Aleix Prat

ORCID: 0000-0003-2377-540X
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About
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Research Areas
  • HER2/EGFR in Cancer Research
  • Advanced Breast Cancer Therapies
  • Breast Cancer Treatment Studies
  • Cancer Treatment and Pharmacology
  • Cancer Genomics and Diagnostics
  • Cancer Immunotherapy and Biomarkers
  • Estrogen and related hormone effects
  • Lung Cancer Treatments and Mutations
  • Cancer Cells and Metastasis
  • Monoclonal and Polyclonal Antibodies Research
  • BRCA gene mutations in cancer
  • Cancer Research and Treatments
  • Nutrition, Genetics, and Disease
  • PI3K/AKT/mTOR signaling in cancer
  • Radiomics and Machine Learning in Medical Imaging
  • Lung Cancer Research Studies
  • Chronic Lymphocytic Leukemia Research
  • Prostate Cancer Treatment and Research
  • Gene expression and cancer classification
  • Colorectal Cancer Treatments and Studies
  • COVID-19 and healthcare impacts
  • Computational Drug Discovery Methods
  • Esophageal Cancer Research and Treatment
  • Cancer-related Molecular Pathways
  • Ferroptosis and cancer prognosis

Hospital Clínic de Barcelona
2016-2025

Universitat de Barcelona
2016-2025

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer
2016-2025

Solti
2020-2025

Oryzon Genomics (Spain)
2022-2025

Hospital Quirónsalud Barcelona
2021-2025

Breast Cancer Research Foundation
2016-2024

Target (United States)
2016-2024

Biomedical Research Institute
2016-2024

Fundació de Recerca Clínic Barcelona-Institut d’Investigacions Biomèdiques August Pi i Sunyer
2024

Daniel C. Koboldt Robert S. Fulton Michael D. McLellan Heather K. Schmidt Joelle Kalicki-Veizer and 95 more Joshua F. McMichael Lucinda Fulton David J. Dooling Li Ding Elaine R. Mardis Richard K. Wilson Adrian Ally Miruna Balasundaram Yaron S.N. Butterfield Rebecca Carlsen Candace Carter Andy Chu Eric Chuah Hye Jung E. Chun Robin Coope Noreen Dhalla Ranabir Guin Carrie Hirst Martin Hirst Robert A. Holt Darlene Lee Haiyan I. Li Michael Mayo Richard A. Moore Andrew J. Mungall Erin Pleasance A. Gordon Robertson Jacqueline E. Schein Arash Shafiei Payal Sipahimalani Jared R. Slobodan Dominik Stoll Angela Tam Nina Thiessen Richard Varhol Natasja Wye Thomas Zeng Yongjun Zhao İnanç Birol Steven J.M. Jones Marco A. Marra Andrew D. Cherniack Gordon Saksena Robert C. Onofrio Nam Pho Scott L. Carter Steven E. Schumacher Barbara Tabak Bryan Hernandez Jeff Gentry Huy Nguyen Andrew Crenshaw Kristin Ardlie Rameen Beroukhim Wendy Winckler Gad Getz Stacey Gabriel Matthew Meyerson Lynda Chin Raju Kucherlapati Katherine A. Hoadley J. Todd Auman Huihui Fan Yidi J. Turman Yan Shi Ling Li Michael D. Topal Xiaping He Hann Hsiang Chao Aleix Prat Grace O. Silva Michael D. Iglesia Zhao Wei Jerry Usary Jonathan S. Berg Michael C. C. Adams Jessica K. Booker Junyuan Wu Anisha Gulabani Tom Bodenheimer Alan P. Hoyle Janae V. Simons Matthew G. Soloway Lisle E. Mose Joshua M. Stuart Saianand Balu Peter J. Park D. Neil Hayes Charles M. Perou Simeen Malik Swapna Mahurkar‐Joshi Hui Shen Daniel J. Weisenberger Timothy J. Triche Phillip H. Lai

We analysed primary breast cancers by genomic DNA copy number arrays, methylation, exome sequencing, messenger RNA microRNA sequencing and reverse-phase protein arrays. Our ability to integrate information across platforms provided key insights into previously defined gene expression subtypes demonstrated the existence of four main cancer classes when combining data from five platforms, each which shows significant molecular heterogeneity. Somatic mutations in only three genes (TP53, PIK3CA...

10.1038/nature11412 article EN cc-by-nc-sa Nature 2012-09-21

Abstract Introduction In breast cancer, gene expression analyses have defined five tumor subtypes (luminal A, luminal B, HER2-enriched, basal-like and claudin-low), each of which has unique biologic prognostic features. Here, we comprehensively characterize the recently identified claudin-low subtype. Methods The clinical, pathological biological features tumors were compared to other using an updated human database multiple independent data sets. These main also evaluated in a panel cancer...

10.1186/bcr2635 article EN cc-by Breast Cancer Research 2010-09-02

Among breast cancers without human epidermal growth factor receptor 2 (HER2) amplification, overexpression, or both, a large proportion express low levels of HER2 that may be targetable. Currently available HER2-directed therapies have been ineffective in patients with these "HER2-low" cancers.

10.1056/nejmoa2203690 article EN New England Journal of Medicine 2022-06-05

Advanced Breast Cancer (ABC) comprises both locally advanced breast cancer (LABC) and metastatic (MBC) [1.Cardoso F. Costa A. Norton L. ESO-ESMO 2nd International Consensus Guidelines for (ABC2). Simultaneous publication in.Breast. 2014; 23: 489-502Abstract Full Text PDF PubMed Scopus (252) Google Scholar]. Although treatable, MBC remains virtually an incurable disease with a median overall survival (OS) of ∼3 years 5-year only ∼25% [2.Cardoso Spence D. Mertz S. et al.Global analysis...

