John H. Healey

ORCID: 0000-0002-0802-1186
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About
Contact & Profiles
Research Areas
  • Sarcoma Diagnosis and Treatment
  • Bone Tumor Diagnosis and Treatments
  • Management of metastatic bone disease
  • Musculoskeletal synovial abnormalities and treatments
  • Orthopaedic implants and arthroplasty
  • Vascular Tumors and Angiosarcomas
  • Orthopedic Infections and Treatments
  • Cancer Genomics and Diagnostics
  • Reconstructive Surgery and Microvascular Techniques
  • Cardiac tumors and thrombi
  • Bone health and treatments
  • Lymphoma Diagnosis and Treatment
  • Oral and Maxillofacial Pathology
  • Total Knee Arthroplasty Outcomes
  • Cancer Diagnosis and Treatment
  • Immune cells in cancer
  • Bone fractures and treatments
  • Cancer Cells and Metastasis
  • Cancer-related molecular mechanisms research
  • Cancer, Hypoxia, and Metabolism
  • Neuroblastoma Research and Treatments
  • CAR-T cell therapy research
  • Surgical site infection prevention
  • Tendon Structure and Treatment
  • Lung Cancer Treatments and Mutations

Memorial Sloan Kettering Cancer Center
2016-2025

Kettering University
2007-2024

Wollongong Hospital
2023

Cornell University
2013-2022

Hospital for Special Surgery
1989-2021

Columbus Oncology and Hematology Associates
2021

Clinical Orthopaedics and Related Research
2018-2020

Stryker (United States)
2020

Sanden (Japan)
2020

National Institutes of Health
2018-2019

Ayuko Hoshino Han Sang Kim Linda Bojmar Kofi Ennu Gyan Michele Cioffi and 95 more Jonathan M. Hernandez Constantinos P. Zambirinis Gonçalo Rodrigues Henrik Molina Søren Heissel Milica Tešić Mark Loïc Steiner Alberto Benito‐Martín Serena Lucotti Angela Di Giannatale Katharine Offer Miho Nakajima Caitlin Williams Laura Nogués Fanny A. Pelissier Vatter Ayako Hashimoto Alexander E. Davies Daniela Freitas Candia M. Kenific Yonathan Ararso Weston Buehring Pernille Lauritzen Yusuke Ogitani Kei Sugiura Naoko Takahashi Maša Alečković Kayleen Bailey Joshua S. Jolissant Huajuan Wang Ashton Harris Laurent Schaeffer Guillermo García‐Santos Zoe Posner Vinod P. Balachandran Yasmin Khakoo G. Praveen Raju Avigdor Scherz Irit Sagi Ruth Scherz‐Shouval Yosef Yarden Moshe Oren Mahathi Malladi Mary Petriccione Kevin C. De Braganca Maria Donzelli Cheryl Fischer Stephanie Vitolano Geraldine P. Wright Lee Ganshaw Mariel Marrano Amina Ahmed Joe DeStefano Enrico Danzer Michael H. A. Roehrl Norman J. Lacayo Theresa C. Vincent Martin R. Weiser Mary S. Brady Paul A. Meyers Leonard H. Wexler Srikanth R. Ambati Alexander J. Chou Emily K. Slotkin Shakeel Modak Stephen S. Roberts Ellen M. Basu Daniel Diolaiti Benjamin A. Krantz Fátima Cardoso Amber L. Simpson Michael F. Berger Charles M. Rudin Diane M. Simeone Maneesh Jain Cyrus M. Ghajar Surinder K. Batra Ben Z. Stanger Jack D. Bui Kristy A. Brown Vinagolu K. Rajasekhar John H. Healey Maria de Sousa Kim Kramer Sujit Sheth Jeanine Baisch Virginia Pascual Todd E. Heaton Michael P. LaQuaglia David J. Pisapia Robert E. Schwartz Haiying Zhang Yuan Liu Arti Shukla Laurence Blavier Yves A. DeClerck

10.1016/j.cell.2020.07.009 article EN publisher-specific-oa Cell 2020-08-01

To compare three-drug chemotherapy with cisplatin, doxorubicin, and methotrexate four-drug methotrexate, ifosfamide for the treatment of osteosarcoma. determine whether addition muramyl tripeptide (MTP) to enhances event-free survival (EFS) overall in newly diagnosed patients osteosarcoma.Six hundred sixty-two osteosarcoma without clinically detectable metastatic disease whose was considered resectable received one four prospectively randomized treatments. All identical cumulative doses...

