chinese Academy of Medical Sciences &Peking Union Medical College Tianjin China Department of Cell Systems and Anatomy UT Health San Antonio San Antonio TX Department of Pathology and Laboratory Medicine UT Health San Antonio San Antonio TX State Key Laboratory of Experimental Hematology National Clinical Research Center for Blood Diseases Haihe Laboratory of Cell Ecosystem Institute of Hematology & Blood Diseases Hospital CAMS & PUMC Tianjin China Leukemia Service Department of Medicine Memorial Sloan Kettering Cancer Institute New York NY Memorial Sloan Kettering Cancer Center New York NY Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY State Key Laboratory of Experimental Hematology National Clinical Research Center for Blood Diseases Haihe Laboratory of Cell Ecosystem Institute of Hematology & Blood Diseases Hospital Chinese Academy of Medical Sciences&Peking Union Medical College Tianjin China

Background: Several studies have shown monocytes were the major cellular source of proinflammatory cytokines and monocyte-derived fibrocytes, playing an important role in myelofibrosis (MF). We aim to investigate the role of monocytes in MF acceleration and explore the mechanism. Method: We analyzed the clinical data from 387 MF patients and generated inducible Nras G12D and Jak2 V617F (NJ) knock-in mice to explore the mechanism. Results: In 387 PMF patients, there were 63 cases with monocytosis (≥1x10 9 /L). Patients with monocytosis had a higher MF grade (Grade2-3: 88.5% vs 74.2%, p =0.02), inferior OS (37 months vs NOT reached, p =0.004). Patients with monocytosis were more likely to have mutated ASXL1 (49.2% vs 25.2%; p< 0.001), SRSF2 (12.7% vs 5.5%; p =0.03), NRAS (11.1% vs 3.7%; p =0.02) and RUNX1 (7.9% vs 2.2%; p =0.02). In mouse model, peripheral blood (PB) count showed an obvious monocytosis accompanied with a significant increase in the percentage of CD11b + CD115 + monocytes in NJ recipient mice at 8 weeks after transplantation. At 28 weeks after transplantation, most of NJ revealed a decrease in hemoglobin, splenomegaly, reticulin infiltration and BM failure (mean ckit + cells per Femur: Jak2 V617F (J) 2.52x10 7 (n=5) vs NJ 0.99x10 7 (n=6), p =0.0238), but not in other age-matched mice with Nras G12D (N) or Jak2 V617F . Both at 20 weeks (pre-fibrotic stage) and 28 weeks (fibrotic stage), NJ presented a significantly higher percentage of CD11b + CD115 + monocytes in BM. Relative to the fibrotic stage, the increase in the CD11b + CD115 + Ly6c high monocyte was more obvious in the pre-fibrotic stage. In vitro, the differentiation assay revealed that monocyte-derived fibrocytes mainly differentiated from the Ly6c high subpopulation and significantly increased in N and NJ. Although Ly6c high monocytes from both N and NJ were more likely to differentiate to fibrocytes in vitro, only NJ presented MF phenotype. Therefore, we further explored the gene expression

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Deconvoluting clonal and cellular architecture in IDH-mutant acute myeloid leukemia

