Raquel Buj-Gomez, PhD

Research Instructor

Hillman Cancer Center, Research Pavilion
5115 Centre Avenue, Suite 1.48
Pittsburgh, PA 15232
Phone: 412-623-3241

Education

BS (Biology), University of Valencia, Valencia, Spain, 2010
MS (Developmental genetics and genomics). University of Barcelona, Barcelona, Spain, 2011
PhD (Cancer epigenetics), University of Barcelona, Barcelona, Spain, 2017
 
Raquel Buj-Gomez, PhD
Dr. Buj's research is focused on understanding the fundamental metabolic and epigenetic mechanisms that drive malignant transformation and tumorigenesis downstream p16 loss. p16 is an important tumor suppressor protein suppressed in ~50% of human cancers and is highly upregulated in many types of senescence. Senescence is a stable cell cycle arrest also characterized by high metabolic activity and epigenomic reorganization. Senescence acts as a double-edge sword in human cancer. On one hand, senescence is a tumor suppressor mechanism that maintains the cell cycle arrest in part by overexpressing p16. On the other hand, senescent cells acquire a senescence-associated secretory phenotype (SASP) that promotes chronic inflammation and tumorigenesis. Dr. Buj's research program aim to understand the metabolic and epigenetic mechanisms that promote senescence-bypass and malignant transformation downstream of p16 loss with the ultimate goal of developing new targeted therapies for patients with null or very low p16 expression.
 
Currently, Dr. Buj is involved in two major lines of research:
 
1) To investigate whether altered metabolism and epigenome downstream of p16 loss leads to reprogrammed SASP and tumor microenvironment, impairing tumor immunosurveillance.

2) To investigate the coordinated mechanism between mTORC1 and the Hippo pathway to alleviate oxidative stress and promote malignant transformation downstream of loss of p16.
 

Journal Articles

Leon KE, Tangudu NK, Aird KM and Buj R. Loss of p16: a bouncer of the immunological surveillance? Life (Basel). 2021 Apr 2;11(4):309. Doi: 10.3390/life11040309.
Buj R, Leon KE and Aird KM. Suppression of p16 alleviates the senescence-associated secretory phenotype. Aging (Albany NY). 2020 Feb 6; 13(3):3290-3312. doi: 10.18632/aging.202640.
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 Induces mTORC1- Mediated Nucleotide Metabolic Reprogramming. Cell Rep. 2019 Aug 20;28(8):1971-1980.e8. doi: 10.1016/j.celrep.2019.07.084.
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 Induces mTORC1- Mediated Nucleotide Metabolic Reprogramming. Cell Rep. 2019 Aug 20;28(8):1971-1980.e8. doi: 10.1016/j.celrep.2019.07.084.
Buj R and Aird KM. p16: cycling off the beaten path. Mol Cell Oncol. 2019;6(6):e1677140. doi: 10.1080/23723556.2019.1677140.
Buj R, Mallona I, Díez-Villanueva A, Zafon C, Mate JL, Roca M, Puig-Domingo M, Reverter JL, Mauricio D, Peinado MA and Jordà M. Kallikreins Stepwise Scoring Reveals Three Subtypes of Papillary Thyroid Cancer with Prognostic Implications. Thyroid. 2018 May;28(5):601-612. doi: 10.1089/thy.2017.0501.
Buj R, Mallona I, Díez-Villanueva A, Barrera V, Mauricio D, Puig-Domingo M, Reverter JL, Matias-Guiu X, Azuara D, Ramírez JL, Alonso S, Rosell R, Capellà G, Perucho M, Robledo M, Peinado MA and Jordà M. Quantification of unmethylated Alu (QUAlu): a tool to assess global hypomethylation in routine clinical samples. Oncotarget. 2016 Mar 1;7(9):10536-46. doi: 10.18632/oncotarget.7233.
Buj R, Iglesias N, Planas AM and Santalucía T. A plasmid toolkit for cloning chimeric cDNAs encoding customized fusion proteins into any Gateway destination expression vector. BMC Mol Biol. 2013 Aug 20;14(1):18. doi: 10.1186/1471-2199-14-18.