10.1200/jco.2008.14.0095 article EN Journal of Clinical Oncology 2008-01-30

To determine whether the addition of ifosfamide and/or muramyl tripeptide (MTP) encapsulated in liposomes to cisplatin, doxorubicin, and high-dose methotrexate (HDMTX) could improve probability for event-free survival (EFS) newly diagnosed patients with osteosarcoma (OS).Six hundred seventy-seven OS without clinically detectable metastatic disease were treated one four prospectively randomized treatments. All received identical cumulative doses HDMTX underwent definitive surgical resection...

10.1200/jco.2005.06.031 article EN Journal of Clinical Oncology 2005-03-18

Chemotherapy with alternating vincristine-doxorubicin-cyclophosphamide and ifosfamide-etoposide cycles primary tumor treatment surgery and/or radiation therapy constitute the usual approach to localized Ewing sarcoma in North America. We tested whether chemotherapy intensification through interval compression could improve outcome.This was a prospective, randomized controlled trial for patients younger than 50 years old newly diagnosed extradural sarcoma. Patients assigned standard...

10.1200/jco.2011.41.5703 article EN Journal of Clinical Oncology 2012-10-23

PURPOSE Adjuvant chemotherapy improves disease-free survival (DFS) for patients with osteogenic sarcoma (OS). We reviewed our experience OS to determine prognostic factors, the role of preoperative and subsequent histologic response, salvage after poor initial response. METHODS From 1975 1984, we saw 279 previously untreated without metastasis. All received intensive underwent surgical resection primary tumor. Chemotherapy included high-dose methotrexate; Adriamycin (doxorubicin; Adria...

10.1200/jco.1992.10.1.5 article EN Journal of Clinical Oncology 1992-01-01

Synovial sarcomas account for up to 10 percent of soft-tissue and include two major histologic subtypes, biphasic monophasic, defined respectively by the presence absence glandular epithelial differentiation in a background spindle tumor cells. A characteristic SYT–SSX fusion gene resulting from chromosomal translocation t(X;18)(p11;q11) is detectable almost all synovial sarcomas. The fuses SYT chromosome 18 either highly homologous genes at Xp11, SSX1 or SSX2. SYT–SSX1 SYT–SSX2 are thought...

10.1056/nejm199801153380303 article EN New England Journal of Medicine 1998-01-15

The human fibroblast activation protein alpha (FAP alpha) is a M(r) 95,000 cell surface antigen selectively expressed in reactive stromal fibroblasts of epithelial cancers, granulation tissue healing wounds, and malignant cells bone soft sarcomas. Normal adult tissues are generally FAP alpha-, but some fetal mesenchymal transiently express the molecule. Because its restricted normal distribution abundant expression stroma over 90% breast, colorectal, lung carcinomas, under clinical...

10.1073/pnas.91.12.5657 article EN Proceedings of the National Academy of Sciences 1994-06-07

PURPOSE More than 90% of Ewing's sarcomas (ES) contain a fusion the EWS and FLI1 genes, due to t(11;22)(q24;q12) translocation. At molecular level, EWS-FLI1 rearrangements show great diversity. Specifically, many different combinations exons from encode in-frame transcripts result in differences length composition chimeric protein, which functions as an oncogenic aberrant transcription factor. In most common type (type 1), exon 7 is linked frame with 6 FLI1. As fundamental pathogenetic...

10.1200/jco.1998.16.4.1248 article EN Journal of Clinical Oncology 1998-04-01

Expression of the colony-stimulating factor 1 (CSF1) gene is elevated in most tenosynovial giant-cell tumors. This observation has led to discovery and clinical development therapy targeting CSF1 receptor (CSF1R).Using x-ray co-crystallography guide our drug-discovery research, we generated a potent, selective CSF1R inhibitor, PLX3397, that traps kinase autoinhibited conformation. We then conducted multicenter, phase trial two parts analyze this compound. In first part, evaluated escalations...

