Andrew Volk.

Andrew Volk, PhD

  • Assistant Professor, UC Department of Pediatrics



Our lab studies the genetic and epigenetic drivers of leukemia. Our gene of interest, CHAF1B, is located within the Down syndrome critical region of chromosome 21. Children with Down syndrome are predisposed to leukemias, suggesting that elevated expression of genes on chromosome 21 is somehow involved in leukemia progression.

We are excited to make fundamental discoveries about the molecular drivers of leukemia and are always trying to understand how cells use the process of chromatin assembly to maintain their state. Defects in this process lead to cancer or tissue failure. We found that chromatin assembly is directly linked to transcriptional regulation in acute myeloid leukemia, and that leukemias are driven by CHAF1B and the chromatin assembly complex binding regions of DNA associated with stem cell differentiation genes, repressing their expression.

I am honored to be a Transition to Independence Award recipient from the National Cancer Institute (NCI) K99/R00 (2019). My work has been published in many well-respected journals, including Genes and Development, Clinical Cancer Research, Cancer Cell, Leukemia, Cell, Molecular Cell, Stem Cells and Biochimica et Biophysica Acta-Gene Regulatory Mechanisms. I have more than 11 years of research experience, and I began my work at Cincinnati Children’s in 2020.

BS: Baylor University, Waco, TX.

PhD: Loyola University Chicago, Chicago, IL.

Post-doctoral Fellowship: Northwestern University, Evanston, IL.

Services and Specialties

Cancer and Blood Diseases, Cancer Blood Disease Institute


Epigenetics; chromatin assembly; Acute Myeloid Leukemia; down syndrome; genetic drivers of leukemia and bone marrow failure

Research Areas

Experimental Hematology and Cancer Biology


Paralog-specific signaling by IRAK1/4 maintains MyD88-independent functions in MDS/AML. Bennett, J; Ishikawa, C; Agarwal, P; Yeung, J; Sampson, A; Uible, E; Vick, E; Bolanos, LC; Hueneman, K; Wunderlich, M; et al. Blood. 2023; 142:989-1007.

Repression of TRIM13 by chromatin assembly factor CHAF1B is critical for AML development. Dean, ST; Ishikawa, C; Zhu, X; Walulik, S; Nixon, T; Jordan, JK; Henderson, S; Wyder, M; Salomonis, N; Wunderlich, M; et al. Blood Advances. 2023; 7:4822-4837.

Regulation of chromatin accessibility by the histone chaperone CAF-1 sustains lineage fidelity. Franklin, R; Guo, Y; He, S; Chen, M; Ji, F; Zhou, X; Frankhouser, D; Do, BT; Chiem, C; Jang, M; et al. Nature Communications. 2022; 13:2350.

TRIM13 Is a Novel Cell Cycle Hub Regulated By CHAF1B to Promote Acute Myeloid Leukemogenesis. Dean, S; Ishikawa, C; Zhu, X; Nixon, T; Walulik, S; Wyder, M; Jordan, J; Wunderlich, M; Starczynowski, DT; Salomonis, N; et al. Blood. 2022; 140:2978-2979.

IRAK1 Contributes to IRAK4 Inhibitor Resistance Via Non-Canonical Signaling Mechanisms in MDS/AML. Bennett, J; Yeung, J; Sampson, A; Hueneman, K; Wunderlich, M; Choi, K; Volk, A; Hoyt, SB; Thomas, CJ; Starczynowski, DT. Blood. 2022; 140:2240-2241.

UBE2N Is a Druggable Target and an Essential Ubiquitin-Conjugating Enzyme in Myeloid Malignancies. Ishikawa, C; Barreyro, L; Sampson, A; Hueneman, K; Choi, K; Bolanos, LC; Volk, A; Greis, KD; Starczynowski, DT. Blood. 2022; 140:5830.

Ticket to divide: m6A reader YTHDC1 drives acute myeloid leukemia proliferation. Volk, A. Blood. 2021; 138:2748-2750.

NOTCH-ing up nucleotide metabolism in T-cell acute lymphoblastic leukemia. Volk, A. Communications Biology. 2021; 4:809.

LKB1/STK11 Is a Tumor Suppressor in the Progression of Myeloproliferative Neoplasms. Marinaccio, C; Suraneni, P; Celik, H; Volk, A; Wen, QJ; Ling, T; Bulic, M; Lasho, T; Koche, RP; Famulare, CA; et al. Cancer Discovery. 2021; 11:1398-1410.