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Cell stem cell 2025年

作者： Maria Sirenko Soobeom Lee Zhengxi Sun Ronan Chaligne Sanam Loghavi Georgios Asimomitis Charlotte K Brierley Elsa Bernard Sheng F Cai Robert M Myers Bettina Nadorp Junya Sango Morgan Lallo Max F Levine Dylan Domenico Juan E Arango Ossa Juan S Medina-Martinez Kamal Menghrajani Audrey Lasry Alice S Mims Helee Desai Andrea Laganson Chris Famulare Minal Patel Gerard Lozanski Kelly L Bolton Aaron D Viny Mikhail Roshal Ross L Levine Eirini P Papapetrou Eytan M Stein Dan A Landau Ann-Kathrin Eisfeld Iannis Aifantis Elli Papaemmanuil Department of Pathology New York University Grossman School of Medicine New York NY USA Laura and Isaac Perlmutter Cancer Center New York University Grossman School of Medicine New York NY USA Louis V. Gerstner Jr. Graduate School of Biomedical Sciences Memorial Sloan Kettering Cancer Center New York NY USA Computational Oncology Service Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center New York NY USA. Department of Biology New York University New York NY USA. Laura and Isaac Perlmutter Cancer Center New York University Grossman School of Medicine New York NY USA. Program for Computational and Systems Biology Sloan Kettering Institute Memorial Sloan Kettering Cancer Center New York NY 10065 USA. Department of Hematopathology The University of Texas MD Anderson Cancer Center Houston TX USA. Computational Oncology Service Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center New York NY USA Biomedical Systems Laboratory Department of Mechanical Engineering National Technical University of Athens Athens Greece. Medical Research Council Weatherall Institute of Molecular Medicine University of Oxford Oxford UK NIHR Biomedical Research Centre University of Oxford Oxford UK. Leukemia Service Department of Medicine Center for Hematologic Malignancies Memorial Sloan Kettering Cancer Center New York NY USA Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY USA. Tri-Institutional MD-PhD Program Weill Cornell Medicine Rockefeller University Memorial Sloan Kettering Cancer Center New York NY USA. Division of Precision Medicine Department of Medicine New York University School of Medicine New York NY USA. Department of Oncological Sciences Tisch Cancer Institute Center for Advancement of Blood Cancer Therapies Icahn School of Medicine at Mount Sinai New York NY USA. Vilcek Institute of Graduate Biomedical Sciences NYU Grossman School of Medicine N

Isocitrate dehydrogenase 1/2 (IDH) mutations are early initiating events in acute myeloid leukemia (AML). The complex clonal architecture and cellular heterogeneity in IDH-mutant AML underlies the heterogeneous clinical presentation and outcomes. Integrating single-cell genotyping and transcriptomics, we demonstrate a stem-like and inflammatory phenotype of IDH-mutant AML and identify clone-specific programs associated with NPM1, NRAS, and SRSF2 co-mutations. Furthermore, these clones had distinct responses to treatment with combination IDH inhibitors and chemotherapy, including elimination, reconstitution of myeloid differentiation, or retention within progenitor populations. At relapse after IDH inhibitor monotherapy, we identify upregulated stemness, inflammation, mitochondrial metabolism, and anti-apoptotic factors, as well as downregulated major histocompatibility complex (MHC) class II antigen presentation. At the pre-leukemic stage, we observe upregulation of IDH2-associated pathways, including inflammation. We deliver a detailed phenotyping of IDH-mutant AML and a framework for dissecting contributions of recurrently mutated genes in AML at diagnosis and following therapy, with implications for precision medicine.

关键词： IDH inhibitors IDH1/2 mutations acute myeloid leukemia cellular hierarchy clonal architecture clonal evolution relapse single-cell transcriptomics targeted therapy treatment resistance

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Phase 1 Trial of Vodobatinib, a Novel Oral BCR-ABL1 Tyrosine Kinase Inhibitor (TKI): Activity in CML Chronic Phase Patients Failing TKI Therapies Including Ponatinib

