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Katherine Aird, PhD

Associate Professor
1.46d Hillman Cancer Center
Pittsburgh, PA 15232
Phone: 412-623-7709


BA (Biology), Johns Hopkins University, Baltimore, MD, 2004
PhD (Pathology), Duke University, Durham, NC, 2010
Headshot of Katherine Aird, PhD
The Aird lab has two main areas of investigation: 1) mechanisms and pathological implications of cellular senescence; and 2) metabolic reprogramming during tumorigenesis in ovarian cancer and melanoma. More information can be found at:

1) The mechanisms and pathological implications of cellular senescence.  Cellular senescence is a stable cell cycle arrest that plays a role in both cancer and aging. While some aspects of senescence are beneficial, such as the tumor suppressive loss of proliferation, others are detrimental. For instance, expression of the senescence-associated secretory phenotype (SASP) promotes chronic inflammation, which has negative effects on the senescent cell and tumor microenvironment. The lab is particularly interested in the intersection between metabolism, the epigenome, and the microenvironment during senescence.  Understanding the mechanisms of how cells undergo and overcome senescence, and its role on the microenvironment, may lead to novel therapeutic strategies for both cancer and aging.
2) Metabolic reprogramming during tumorigenesis.  It is well-appreciated that cellular metabolism is altered in tumors as an adaptive response to nutrient- and oxygen-poor conditions. However, in the past few years, it is becoming more apparent that metabolism is changed early in tumorigenesis and may contribute to driving tumorigenic phenotypes. The lab aims to characterize and mechanistically probe the role of altered metabolism in the earliest events in tumorigenesis. Projects are related to: 1) how metabolites affect histone modifications to influence DNA damage response and repair; and 2) how tumor suppressors such as p16 and ATM affect metabolic programs outside of their canonical roles. These mechanistic insights will lead to novel targets to explore for therapeutic intervention.

Journal Articles

Buj R, Chen CW, Dahl ES, Leon KE, Kuskovsky R, Maglakelidze N, Navaratnarajah M, Zhang G, Doan MT, Jiang H,Zaleski M,Kutzler L, Lacko H. Lu Y, Mills GB, Gowda R, Robertson GP, Warrick JI, Herlyn M, Imamura Y, Kimball SR, DeGraff DJ, Snyder NW and Aird KM. Suppression of p16 increases nucleotide synthesis via mTORC1. Cell Reports 28:1971-1980, 2019.
Chen CW, Buj R, Dahl ES, Leon KE, Varner EL, von Krusenstiern E, Snyder NW and Aird KM. ATM inhibition drives metabolic adaptation via induction of macropinocytosis. bioRxiv. doi: /10.1101/2020.04.06.027565 
Chen CW, Buj R, Dahl ES, Leon KE and Aird KM. ATM inhibition synergizes with fenofibrate in high grade serous ovarian cancer cells. bioRxiv. 
Dahl ES, Buj R, Leon KE, Newell JM, Bitler BG, Snyder NW and Aird KM. Targeting IDH1 as a pro-senescent therapy for high grade serous ovarian cancer. Molecular Cancer Research 17:1710-1720, 2019.
Aird KM, Worth AJ, Snyder NW, Lee JV, Sivanand S, Blair IA, Wellen KE and Zhang R. ATM couples replication stress and metabolism reprogramming during cellular senescence. Cell Reports 11:893-901, 2015. 
Aird KM, Li H, Xin F, Konstantinopoulos PA and Zhang R. Identification of ribonucleotide reductase M2 as a potential target for pro-senescence therapy in epithelial ovarian cancer.Cell Cycle 13(2), 2013.
Aird KM, Zhang G, Li H, Tu Z, Bitler BG, Garipov A, Wu H, Wei Z, Wagner SN, Herlyn M and Zhang R. Suppression of nucleotide metabolism underlies the establishment and maintenance of oncogene-induced senescence. Cell Reports 3:1252-1265, 2013.