10.1093/annonc/mdy192 article EN publisher-specific-oa Annals of Oncology 2018-05-24

To characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained high fidelity. However, at single-nucleotide level, variable numbers PDX-specific somatic events documented, although they only rarely functionally significant. Variant allele frequencies often preserved in PDXs, demonstrating that clonal...

10.1016/j.celrep.2013.08.022 article EN cc-by Cell Reports 2013-09-01

PARP inhibitors are active in tumors with defects DNA homologous recombination (HR) due to BRCA1/2 mutations. The phosphoinositide 3-kinase (PI3K) signaling pathway preserves HR steady state. We hypothesized that BRCA-proficient triple-negative breast cancer (TNBC), PI3K inhibition would result impairment and subsequent sensitization inhibitors. show TNBC cells leads damage, downregulation of BRCA1/2, gain poly-ADP-ribosylation, inhibition. In patient-derived primary tumor xenografts, dual...

10.1158/2159-8290.cd-11-0348 article EN Cancer Discovery 2012-08-23

Purpose Current immunohistochemical (IHC)-based definitions of luminal A and B breast cancers are imperfect when compared with multigene expression-based assays. In this study, we sought to improve the IHC subtyping by examining pathologic gene expression characteristics genomically defined subtypes. Patients Methods Gene features were collected from primary tumors across five independent cohorts: British Columbia Cancer Agency (BCCA) tamoxifen-treated only, Grupo Español de Investigación en...

10.1200/jco.2012.43.4134 article EN Journal of Clinical Oncology 2012-12-12

Preoperative aromatase inhibitor (AI) treatment promotes breast-conserving surgery (BCS) for estrogen receptor (ER)-positive breast cancer. To study this option, responses to three AIs were compared in a randomized phase II neoadjuvant trial designed select agents III investigations.Three hundred seventy-seven postmenopausal women with clinical stage ER-positive (Allred score 6-8) cancer randomly assigned receive exemestane, letrozole, or anastrozole. The primary end point was response....

10.1200/jco.2010.31.6950 article EN Journal of Clinical Oncology 2011-05-10

Novel antibody-drug conjugates against HER2 are showing high activity in HER2-negative breast cancer (BC) with low expression (i.e., 1+ or 2+ and lack of ERBB2 amplification). However, the clinical molecular features HER2-low BC yet to be elucidated. Here, we collected retrospective clinicopathological PAM50 data from 3,689 patients disease made following observations. First, proportion was higher HR-positive (65.4%) than triple-negative (TNBC, 36.6%). Second, within disease, luminal-related...

10.1038/s41523-020-00208-2 article EN cc-by npj Breast Cancer 2021-01-04

Abstract Breast cancer research is hampered by difficulties in obtaining and studying primary human breast tissue, the lack of vivo preclinical models that reflect patient tumor biology accurately. To overcome these limitations, we propagated a cohort tumors grown epithelium-free mammary fat pad severe combined immunodeficient (SCID)/Beige nonobese diabetic (NOD)/SCID/IL-2γ-receptor null (NSG) mice under series transplant conditions. Both yielded stably transplantable xenografts at...

10.1158/0008-5472.can-12-4081 article EN Cancer Research 2013-06-05

Antibody targeting of the immune checkpoint receptor PD1 produces therapeutic activity in a variety solid tumors, but most patients exhibit partial or complete resistance to treatment for reasons that are unclear. In this study, we evaluated tumor specimens from 65 with melanoma, lung nonsquamous, squamous cell head and neck cancers who were treated approved PD1-targeting antibodies pembrolizumab nivolumab. Tumor RNA before anti-PD1 therapy was analyzed on nCounter system using PanCancer...

10.1158/0008-5472.can-16-3556 article EN Cancer Research 2017-05-10

Abstract Summary: Breast cancer is one of the most frequent cancers among women. Extensive studies into molecular heterogeneity breast have produced a plethora subtype classification and prognosis prediction algorithms, as well numerous gene expression signatures. However, reimplementation these algorithms tedious but important task to enable comparison existing signatures models between each other with new models. Here, we present genefu R/Bioconductor package, multi-tiered compendium...

10.1093/bioinformatics/btv693 article EN Bioinformatics 2015-11-24

Many methodologies have been used in research to identify the "intrinsic" subtypes of breast cancer commonly known as Luminal A, B, HER2-Enriched (HER2-E) and Basal-like. The PAM50 gene set is often for expression-based subtyping; however, surrogate subtyping using panels immunohistochemical (IHC) markers are still widely clinically. Discrepancies between these methods may lead different treatment decisions.We RT-qPCR assay expression profile 814 tumors from GEICAM/9906 phase III clinical...

10.1186/1755-8794-5-44 article EN cc-by BMC Medical Genomics 2012-10-04

Clinical benefits from trastuzumab and other anti-HER2 therapies in patients with HER2 amplified breast cancer remain limited by primary or acquired resistance. To identify potential mechanisms of resistance, we established trastuzumab-resistant cells chronic exposure to treatment. Genomewide copy-number variation analyses the resistant compared parental revealed a focal amplification genomic DNA containing cyclin E gene. In cohort 34 + treated trastuzumab-based therapy, found that...

10.1073/pnas.1014835108 article EN Proceedings of the National Academy of Sciences 2011-02-14
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