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BLOOD 2020年 136卷 51-52页

作者： Cortes, Jorge E. Saikia, Tapan Kim, Dong-Wook Alvarado, Yesid Nicolini, Franck E. Khattry, Navin Rathnam, Krishnakumar Apperley, Jane Deininger, Michael W. de Lavallade, Hugues Charbonnier, Aude Granacher, Nikki Gambacorti-Passerini, Carlo Lucchesi, Alessandro Mauro, Michael J. Verhoef, Gregor Vandenberghe, Peter Whiteley, Andrew R. Apte, Shashikant Yao, Siu-Long Kothekar, Mudgal Sreenivasan, Jayasree Bimba, H., V Chimote, Geetanjali Georgia Cancer Center Augusta University Augusta GA Prince Aly Khan Hospital Mumbai India Seoul St. Mary's Hospital The Catholic University of Korea Seoul South Korea Department of Hematology Seoul St. Mary's Hospital The Catholic University of Korea Seoul Korea Republic of (South) Department of Leukemia MD Anderson Cancer Center Houston TX Hematology department & ISERM U590 Centre Hospitalier Lyon Sud LYON Cedex 03 France BMT unit Department of Medical oncology ACTREC. Tata Memorial Centre Navi Mumbai India Lake Area Melur Main Rd Meenakshi Mission Hospital and Research Centre Tamil Nadu India Centre for Haematology Department of Medicine Hammersmith Hospital Imperial College London United Kingdom Department of Internal Medicine Division of Hematology and Hematologic Malignancies University of Utah Salt Lake City UT Department of Haematological Medicine Kings College Hospital NHS Foundation Trust London United Kingdom Onco-Hematology Department Paoli-Calmette Cancer Institute Marseille France Ziekenhuis Netwerk Antwerpen Antwerp Belgium Dept of Medicine and Surgery University of Milano Bicocca Monza Italy Hematology Unit Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS Meldola (FC) Italy Myeloproliferative Neoplasms Program Leukemia Service Memorial Sloan Kettering Cancer Center New York NY Department of Hematology University Hospitals Leuven Leuven Belgium Center for Human Genetics University of Leuven Center for Human Genetics Leuven Belgium Baylor University Medical Center Dallas TX Department of Haematology Sahyadri Specialty Hospitals Pune India Sun Pharmaceutical Industries Inc. Princeton NJ Clinical Research Department Sun Pharma Advanced Research Company Mumbai India

Introduction: Vodobatinib, a novel 3 rd generation (3G) TKI effective against wild-type and mutated BCR-ABL1 with limited off-target activity, was evaluated in a Phase I multicentre dose-escalation study in chronic myeloid leukemia (CML) patients (pts) who failed ≥ 3 TKIs or less (if not eligible for other approved 3G TKIs) (NCT02629692). The activity and safety of vodobatinib was evaluated in ponatinib treated (PT) and ponatinib naïve (PN) chronic phase (CP)-CML subjects in an exploratory analysis. Methods: Multiple escalating doses of vodobatinib (once daily) in 28-day cycles were evaluated in a 3+3 study design. The primary objective was determination of the maximal tolerated dose (MTD) or recommended phase 2 dose (RP2D) along with safety and a secondary objective was to evaluate anti-leukemic activity. Dose escalation involved dose doubling until 2 pts in a cohort experienced Grade 2 toxicity, or 1 pt experienced Grade 3 or 4 toxicity, after which dose escalation was reduced to 40% increments. Treatment continued until unacceptable toxicity, disease progression (PD), consent withdrawal, or death. Results: As of 15 Jul 2020, 31 CP-CML pts received vodobatinib at doses of 12 to 240 mg; 16 pts (9 males) in ponatinib treated (PT) cohort [7 (44%) ponatinib was the immediate prior TKI] and 15 pts (7 males) in the ponatinib naïve (PN) cohort . The baseline demographics and disease history are represented in Table 1. Efficacy: Median duration of treatment was 17.3 (0.6-36) and 14.8 (0.5- 42) months in the Ponatinib treated and naive groups, respectively; 11 pts in the PT group [2 in Deep molecular response (DMR), 3 in MMR; 5 in MCyR (2 in CCyR and 3 in PCyR); 1 in stable disease] and 10 pts in the PN group (2 in DMR, 4 in MMR and 3 in CCyR, 1 in stable disease) are continuing on treatment. Overall efficacy outcomes are included in Tables 2 and 3. Of 16 PT pts, 2 (13%) pts, both with double mutations, had disease progression. Of 15 PN pts, 4 (26%) pts (with baseline muta

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Publisher Correction: Lineage plasticity in cancer: a shared pathway of therapeutic resistance

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Nature reviews. Clinical oncology 2020年第6期17卷 382页

