About

Houda Alachkar, PharmD, PhD, is an Associate Professor of Clinical Pharmacy at the Titus Family Department of Clinical Pharmacy at USC Alfred E. Mann School of Pharmacy and Pharmaceutical Sciences. She received her PharmD degree from Ohio Northern University and her PhD in biomedical sciences from Ohio State University. She completed postdoctoral fellowship training in clinical pharmacology and pharmacogenomics at the University of Chicago. Her research focuses on applying genomic information to the identification and functional characterization of cancer targets, with particular interest in acute myeloid leukemia (AML). Her lab investigates the role of cancer pharmacogenomic variation, somatic changes in cancer cells, and germline variants in influencing disease outcomes and treatment responses. Her work includes exploring targeted therapeutic approaches, such as engineered fusion proteins and nanoparticles, to develop novel treatments for AML. Dr. Alachkar's contributions advance understanding of the molecular mechanisms underlying leukemia progression and resistance, aiming to translate genomic discoveries into clinical applications.

Research topics

• Immunology
• Virology
• Medicine
• Computer Science
• Sociology
• Psychology
• Biology
• Cognitive science
• Evolutionary biology
• Art
• Computational biology
• Genetics
• Communication
• Social psychology
• Neuroscience
• Pathology
• Anthropology
• Internal medicine

Selected publications

• Abstract 7413: CD36 influences leukemia progression in MLL-AF9-driven AML by modulating the leukemia immune microenvironment

  Cancer Research · 2026-04-03

  articleSenior author

  Abstract CD36, a fatty acid translocase, is recognized as a potential therapeutic target in acute myeloid leukemia (AML), where its overexpression is associated with disease progression, yet its role in leukemogenesis remains to be elucidated. This study investigates the role of CD36 in leukemia initiation using the MLL-AF9 mouse model, where hematopoietic stem progenitor cells (HSPCs) from Cd36 knockout (KO) or wild-type (WT) mice were transduced with MLL-AF9 virus and evaluated for leukemogenic potential through in vitro and in vivo assays, and comprehensive transcriptomic, metabolomic, and immune profiling. Both Cd36KO and Cd36WT HSPCs transformed into leukemic cells, but Cd36 deletion led to a less aggressive leukemia phenotype, with reduced leukemia burden and extended median survival in sublethaly irradiated mice (15 vs. 22 days, P = 0.001). Leukemia engraftment was significantly higher in Cd36WT-MA9 compared with Cd36KO-MA9 transplanted mice in spleen (74.99% vs. 38.67%, P = 0.008) and blood (85.49% vs. 26.84%, P < 0.001) relative to bone marrow (BM). Increased CD4 (13.93% vs. 36.78%, P = 0.025) and CD8 T cells (7.62% vs. 16.06%, P = 0.02) and less CD4CD25 T cells (34.53% vs. 19.24%, P = 0.006) were observed in mice engrafted with Cd36KO-MA9 cells compared with Cd36WT-MA9 mice. qPCR analysis shows elevated Gzmb (2.43-fold, P < 0.001), and Tim3 (5.88-fold, P = 0.002) mRNA expression in Cd36WT-MA9 compared with Cd36KO-MA9 mice, while Foxp3, Lag3, and Pd1 showed no significant differences. A more pronounced phenotypic was observed in immunocompetent, non-irradiated mice; Cd36WT-MA9 cells displayed significantly greater leukemia engraftment (BM: 98.58% vs. 0.73%, P < 0.0001; spleen: 64.60% vs. 0.79%, P < 0.001, and blood: 89.08% vs. 10.20%, P = 0.014) compared with Cd36KO-MA9 cells. Cd36KO-MA9 mice showed enhanced immune responses with higher CD3+ (10.87% vs. 37.82%, P < 0.001), CD4 (27.77% vs. 55.19%, P = 0.008), CD8 T cells (17.84% vs. 31.24%, P < 0.001), and NK1.1 cells (14.47% vs. 29.83%, P < 0.0001), but lower CD4CD25 (11.11% vs. 5.55%, P = 0.045), DN-T cells (51.95% vs. 10.46%, P < 0.001), and CD25 DN T cells (17.77% vs. 4.00%, P < 0.001) compared with Cd36WT-MA9 mice, suggesting Cd36 deletion reduces leukemia progression by enhancing anti-leukemic immunity. RNA-sequencing and gene set enrichment analysis indicated enrichment of inflammatory (TNFA, FDR < 0.001) and metabolic pathways (oxidative phosphorylation, FDR < 0.001) in Cd36WT-MA9 cells compared with Cd36KO-MA9 mice. Metabolomic analysis identified 124 metabolites, with Cd36KO-MA9 cells showing a significant increase in asparagine (10.00-fold, unadj P = 0.009) and a decrease in purine (7.68-fold, unadj P < 0.0001) compared with Cd36WT-MA9 cells. While Cd36 deletion does not prevent leukemogenesis, it alters the leukemia immune microenvironment and slows leukemia progression, highlighting its role in modulating leukemia development. Citation Format: Yiting Meng, Wenda Zhu, Mateusz Pospiech, Long Huynh, Kalyani Divgi, Yiyu Xiao, Qianqian Peng, Nicholas A. Graham, Houda Alachkar. CD36 influences leukemia progression in MLL-AF9-driven AML by modulating the leukemia immune microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 7413.

