Andrew Volk.

Assistant Professor, UC Department of Pediatrics

513-636-1844

Biography & Affiliation

Biography

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.

Research Interests

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

Academic Affiliation

Assistant Professor, UC Department of Pediatrics

Research Divisions

Experimental Hematology and Cancer Biology

Education

BS: Baylor University, Waco, TX.

PhD: Loyola University Chicago, Chicago, IL.

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

Publications

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.

Loss of LKB1/STK11 Facilitates Leukemic Progression of the Myeloproliferative Neoplasms. Marinaccio, C; Suraneni, PK; Celik, H; Volk, A; Wen, JQ; Ling, T; Lasho, T; Koche, RP; Famulare, C; Stein, BL; et al. Blood. 2020; 136:1-1.

Regulation of MLL/COMPASS stability through its proteolytic cleavage by taspase1 as a possible approach for clinical therapy of leukemia. Zhao, Z; Wang, L; Volk, AG; Birch, NW; Stoltz, KL; Bartom, ET; Marshall, SA; Rendleman, EJ; Nestler, CM; Shilati, J; et al. Genes and Development. 2019; 33:61-74.

USP7 Cooperates with NOTCH1 to Drive the Oncogenic Transcriptional Program in T-Cell Leukemia. Jin, Q; Martinez, CA; Arcipowski, KM; Zhu, Y; Gutierrez-Diaz, BT; Wang, KK; Johnson, MR; Volk, AG; Wang, F; Wu, J; et al. Clinical Cancer Research. 2019; 25:222-239.

A CHAF1B-Dependent Molecular Switch in Hematopoiesis and Leukemia Pathogenesis. Volk, A; Liang, K; Suraneni, P; Li, X; Zhao, J; Bulic, M; Marshall, S; Pulakanti, K; Malinge, S; Taub, J; et al. Cancer Cell. 2018; 34:707-723.e7.

Sensitizing acute myeloid leukemia cells to induced differentiation by inhibiting the RIP1/RIP3 pathway. Xin, J; You, D; Breslin, P; Li, J; Wei, W; Cannova, J; Volk, A; Gutierrez, R; Xiao, Y; Ni, A; et al. Leukemia. 2017; 31:1154-1165.

Not All H3K4 Methylations Are Created Equal: Mll2/COMPASS Dependency in Primordial Germ Cell Specification. Hu, D; Gao, X; Cao, K; Morgan, MA; Mas, G; Smith, ER; Volk, AG; Bartom, ET; Crispino, JD; Di Croce, L; et al. Molecular Cell. 2017; 65:460-475.e6.

Sensitizing leukemia stem cells to NF-κB inhibitor treatment in vivo by inactivation of both TNF and IL-1 signaling. Li, J; Volk, A; Zhang, J; Cannova, J; Dai, S; Hao, C; Hu, C; Sun, J; Xu, Y; Wei, W; et al. Oncotarget. 2017; 8:8420-8435.

Therapeutic Targeting of MLL Degradation Pathways in MLL-Rearranged Leukemia. Liang, K; Volk, AG; Haug, JS; Marshall, SA; Woodfin, AR; Bartom, ET; Gilmore, JM; Florens, L; Washburn, MP; Sullivan, KD; et al. Cell. 2017; 168:59-72.e13.

Hematopoietic Stem Cell Activity Is Regulated by Pten Phosphorylation Through a Niche-Dependent Mechanism. Li, J; Zhang, J; Tang, M; Xin, J; Xu, Y; Volk, A; Hao, C; Hu, C; Sun, J; Wei, W; et al. Stem Cells. 2016; 34:2130-2144.