作者： Álvaro Quintanal-Villalonga Joseph M Chan Helena A Yu Dana Pe'er Charles L Sawyers Triparna Sen Charles M Rudin Department of Medicine Thoracic Oncology Service Memorial Sloan Kettering Cancer Center New York NY USA. Program for Computational and Systems Biology Sloan Kettering Institute Memorial Sloan Kettering Cancer Center New York NY USA. Parker Institute for Cancer Immunotherapy Memorial Sloan Kettering Cancer Center New York NY USA. Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY USA. Howard Hughes Medical Institute Chevy Chase MD USA. Department of Medicine Thoracic Oncology Service Memorial Sloan Kettering Cancer Center New York NY USA. sent@***. Department of Medicine Thoracic Oncology Service Memorial Sloan Kettering Cancer Center New York NY USA. rudinc@***.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Genetic diversity of tumors with mismatch repair deficiency influences anti-PD-1 immunotherapy response

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Science 2019年第6439期364卷 485-491页

作者： Mandal, Rajarsi Samstein, Robert M. Lee, Ken-Wing Havel, Jonathan J. Wang, Hao Krishna, Chirag Sabio, Erich Y. Makarov, Vladimir Kuo, Fengshen Blecua, Pedro Ramaswamy, Apoorva T. Durham, Jennifer N. Bartlett, Bjarne Ma, Xiaoxiao Srivastava, Raghvendra Middha, Sumit Zehir, Ahmet Hechtman, Jaclyn F. Morris, Luc Gt Weinhold, Nils Riaz, Nadeem Le, Dung T. Diaz, Luis A. Chan, Timothy A. Department of Otolaryngology-Head and Neck Surgery Johns Hopkins University Baltimore 21287 MD United States Bloomberg-Kimmel Institute for Cancer Immunotherapy at Johns Hopkins Baltimore 21287 MD United States Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York 10065 NY United States Department of Radiation Oncology Memorial Sloan Kettering Cancer Center New York 10065 NY United States Immunogenomics and Precision Oncology Platform Memorial Sloan Kettering Cancer Center New York 10065 NY United States Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins Baltimore 21287 MD United States Computational and Systems Biology Program Memorial Sloan Kettering Cancer Center New York 10065 NY United States Department of Otolaryngology-Head and Neck Surgery Weill Cornell New York Presbyterian Hospital New York 10065 NY United States Swim Across America Laboratory at Johns Hopkins Baltimore 21287 MD United States Department of Pathology Memorial Sloan Kettering Cancer Center New York 10065 NY United States Head and Neck Service Department of Surgery Memorial Sloan Kettering Cancer Center New York 10065 NY United States Division of Solid Tumor Oncology Department of Medicine Memorial Sloan Kettering Cancer Center New York 10065 NY United States Johns Hopkins Department of Otolaryngology-Head and Neck Surgery Bloomberg-Kimmel Institute for Cancer Immunotherapy at Johns Hopkins Baltimore 21287 MD United States

Tumors with mismatch repair deficiency (MMR-d) are characterized by sequence alterations in microsatellites and can accumulate thousands of mutations. This high mutational burden renders tumors immunogenic and sensitive to programmed cell death-1 (PD-1) immune checkpoint inhibitors. Yet, despite their tumor immunogenicity, patients with MMR-deficient tumors experience highly variable responses, and roughly half are refractory to *** present experimental and clinical evidence showing that the degree of microsatellite instability (MSI) and resultant mutational load, in part, underlies the variable response to PD-1 blockade immunotherapy in MMR-d human and mouse tumors. The extent of response is particularly associated with the accumulation of insertion-deletion (indel) mutational load. This study provides a rationale for the genome-wide characterization of MSI intensity and mutational load to better profile responses to anti-PD-1 immunotherapy across MMR-deficient human cancers. © 2019 American Association for the Advancement of Science. All rights reserved.