10.1056/nejmoa1411366 article EN New England Journal of Medicine 2015-07-29

Abstract The classification of epithelioid vascular tumors remains challenging, as there is considerable morphological overlap between tumor subtypes, across the spectrum from benign to malignant categories. A t(1;3)(p36.3;q25) translocation was reported in two cases hemangioendothelioma (EHE), however, no follow‐up studies have been performed identify gene fusion or assess its prevalence a larger cohort patients. We undertook systematic molecular analysis 17 EHE, characterized by classic...

10.1002/gcc.20886 article EN Genes Chromosomes and Cancer 2011-05-16

Chemotherapy and surgery have improved the length of survival for patients with osteogenic sarcoma (OS) who present without metastatic disease. We reviewed our experience OS presented clinically detectable metastasis to determine prognostic factors effects on primary tumor disease.From 1975 1984 we treated 62 had previously untreated detected at presentation. All these received intensive chemotherapy that included high-dose methotrexate; doxorubicin; bleomycin, cyclophosphamide, dactinomycin...

10.1200/jco.1993.11.3.449 article EN Journal of Clinical Oncology 1993-03-01

The Ewing sarcoma family of tumors (ESFT) is a group malignant soft tissue and bone sharing chromosomal translocation affecting the EWS locus. Intergroup INT-0091 demonstrated superiority regimen vincristine, cyclophosphamide, doxorubicin (VDC), dactinomycin alternating with ifosfamide etoposide (IE) over VDC for patients nonmetastatic ESFT bone. goal this study was to determine whether dose-intensified IE would further improve outcome or tissue.Patients previously untreated, were eligible....

10.1200/jco.2008.19.1478 article EN Journal of Clinical Oncology 2009-04-07

A hallmark of metastasis is the adaptation tumor cells to new environments. Metabolic constraints imposed by serine and glycine-limited brain environment restrict metastatic growth. How metastases overcome these growth-prohibitive conditions poorly understood. Here, we demonstrate that 3-phosphoglycerate dehydrogenase (PHGDH), which catalyzes rate-limiting step glucose-derived synthesis, a major determinant in multiple human cancer types preclinical models. Enhanced synthesis proved...

10.1158/2159-8290.cd-19-1228 article EN Cancer Discovery 2020-06-22

Colony-stimulating factor 1 (CSF1) is a primary regulator of the survival, proliferation, and differentiation monocyte/macrophage that sustains protumorigenic functions tumor-associated macrophages (TAMs). Considering current advances in understanding role inflammatory tumor microenvironment, targeting components sarcoma such as TAMs, viable strategy. Here, we investigated effect PLX3397 (pexidartinib) potent inhibitor CSF1 receptor (CSF1R). was recently approved by Food Drug Administration...

10.1158/1535-7163.mct-20-0591 article EN Molecular Cancer Therapeutics 2021-06-04

Abstract The genetic, biologic, and clinical heterogeneity of sarcomas poses a challenge for the identification therapeutic targets, research, advancing patient care. Because there are > 100 sarcoma subtypes, in-depth genetic studies have focused on one or few subtypes. Herein, we report comparative analysis 2,138 representing 45 pathological entities. This cohort is prospectively analyzed using targeted sequencing to characterize subtype-specific somatic alterations in targetable...

10.1038/s41467-022-30453-x article EN cc-by Nature Communications 2022-06-15

Abstract There are more than 70 distinct sarcomas, and this diversity complicates the development of precision-based therapeutics for these cancers. Prospective comprehensive genomic profiling could overcome challenge by providing insight into sarcomas’ molecular drivers. Through targeted panel sequencing 7494 sarcomas representing 44 histologies, we identify highly recurrent type-specific alterations that aid in diagnosis treatment decisions. Sequencing lead to refinement or reassignment...

10.1038/s41467-022-30496-0 article EN cc-by Nature Communications 2022-06-15

The tumor microenvironment presents many obstacles to effective chimeric antigen receptor (CAR) T cell therapy, including glucose competition from and myeloid cells. Using mouse models of acute lymphoblastic leukemia (ALL), renal carcinoma (RCC), glioblastoma (GBM), we show that enforced expression the transporter GLUT1 enhances anti-tumor efficacy promotes favorable CAR-T phenotypes for two clinically relevant CAR designs, 19-28z IL13Rα2-BBz. In NALM6 ALL model, 19-28z-GLUT1 stem cell-like...

10.1016/j.ymthe.2024.05.006 article EN cc-by-nc-nd Molecular Therapy 2024-05-07
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