Luis Francisco Zirnberger Batista

Luis Francisco Zirnberger Batista, PhD

Languages spoken: English

Academic Information

Departments Adjunct - Radiation Oncology , Primary - Internal Medicine , Adjunct - Oncological Sciences

Divisions: Hematology & Hematologic Malignancies

Academic Office Information

luis.batista@hci.utah.edu

Dr. Luis Batista holds the HCI Presidential Endowed Professor Chair in Hematologic Malignancies, with a primary appointment in the Department of Medicine and adjunct appointment in the Department of Oncological Sciences. Dr. Batista is a member of the Genomics, Epigenetics and Metabolism Program at the Huntsman Cancer Institute, where he also runs the Center for Telomere Biology Disorders and organizes the Genome Stability and Cancer (GStaC) Seminar Series.



The overarching goal of the Batista lab is to understand the consequences of telomere dysfunction and DNA damage during tissue development. The Batista lab pioneered the use of targeted differentiation of human pluripotent stem cells towards hematopoietic progenitors to decipher how telomerase is regulated during hematopoiesis, and to uncover pathways leading from telomere shortening to hematopoietic failure. The lab has also uncovered novel non-coding RNA processing mechanisms that can be modulated to restore hematopoietic development in mutant cells. The Batista lab continues to break new ground by coupling molecular and biochemical assays with the ability to generate specific cell types that are impaired in patients. This approach has led the team to discover USB1, which is mutated in patients suffering with poikiloderma with neutropenia, as being a novel 3’- end miRNA deadenylase. Research in the Batista lab has opened novel alternatives that can be explored for treatment of aplastic anemia, bone marrow failure, and cancer.



Originally from Porto, Portugal, Dr. Batista performed his PhD under the guidance of Dr. Carlos Menck (University of Sao Paulo) and Bernd Kaina (University of Mainz), working on DNA damage pathways in cancer. Dr. Batista then moved to Stanford University for his postdoctoral training, where he was awarded a Pew Fellowship, a CIRM postdoctoral fellowship, and a K99/R00 grant from the NIH to study telomerase regulation and telomere biology syndromes. In 2014 Dr. Batista started his independent career at Washington University in St. Louis where he was an Associate Professor of Medicine and served as Associate Director of the Center for Genome Integrity at the Siteman Cancer Center. In 2026, Dr. Batista relocated to the Huntsman Cancer Institute at the University of Utah. Dr. Batista’s work has been continuously funded by the National Institutes of Health and numerous grants from the Department of Defense (DOD). Dr. Batista has also been awarded grants from different foundations, including the American Cancer Society, the Edward Mallinckrodt Jr. Foundation, the V Foundation for Cancer Research, and the American Federation for Aging Research.

Education History

Undergraduate University of Sao Paulo
 BSc
Doctoral Training University of Sao Paulo (Brazil) and University of Mainz (Germany)
 PhD
Postdoctoral Training Stanford University
 Postdoctoral Scholar