关键词： Rajarsi Mandal[1] [2] [3] † Robert M. Samstein[3] [4] Ken-Wing Lee[3] Jonathan J. Havel[3] [5] Hao Wang[6] Chirag Krishna[7] Erich Y. Sabio[3] Vladimir Makarov[3] [5] Fengshen Kuo[5] Pedro Blecua[4] Apoorva T. Ramaswamy[8] Jennifer N. Durham[2] [6] [9] Bjarne Bartlett[9] Xiaoxiao Ma[3] Raghvendra Srivastava[5] Sumit Middha[10] Ahmet Zehir[10] Jaclyn F. Hechtman[10] Luc GT Morris[3] [5] [11] Nils Weinhold[4] Nadeem Riaz[3] [4] [5] Dung T. Le[2] [6] [9] Luis A. Diaz Jr.[5] [12] Timothy A. Chan[3] [4] [5] ‡

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Author Correction: High p16 expression and heterozygous RB1 loss are biomarkers for CDK4/6 inhibitor resistance in ER+ breast cancer

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Nature communications 2022年第1期13卷 6928页

作者： Marta Palafox Laia Monserrat Meritxell Bellet Guillermo Villacampa Abel Gonzalez-Perez Mafalda Oliveira Fara Brasó-Maristany Nusaibah Ibrahimi Srinivasaraghavan Kannan Leonardo Mina Maria Teresa Herrera-Abreu Andreu Òdena Mònica Sánchez-Guixé Marta Capelán Analía Azaro Alejandra Bruna Olga Rodríguez Marta Guzmán Judit Grueso Cristina Viaplana Javier Hernández Faye Su Kui Lin Robert B Clarke Carlos Caldas Joaquín Arribas Stefan Michiels Alicia García-Sanz Nicholas C Turner Aleix Prat Paolo Nuciforo Rodrigo Dienstmann Chandra S Verma Nuria Lopez-Bigas Maurizio Scaltriti Monica Arnedos Cristina Saura Violeta Serra Experimental Therapeutics Group Vall d'Hebron Institute of Oncology Barcelona Spain. Breast Cancer and Melanoma Group Vall d'Hebron Institute of Oncology Barcelona Spain. Department of Medical Oncology Hospital Vall d'Hebron Barcelona Spain. Oncology Data Science Group Vall d'Hebron Institute of Oncology Barcelona Spain. Institute for Research in Biomedicine (IRB Barcelona) Barcelona Spain. Research Program on Biomedical Informatics Universitat Pompeu Fabra Barcelona Spain. Translational Genomics and Targeted Therapies in Solid Tumors August Pi i Sunyer Biomedical Research Institute (IDIBAPS) Barcelona Spain. Service de Biostatistique et d'Epidémiologie Gustave Roussy Villejuif France. Oncostat U1018 Inserm University Paris-Saclay Villejuif France. Bioinformatics Institute (A*STAR) Singapore Singapore. Medica Scientia Innovation Research (MedSIR) Barcelona Spain. The Breast Cancer Now Research Centre London UK. Preclinical Modelling of Pediatric Cancer Evolution Group The Institute of Cancer Research London UK. Translational Molecular Pathology Vall d'Hebron Institute of Research (VHIR) Barcelona Spain. Novartis Pharmaceuticals East Hanover NJ USA. Genentech Inc. South San Francisco California USA. Breast Biology Group Manchester Breast Centre Manchester UK. Cancer Research UK Cambridge UK. CIBERONC Vall d'Hebron Institute of Oncology Barcelona Spain. Growth Factors Laboratory Vall d'Hebron Institute of Oncology Barcelona Spain. Department of Biochemistry and Molecular Biology Universitat Autònoma de Barcelona Barcelona Spain. IMIM (Hospital del Mar Medical Research Institute) Barcelona Spain. Institució Catalana de Recerca i Estudis Avançats (ICREA) Barcelona Spain. University of Barcelona Barcelona Spain. Department of Medical Oncology Hospital Clinic Barcelona Spain. SOLTI Breast Cancer Research Group Barcelona Spain. Department of Oncology IOB Institute of Oncology Barcelona Spain. Molecular Oncology Group Vall d'Hebron Institute of On

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Dual Targeting of Oncogenic Activation and Inflammatory Signaling Increases Therapeutic Efficacy in Myeloproliferative Neoplasms (vol 33, pg 29, 2018)

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CANCER CELL 2018年第4期33卷 785-787页

