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Hyperactivated mTOR and JAK2/STAT3 Pathways: Molecular Drivers and Potential Therapeutic Targets of Inflammatory and Invasive Ductal Breast Cancers After Neoadjuvant Chemotherapy.
Jhaveri, Komal; Teplinsky, Eleonora; Silvera, Deborah; Valeta-Magara, Amanda; Arju, Rezina; Giashuddin, Shah; Sarfraz, Yasmeen; Alexander, Melissa; Darvishian, Farbod; Levine, Paul H; Hashmi, Salman; Zolfaghari, Ladan; Hoffman, Heather J; Singh, Baljit; Goldberg, Judith D; Hochman, Tsivia; Formenti, Silvia; Esteva, Francisco J; Moran, Meena S; Schneider, Robert J.
Afiliación
  • Jhaveri K; Laura and Isaac Perlmutter Cancer Center, New York University Langone Medical Center, New York, NY. Electronic address: jhaverik@mskcc.org.
  • Teplinsky E; Division of Hematology & Medical Oncology, Department of Medicine, New York University School of Medicine, New York, NY.
  • Silvera D; Department of Microbiology, New York University School of Medicine, New York, NY.
  • Valeta-Magara A; Department of Microbiology, New York University School of Medicine, New York, NY.
  • Arju R; Department of Microbiology, New York University School of Medicine, New York, NY.
  • Giashuddin S; Department of Pathology, The Brooklyn Hospital Center, Brooklyn, NY.
  • Sarfraz Y; Department of Microbiology, New York University School of Medicine, New York, NY.
  • Alexander M; Department of Pathology, The Brooklyn Hospital Center, Brooklyn, NY.
  • Darvishian F; Department of Pathology, The Brooklyn Hospital Center, Brooklyn, NY.
  • Levine PH; Department of Epidemiology and Biostatistics, George Washington University, Washington, DC.
  • Hashmi S; Division of Biostatistics, New York University School of Medicine, New York, NY.
  • Zolfaghari L; Division of Biostatistics, New York University School of Medicine, New York, NY.
  • Hoffman HJ; Division of Biostatistics, New York University School of Medicine, New York, NY.
  • Singh B; Department of Epidemiology and Biostatistics, George Washington University, Washington, DC.
  • Goldberg JD; Division of Biostatistics, New York University School of Medicine, New York, NY.
  • Hochman T; Division of Biostatistics, New York University School of Medicine, New York, NY.
  • Formenti S; Department of Radiation Oncology, Weill Cornell Medical College, New York, NY.
  • Esteva FJ; Laura and Isaac Perlmutter Cancer Center, New York University Langone Medical Center, New York, NY.
  • Moran MS; Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT.
  • Schneider RJ; Laura and Isaac Perlmutter Cancer Center, New York University Langone Medical Center, New York, NY; Department of Microbiology, New York University School of Medicine, New York, NY.
Clin Breast Cancer ; 16(2): 113-22.e1, 2016 Apr.
Article en En | MEDLINE | ID: mdl-26774497
INTRODUCTION: Inflammatory breast cancer (IBC) is an aggressive and rare cancer with a poor prognosis and a need for novel targeted therapeutic strategies. Preclinical IBC data showed strong activation of the phosphatidylinositide-3-kinase/mammalian target of rapamycin (mTOR) and Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathways, and expression of inflammatory cytokines and tumor-associated macrophages (TAMs). PATIENTS AND METHODS: Archival tumor tissue from 3 disease types (IBC treated with neoadjuvant chemotherapy [NAC], n = 45; invasive ductal carcinoma [IDC] treated with NAC [n = 24; 'treated IDC'; and untreated IDC [n = 27; 'untreated IDC']) was analyzed for the expression of biomarkers phospho-S6 (pS6) (mTOR), phospho-JAK2 (pJAK2), pSTAT3, interleukin (IL)-6, CD68 (monocytes, macrophages), and CD163 (TAMs). Surrounding nontumor tissue was also analyzed. RESULTS: Biomarker levels and surrogate activity according to site-specific phosphorylation were shown in the tumor tissue of all 3 disease types but were greatest in IBC and treated IDC and least in untreated IDC for pS6, pJAK2, pSTAT3, and IL-6. Of 37 IBC patients with complete biomarker data available, 100% were pS6-positive and 95% were pJAK2-positive. In nontumor tissue, biomarker levels were observed in all groups but were generally greatest in untreated IDC and least in IBC, except for JAK2. CONCLUSION: IBC and treated IDC display similar levels of mTOR and JAK2 biomarker activation, which suggests a potential mechanism of resistance after NAC. Biomarker levels in surrounding nontumor tissue suggested that the stroma might be activated by chemotherapy and resembles the oncogenic tumor-promoting environment. Activation of pS6 and pJAK2 in IBC might support dual targeting of the mTOR and JAK/STAT pathways, and the need for prospective studies to investigate combined targeted therapies in IBC.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias de la Mama / Protocolos de Quimioterapia Combinada Antineoplásica / Carcinoma Ductal de Mama / Terapia Neoadyuvante / Factor de Transcripción STAT3 / Janus Quinasa 2 / Neoplasias Inflamatorias de la Mama / Serina-Treonina Quinasas TOR Tipo de estudio: Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Adult / Aged / Aged80 / Female / Humans / Middle aged Idioma: En Revista: Clin Breast Cancer Asunto de la revista: NEOPLASIAS Año: 2016 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias de la Mama / Protocolos de Quimioterapia Combinada Antineoplásica / Carcinoma Ductal de Mama / Terapia Neoadyuvante / Factor de Transcripción STAT3 / Janus Quinasa 2 / Neoplasias Inflamatorias de la Mama / Serina-Treonina Quinasas TOR Tipo de estudio: Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Adult / Aged / Aged80 / Female / Humans / Middle aged Idioma: En Revista: Clin Breast Cancer Asunto de la revista: NEOPLASIAS Año: 2016 Tipo del documento: Article Pais de publicación: Estados Unidos