Matthew
Middle Name
J.
Ellis, MD, BChir, BSc., PhD, FRCP
Middle Name
J.
Picture
Positions
- Professor / Director
-
Lester and Sue Smith Breast Center - Administrative
Oncology/Medicine and MCB
Baylor College of Medicine
Houston, TX US
- McNair Scholar
-
Baylor College of Medicine
Houston, Texas United States
- Associate Director of Precision Medicine
-
Dan L Duncan Comprehensive Cancer Center
Baylor College of Medicine
Houston, Texas United States
Addresses
- BCM-Cullen Building (Office)
-
Room: BCMC-335
Houston, TX 77030
United States
Education
- MD from University of Cambridge
- 05/1984 - Cambridge, England
- MB., BChir.
- PhD from University of London
- 05/1992 - London, United Kingdom
- Molecular Biology
- Fellowship at Georgetown University Hospital
- 06/1994 - Washington, District of Columbia United States
- Medical Oncology
- Residency at Royal College of Physicians
- 06/1988 - London, United Kingdom
- Medicine
- BSc from University of London
- 05/1980 - London, United Kingdom
- Pathology
Honors & Awards
- CPRIT Scholar in Cancer Research
- C. Kent Osborne Endowed Chair
- Baylor College of Medicine
- Gianni Bonadonna Breast Cancer Award
- American Society of Clinical Oncology (06/2015)
- Elected Member
- Association of American Physicians (04/2018)
Professional Interests
- Breast Cancer Oncology
- Breast Cancer Genomics
- Metastatic Breast Cancer
- Clinical Trials
Professional Statement
As the Director for the Lester and Sue Smith Breast Center I coordinate an interdisciplinary team of oncologists, pathologists, epidemiologists, basic scientists and statisticians focused on improving our ability to prevent, detect and treat breast cancer. I bring to this position considerable experience in the oversight and execution of large projects and protocols of a collaborative nature on a nationwide basis. I have a strong background in molecular cell biology, molecular pharmacology, genomics and proteomics. I have been an active member of The Breast Cancer Intergroup of North America (TCBI) since 1998 (now NCTN) and I am Co-Chair of the translational medicine committee for the NRG cooperative group. I was also Co-leader for The Cancer Genome Atlas (TCGA) Breast Project where I established collaborations with several Genome Centers on massive parallel sequencing of breast cancer (Nature 2010, 2012). I served as a Co-PI for the second phase Clinical Proteomic Tumor Analysis Consortium (CPTAC2) grant when I was at Washington University in St Louis. During CPTAC2 I established collaborative interactions with the Broad Institute that led to several publications on the proteogenomic analysis of breast cancer (Nature 2016, Cell 2020 in press). I am also a U01 funded principal investigator in CPTAC3 where I continue to translate proteogenomic findings to improve the diagnosis and treatment of breast and other cancers. Finally I am principal investigator of the Baylor College of Medicine Breast Cancer SPORE.Websites
Selected Publications
- "Activating HER2 mutations in HER2 gene amplification negative breast cancer." Cancer discovery. 2013;3(2):224-37. 2013 :
- "Whole-genome analysis informs breast cancer response to aromatase inhibition." Nature. 2012;486(7403):353-60.. 2012 :
- "Connecting genomic alterations to cancer biology with proteomics: the NCI Clinical Proteomic Tumor Analysis Consortium." Cancer discovery. 2013;3(10):1108-12. 2012 :
- "The genomic landscape of breast cancer as a therapeutic roadmap." Cancer discovery. 2013;3(1):27-34. 2013 :
- "New concepts in breast cancer genomics and genetics.." Breast cancer research : BCR. 2014;16(5):460.. 2014 :
- "Endocrine-therapy-resistant ESR1 variants revealed by genomic characterization of breast-cancer-derived xenografts." Cell reports. 2013;4(6):1116-30. 2013 :
- "Incorporating genomics into breast cancer clinical trials and care." Clinical cancer research: an official journal. 2013 :
- Li Ding, Amanda G Paulovich, David Fenyö, Matthew J Ellis, Steven A Carr, "Proteogenomics connects somatic mutations to signalling in breast cancer." 2016 June 2; 534 (7605): 55-62. Pubmed PMID: 27251275
- Sherri R Davies, Kelly Hunt, Vera J Suman, Jacqueline Snider, Thomas Walsh, Graham A Colditz, Katherine DeSchryver, Richard K Wilson, Elaine R Mardis, Matthew J Ellis "Aromatase inhibition remodels the clonal architecture of estrogen-receptor-positive breast cancers." 2016 August 9; 7 : Pubmed PMID: 27502118
Funding
- Proteogenomics of Endocrine Therapy Resistance (10/01/2019 - 05/31/2021) Grant funding from Komen Leadership Grant
- Conduct Tandem-Mass Tag (TMT) quantitative proteomic and phosphoproteomic analysis of ER+ PDX grown in the presence and absence of estradiol supplementation. Informatic tools will be applied to contrast estradiol-dependent and independent models and metastatic and non-metastatic models.
- Circulating Tumor DNA Based-Monitoring in Early Stage and Advanced Breast Cancer (10/01/2019 - 09/30/2021) The Breast Cancer Research Foundation
- Translational Research in Breast Cancer (08/01/2020 - 07/31/2025) Grant funding from NIH/NCI - Breast SPORE
- Microscaled Proteogenomics for Cancer Clinical Trials (06/01/2017 - 05/31/2022) Grant funding from NIH/NCI - CPTAC
- The overall goal of our proposal leverages state-of-the-art quantitative discovery proteomics and phosphoproteomics as well as targeted assays to measure the kinome and chromatin modifications. These sensitive and reproducible pipelines will be used to analyze preclinical models, well-annotated cohorts and clinical trial samples in an iterative design. A robust proteogenomics pipeline developed by our group will be used to analyze and visualize the data.
- Kinase inhibition for ESR1 fusion-driven breast cancer (10/01/2020 - 09/30/2023) Grant funding from Adrienne Helis Malvin Medical Research Foundation
- This proposal provides strong evidence that ESR1 translocation events are an emerging class of recurrent somatic mutations that lead to not only therapeutic drug resistance but also lethal metastasis in a subset of patients with ER+ breast cancer, a disease not previously considered to be driven by gene fusions. These ESR1 fusions cannot be treated with the current standard-of-care ET, as they produce proteins lacking the ERα LBD. However, we will define gene expression patterns that classify pathogenic ESR1 fusion proteins and their downstream activated kinases to allow new therapeutics to be developed to treat ESR1 translocated breast tumors. Results of this study will also shed new mechanistic insight into how ER+ breast cancer becomes ET-resistant and metastatic, a lethal process that is still poorly understood.
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