Selected Publications

Journal Article

  1. Mendoza-Castrejon J, Yang W, Denby ED, Wang HC, Casey EB, Muthukumar R, Patel RM, Yoon J, Li Y, White JM, Chen R, Batista LFZ, Magee J (2025). Fetal context conveys heritable protection against MLL-rearranged AML that depends on MLL3. Blood,
  2. Camacho V, Bekendam R, Stone AP, Barrachina MN, Branfield S, Carminita E, Becker IC, Lee DH, Walsey E, Payne C, Kaplan JP, Tilburg J, Pal S, Batista LFZ, Italiano JE Jr, Machlus K (2025). Induction of Moderate DNA Damage Enhances Megakaryopoiesis and Platelet Production. Blood advances,
  3. Collins TB, Laranjeira ABA, Kong T, Fulbright MC, Fisher DAC, Sturgeon CM, Batista LFZ, Oh S (2024). Altered erythropoiesis via JAK2 and ASXL1 mutations in myeloproliferative neoplasms. Experimental hematology, 132, 104178.
  4. Jeong HC, Shukla S, Fok WC, Huynh TN, Batista LFZ*, Parker R* (*Co-Corresponding Author (2023). USB1 is a miRNA deadenylase that regulates hematopoietic development. Science (New York, N.Y.), 379(6635), 901-907.
  5. Vessoni AT, Zhang T, Quinet A, Jeong HC, Munroe M, Wood M, Tedone E, Vindigni A, Shay JW, Greenberg RA, Batista LF (2021). Telomere erosion in human pluripotent stem cells leads to ATR-mediated mitotic catastrophe. The Journal of cell biology, 220(6),
  6. Munroe M, Niero EL, Fok WC, Vessoni AT, Jeong HC, Brenner KA, Batista LF (2020). Telomere Dysfunction Activates p53 and Represses HNF4¿ Expression Leading to Impaired Human Hepatocyte Development and Function. Hepatology (Baltimore, Md.), 72(4), 1412-1429.
  7. Shukla S, Jeong HC, Sturgeon CM, Parker R, Batista LF (2020). Chemical inhibition of PAPD5/7 rescues telomerase function and hematopoiesis in dyskeratosis congenita. Blood advances, 4(12), 2717-2722.
  8. Quinet A, Tirman S, Jackson J, ¿vikovi¿ S, Lemaçon D, Carvajal-Maldonado D, González-Acosta D, Vessoni AT, Cybulla E, Wood M, Tavis S, Batista LFZ, Méndez J, Sale JE, Vindigni (2020). PRIMPOL-Mediated Adaptive Response Suppresses Replication Fork Reversal in BRCA-Deficient Cells. Molecular cell, 77(3), 461-474.e9.
  9. Fok WC, Shukla S, Vessoni AT, Brenner KA, Parker R, Sturgeon CM, Batista LF (2019). Posttranscriptional modulation of TERC by PAPD5 inhibition rescues hematopoietic development in dyskeratosis congenita. Blood, 133(12), 1308-1312.
  10. Kreienkamp R, Graziano S, Coll-Bonfill N, Bedia-Diaz G, Cybulla E, Vindigni A, Dorsett D, Kubben N, Batista LFZ, Gonzalo (2018). A Cell-Intrinsic Interferon-like Response Links Replication Stress to Cellular Aging Caused by Progerin. Cell reports, 22(8), 2006-2015.
  11. Brestoff JR, Vessoni AT, Brenner KA, Uy GL, DiPersio JF, Blinder M, Witt CA, Byers DE, Hachem RR, Truclock EP, Early DS, Anadkat MJ, Musiek A, Javidan-Nejad C, Balfe DM, Rosman IS, Liu C, Zhang L, Despotis GJ, Ruzinova MB, Sehn JK, Amarillo I, Heusel JW, Swat W, Kim BS, Wartman LD, Yusen RD, Batista LF (2018). Acute graft-versus-host disease following lung transplantation in a patient with a novel TERT mutation. Thorax, 73(5), 489-492.
  12. Fok WC, Batista LF (2017). Stressed ends: telomere attrition in chronic diseases. Revista brasileira de hematologia e hemoterapia, 39(2), 98-99.
  13. Fok WC, Niero ELO, Dege C, Brenner KA, Sturgeon CM*, Batista LFZ* (*Co-Corresponding Author (2017). p53 Mediates Failure of Human Definitive Hematopoiesis in Dyskeratosis Congenita. Stem cell reports, 9(2), 409-418.
  14. Huh CJ, Zhang B, Victor MB, Dahiya S, Batista LF, Horvath S, Yoo A (2016). Maintenance of age in human neurons generated by microRNA-based neuronal conversion of fibroblasts. eLife, 5,
  15. Kareta MS, Gorges LL, Hafeez S, Benayoun BA, Marro S, Zmoos AF, Cecchini MJ, Spacek D, Batista LF, O'Brien M, Ng YH, Ang CE, Vaka D, Artandi SE, Dick FA, Brunet A, Sage J, Wernig (2015). Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis. Cell stem cell, 16(1), 39-50.
  16. Zhong FL, Batista LF, Freund A, Pech MF, Venteicher AS, Artandi S (2012). TPP1 OB-fold domain controls telomere maintenance by recruiting telomerase to chromosome ends. Cell, 150(3), 481-94.
  17. Batista LF, Pech MF, Zhong FL, Nguyen HN, Xie KT, Zaug AJ, Crary SM, Choi J, Sebastiano V, Cherry A, Giri N, Wernig M, Alter BP, Cech TR, Savage SA, Reijo Pera RA, Artandi S (2011). Telomere shortening and loss of self-renewal in dyskeratosis congenita induced pluripotent stem cells. Nature, 474(7351), 399-402.
  18. Sebastiano V, Maeder ML, Angstman JF, Haddad B, Khayter C, Yeo DT, Goodwin MJ, Hawkins JS, Ramirez CL, Batista LF, Artandi SE, Wernig M, Joung J (2011). In situ genetic correction of the sickle cell anemia mutation in human induced pluripotent stem cells using engineered zinc finger nucleases. Stem cells (Dayton, Ohio), 29(11), 1717-26.
  19. Saffi J, Agnoletto MH, Guecheva TN, Batista LF, Carvalho H, Henriques JA, Stary A, Menck CF, Sarasin (2010). Effect of the anti-neoplastic drug doxorubicin on XPD-mutated DNA repair-deficient human cells. DNA repair, 9(1), 40-7.
  20. Batista LF, Roos WP, Kaina B, Menck C (2009). p53 mutant human glioma cells are sensitive to UV-C-induced apoptosis due to impaired cyclobutane pyrimidine dimer removal. Molecular cancer research, 7(2), 237-46.
  21. Batista LF, Artandi S (2009). Telomere uncapping, chromosomes, and carcinomas. Cancer cell, 15(6), 455-7.
  22. Roos WP, Batista LF, Naumann SC, Wick W, Weller M, Menck CF, Kaina (2007). Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O6-methylguanine. Oncogene, 26(2), 186-97.
  23. Batista LF, Roos WP, Christmann M, Menck CF, Kaina (2007). Differential sensitivity of malignant glioma cells to methylating and chloroethylating anticancer drugs: p53 determines the switch by regulating xpc, ddb2, and DNA double-strand breaks. Cancer research, 67(24), 11886-95.
  24. Batista LF, Chiganças V, Brumatti G, Amarante-Mendes GP, Menck C (2006). Involvement of DNA replication in ultraviolet-induced apoptosis of mammalian cells. Apoptosis, 11(7), 1139-48.
  25. Chiganças V, Batista LF, Brumatti G, Amarante-Mendes GP, Yasui A, Menck C (2002). Photorepair of RNA polymerase arrest and apoptosis after ultraviolet irradiation in normal and XPB deficient rodent cells. Cell death and differentiation, 9(10), 1099-107.