作者： Kleppe, Maria Koche, Richard Zou, Lihua van Galen, Peter Hill, Corinne E. Dong, Lauren De Groote, Sofie Papalexi, Efthymia Somasundara, Amritha V. Hanasoge Cordner, Keith Keller, Matthew Farnoud, Noushin Medina, Juan McGovern, Erin Reyes, Jaime Roberts, Justin Witkin, Matthew Rapaport, Franck Teruya-Feldstein, Julie Qi, Jun Rampal, Raajit Bernstein, Bradley E. Bradner, James E. Levine, Ross L. Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center 1275 York Avenue Box 20 New York NY 10065 USA Human Oncology and Pathogenesis ProgramMemorial Sloan Kettering Cancer Center1275 York AvenueBox 20New YorkNY10065USA Center for Epigenetics Research Memorial Sloan Kettering Cancer Center New York NY 10065 USA Center for Epigenetics ResearchMemorial Sloan Kettering Cancer CenterNew YorkNY10065USA Department of Pathology Massachusetts General Hospital Harvard Medical School Broad Institute of Harvard and MIT Boston MA USA Department of Pathology Massachusetts General HospitalHarvard Medical SchoolBroad Institute of Harvard and MITBostonMAUSA Department of Pediatrics Memorial Sloan Kettering Cancer Center New York NY 10065 USA Department of PediatricsMemorial Sloan Kettering Cancer CenterNew YorkNY10065USA Center for Hematologic Malignancies Memorial Sloan Kettering Cancer Center New York NY 10065 USA Center for Hematologic MalignanciesMemorial Sloan Kettering Cancer CenterNew YorkNY10065USA Department of Medical Oncology Dana-Farber Cancer Institute 44 Binney Street Boston MA 02115 USA Department of Medical OncologyDana-Farber Cancer Institute44 Binney StreetBostonMA02115USA Department of Pathology Icahn School of Medicine Mount Sinai New York NY USA Department of PathologyIcahn School of Medicine Mount SinaiNew YorkNYUSA Leukemia Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA [∗]Corresponding author [∗∗]Corresponding author Lead Contact

Genetic and functional studies underscore the central role of JAK/STAT signaling in myeloproliferative neoplasms (MPNs). However, the mechanisms that mediate transformation in MPNs are not fully delineated, and clinically utilized JAK inhibitors have limited ability to reduce disease burden or reverse myelofibrosis. Here we show that MPN progenitor cells are characterized by marked alterations in gene regulation through differential enhancer utilization, and identify nuclear factor κB (NF-κB) signaling as a key pathway activated in malignant and non-malignant cells in MPN. Inhibition of BET bromodomain proteins attenuated NF-κB signaling and reduced cytokine production in vivo. Most importantly, combined JAK/BET inhibition resulted in a marked reduction in the serum levels of inflammatory cytokines, reduced disease burden, and reversed bone marrow fibrosis in vivo.

关键词： myeloproliferative neoplasms H3K27ac chronic inflammation NF-κB JQ1

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Correction: Integrative analysis identifies an older female-linked AML patient group with better risk in ECOG-ACRIN Cancer Research Group's clinical trial E3999

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Blood cancer journal 2023年第1期13卷 103页

