Prof. Mary Barcellos Hoff

Prof. Mary Barcellos Hoff

Dr. Barcellos-Hoff studies breast cancer, mammary biology, radiation carcinogenesis, and biological mechanisms to augment radiotherapy. Her laboratory has 2 broad objectives: One is to use mouse models to determine critical cell and tissue interactions that modulate mammary carcinogenesis and the spectrum of intrinsic subtypes in breast cancer.

The other is to identify targetable TGFβ biology in tumors and the tumor microenvironment that mediate response to therapy. Dr. Barcellos-Hoff received an undergraduate degree from the University of Chicago and earned a doctoral degree in experimental pathology from the University of California, San Francisco (UCSF).

She conducted postdoctoral research on extracellular matrix and functional differentiation at the Lawrence Berkeley National Laboratory, which she joined as a staff scientist in 1988 and rose to Senior Scientist and Associate Director of the Life Sciences Division before moving to the Department of Radiation Oncology of New York University School of Medicine in 2008. In 2015, she was appointed Professor and Vice Chair of Research in the Department of Radiation Oncology at UCSF.

 

ABSTRACT

Title: Transforming growth factor β: New tricks for an old fox
Mary Helen Barcellos-Hoff, Department of Radiation Oncology, University of California San Francisco

Summary: Repair of DNA damage protects genomic integrity and is key to tissue functional integrity. In cancer, the type and fidelity of DNA damage response is the fundamental basis for clinical response to cytotoxic therapy. Survival of head and neck squamous cell carcinoma (HNSCC) patients with human papilloma virus (HPV) positive cancer is more than double that of HPV-negative HNSCC.

Our studies demonstrate that signaling competency by transforming growth factor-beta (TGFβ), an abundant, pleotropic cytokine in the tumor microenvironment, mediates response DNA damage responses (doi: 10.1158/1078-0432.CCR-18-1346). HPV infection profoundly weakens TGFβ signaling, this loss of TGFβ signaling shifts cancer cells from error-free homologous-recombination DNA double-strand-break (DSB) repair to error-prone alternative end-joining (altEJ); notably, pharmaceutical TGFβ inhibition phenocopies HPV infection.

Cells using altEJ have more mutations, are more sensitive to standard of care radiotherapy and cisplatin, and are sensitized to PARP inhibitors. I will discuss the rationale for the use of TGFβ inhibitors for optimal therapeutic combinations to improve patient outcome.

Donate to Cancer Research

All donations to the IACR go directly towards supporting early-stage oncology scientific researchers in their work.

IACR 2023 Carer’s Bursary €300

Apply for funding towards the additional costs of care while attending conference. Five Bursaries Available. 

Registration/ Membership for IACR 2023

Registration for the 59th Annual Conference in the Radisson Blu hotel, Athlone is Now Open.

EACR Membership is Included

The IACR is an affiliated national society and its members benefit from full membership of the EACR.

Late Breaking Abstracts in Now OPEN!

Biomedical Session Abstracts

Deadline: Midnight, Friday, 20th January 2023

Please note:
- Patrick Johnston Lay submission category is now closed
- Late Breaking Abstracts submitted to the Biomedical Sessions will be considered for Display Poster Presentation. 

Social Nursing and Allied Health (SNAH) Abstracts

Deadline: Midnight, Monday, 9th January 2023

SNAH abstract submissions will remain open until Monday 9th January.

Any questions?
Please contact Sinead on: sinead@sineadcassidy.com

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