Review

  1. Chen L, Batista LF (2025). Biogenesis and Regulation of Telomerase during Development and Cancer (Epub ahead of print). Cold Spring Harbor perspectives in biology,
  2. Batista LFZ*, Dokal I*, Parker R* (*Co-Corresponding Author (2022). Telomere biology disorders: time for moving towards the clinic?. Trends in molecular medicine, 28(10), 882-891.
  3. Vessoni AT, Filippi-Chiela EC, Lenz G, Batista LF (2020). Tumor propagating cells: drivers of tumor plasticity, heterogeneity, and recurrence. Oncogene, 39(10), 2055-2068.
  4. Batista LF, Artandi S (2013). Understanding telomere diseases through analysis of patient-derived iPS cells. Current opinion in genetics & development, 23(5), 526-33.
  5. Batista LFZ, Kaina B, Meneghini R, Menck CF (2009). How DNA lesions are turned into powerful killing structures: insights from UV-induced apoptosis. Mutation research, 681(2-3), 197-208.

Letter

  1. Arruda-Neto JD, Friedberg EC, Bittencourt-Oliveira MC, Segreto HR, Moron MM, Maria DA, Batista LF, Schenberg A (2010). The role played by endogenous and exogenous electric fields in DNA signaling and repair. DNA repair, 9(4), 356-7.

News & Podcasts

Huntsman Cancer Institute News