作者： Franck Rapaport Kenneth Seier Yaseswini Neelamraju Duane Hassane Timour Baslan Daniel T Gildea Samuel Haddox Tak Lee H Moses Murdock Caroline Sheridan Alexis Thurmond Ling Wang Martin Carroll Larry D Cripe Hugo Fernandez Christopher E Mason Elisabeth Paietta Gail J Roboz Zhuoxin Sun Martin S Tallman Yanming Zhang Mithat Gönen Ross Levine Ari M Melnick Maria Kleppe Francine E Garrett-Bakelman Human Oncology and Pathogenesis Program Molecular Cancer Medicine Service Memorial Sloan Kettering Cancer Center New York NY USA. Center for Clinical and Translational Science The Rockefeller University New York NY USA. Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center New York NY USA. Department of Biochemistry and Molecular Genetics University of Virginia Charlottesville VA USA. Division of Hematology and Medical Oncology Department of Medicine Weill Cornell Medicine New York NY USA. Cancer Biology and Genetics Program Sloan Kettering Institute Memorial Sloan Kettering Cancer Center New York NY USA. Division of Hematology and Oncology University of Pennsylvania Perelman School of Medicine Philadelphia PA USA. Simon Cancer Center Indiana University Indianapolis IN USA. Department of Malignant Hematology & Cellular Therapy Moffitt Cancer Center Tampa FL USA. Department of Physiology and Biophysics Weill Cornell Medicine New York NY USA. Institute for Computational Biomedicine Weill Cornell Medicine New York NY USA. The WorldQuant Initiative for Quantitative Prediction Weill Cornell Medicine New York USA. Montefiore Medical Center Bronx NY USA. Weill Cornell Medicine and The New York Presbyterian Hospital New York NY USA. Dana-Farber Cancer Institute Boston MA USA. Memorial Sloan Kettering Cancer Center New York NY USA. Department of Pathology Memorial Sloan Kettering Cancer Center New York NY USA. Department of Biochemistry and Molecular Genetics University of Virginia Charlottesville VA USA. fg5q@virginia.edu. Division of Hematology and Medical Oncology Department of Medicine Weill Cornell Medicine New York NY USA. fg5q@virginia.edu. Department of Medicine University of Virginia Charlottesville VA USA. fg5q@virginia.edu. University of Virginia Cancer Center Charlottesville VA USA. fg5q@virginia.edu.

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Correction to: Primary Tumor Location and Outcomes After Cytoreductive Surgery and Intraperitoneal Chemotherapy for Peritoneal Metastases of Colorectal Origin

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Annals of surgical oncology 2020年第SUPPL 3期27卷 987页

作者： Mohammad Adileh Jonathan B Yuval Henry S Walch Walid K Chatila Rona Yaeger Julio Garcia-Aguilar Nikolaus Schultz Philip B Paty Andrea Cercek Garrett M Nash Colorectal Service Department of Surgery Memorial Sloan Kettering Cancer Center New York NY USA. Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY USA. Marie-Josée and Henry R. Kravis Center for Molecular Oncology Memorial Sloan Kettering Cancer Center New York NY USA. Tri-Institutional Program in Computational Biology and Medicine New York NY USA. Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA. Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center New York NY USA. Colorectal Service Department of Surgery Memorial Sloan Kettering Cancer Center New York NY USA. nashg@***.

In the original article there is a reference missing, in addition to its citations in the text. The reference is as follows.

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Author Correction: Accelerated single cell seeding in relapsed multiple myeloma

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Nature communications 2021年第1期12卷 591页

作者： Heather J Landau Venkata Yellapantula Benjamin T Diamond Even H Rustad Kylee H Maclachlan Gunes Gundem Juan Medina-Martinez Juan Arango Ossa Max F Levine Yangyu Zhou Rajya Kappagantula Priscilla Baez Marc Attiyeh Alvin Makohon-Moore Lance Zhang Eileen M Boyle Cody Ashby Patrick Blaney Minal Patel Yanming Zhang Ahmet Dogan David J Chung Sergio Giralt Oscar B Lahoud Jonathan U Peled Michael Scordo Gunjan Shah Hani Hassoun Neha S Korde Alexander M Lesokhin Sydney Lu Sham Mailankody Urvi Shah Eric Smith Malin L Hultcrantz Gary A Ulaner Frits van Rhee Gareth J Morgan Ola Landgren Elli Papaemmanuil Christine Iacobuzio-Donahue Francesco Maura Adult Bone Marrow Transplant Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA. Department of Medicine Weill Cornell Medical College New York NY USA. Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center New York NY USA. Myeloma Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA. Human Oncology & Pathogenesis Program Memorial Sloan Kettering Cancer Center New York NY USA. NYU Perlmutter Cancer Center New York NY USA. Myeloma Center University of Arkansas for Medical Sciences Little Rock AR USA. Center for Hematological Malignancies Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA. Cytogenetics Laboratory Department of Pathology Memorial Sloan Kettering Cancer Center New York NY USA. Hematopathology Service Department of Pathology Memorial Sloan Kettering Cancer Center New York NY USA. Department of Radiology Memorial Sloan Kettering Cancer Center New York NY USA. Myeloma Service Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA. mauraf@***.

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