  PublisherDOI

• Isoform specific regulation of osteopontin by AKT2 in hepatocytes and livers

  Cellular Signalling · 2025-04-09 · 2 citations

  article
  PublisherDOI

• Acute Myeloid Leukemia With a Non-Canonical <i>FLT3</i> V491L Mutation: A Case Report With <i>Ex Vivo</i> FLT3 Inhibitors Sensitivity Testing

  Journal of Medical Cases · 2025-12-25

  articleOpen access

  Approximately 30% of patients with acute myeloid leukemia (AML) harbor FMS-like tyrosine kinase 3 (FLT3) mutations, which are associated with poor overall survival. Although United States Food and Drug Administration (FDA)-approved FLT3 inhibitors are available, their efficacy against non-canonical FLT3 mutations remains elusive. Here we present a case of a 72-year-old female Jehovah’s Witness with newly diagnosed AML carrying a rare pathogenic FLT3 V491L mutation identified by next-generation sequencing. Given the patient’s religious beliefs, blood transfusion was not an option, making the patient ineligible for high-intensity chemotherapy and leading to alternative treatment approaches. To our knowledge, this is the first case report of the effectiveness of gilteritinib in an older patient with AML with a non-canonical FLT3 mutation and limitation on blood products usage. Initial treatment with hydroxyurea and leukapheresis followed by azacitidine and venetoclax resulted in an inadequate treatment response. Given the lack of research on the FLT3 V491L mutation, we conducted an ex vivo sensitivity study using the patient’s diagnostic bone marrow blasts to assess and compare the anti-leukemic efficacy of midostaurin, quizartinib, and gilteritinib. The ex vivo study revealed the lowest half-maximal inhibitory concentration (IC50) value and the highest number of apoptotic cells in gilteritinib treated patient’s blasts under Flt3 ligand-supplemented conditions. An initial clinical improvement with gilteritinib was observed. However, after the third cycle, gilteritinib was substituted with midostaurin because of high copay costs with gilteritinib. Subsequently, an increase in leukemic blasts was observed, and soon after, the patient expired. Treatment of relapsed AML with a non-canonical mutation is challenging due to the lack of data regarding FLT3 inhibitors. This case highlights the potential role of gilteritinib in targeting the rare FLT3 V491L mutation, underscoring the need for further research and improved accessibility to effective therapies.

  PublisherOA PDFDOI

• Figure S3 from FLT3/CD99 Bispecific Antibody–Based Nanoparticles for Acute Myeloid Leukemia

  2025-03-28

  preprintOpen accessSenior author

  &lt;p&gt;Figure S3 – Western Blot data from USC100 following treatment with FLT3-A192, CD99-A192 and Co-Assembled CD99-A192 and FLT3-A192.&lt;/p&gt;

  PublisherDOI

• Characterizing Kupffer Cell Production of CD5 Antigen-Like and Its Function on Regulating Migration of Natural Killer T Cells

  American Journal Of Pathology · 2025-07-08 · 3 citations

  articleOpen access

  CD5 antigen-like (CD5L) is a multifunctional glycoprotein characterized for its role in the lipid metabolism, particularly within macrophages. In the liver, CD5L strongly correlates with liver injury. This study explored the role of CD5L on liver lipid accumulation and inflammatory response. CD5L promoted lipid uptake in hepatocytes and stellate cells. In multiple models of liver injury, expression of Cd5l was associated with that of Clec4f, a marker for liver macrophages, consistent with its role as a macrophage survival factor. Transwell assay was used to demonstrate a novel function of CD5L on promoting migration of natural killer T cells. This effect was independent of CD36, the characterized receptor of CD5L. This effect was also observed with liver macrophages, which are the cellular source for CD5L, and blocking CD5L attenuated natural killer T cell migration induced by liver macrophages. Finally, plasma levels of CD5L correlated with poor patient response to immune check point therapy that is dependent on response of T-cell populations. In addition, plasma CD5L levels correlated with levels of steatosis and severity of steatotic liver injury. Given the association between liver steatosis and poor response to immune checkpoint therapy, these data suggest that plasma CD5L levels may serve as a predictive biomarker for patient response to immune checkpoint therapy.

  PublisherOA PDFDOI

• Figure S2 from FLT3/CD99 Bispecific Antibody–Based Nanoparticles for Acute Myeloid Leukemia

  2025-03-28

  preprintOpen accessSenior author

  &lt;p&gt;Figure S2 – FLT3 and CD99 surface level expression in primary blasts of sample USC001 and USC100.&lt;/p&gt;

  PublisherDOI

• Figure S1 from FLT3/CD99 Bispecific Antibody–Based Nanoparticles for Acute Myeloid Leukemia

  2025-03-28

  preprintOpen accessSenior author

  &lt;p&gt;Figure S1 – Flow Panels of Annexin and PI staining of U937 Cells following treatment with FLT3-A192, CD99-A192 and Co-Assembled CD99-A192 and FLT3-A192.&lt;/p&gt;

  PublisherDOI

• Recognition, prevention, and management of adverse events associated with asparaginase / pegaspargase treatment of acute lymphoblastic leukemia in adults: consensus of an expert panel

  Haematologica · 2025-03-20 · 5 citations

  articleOpen access

  Asparaginase (ASNase)-based chemotherapy regimens significantly improve survival outcomes in children, adolescents and young adults (AYA), and even adults with acute lymphoblastic leukemia/lymphoma (ALL); however, the incidence and severity of ASNase-associated adverse events (AE) in adults may differ significantly from those reported in children. Strategies to mitigate, monitor for, and manage toxicities that allow adult ALL patients to receive full ASNase courses are needed. A representative 12-member panel of experts who treat AYA and adult ALL patients, incorporate ASNase into their treatment regimens, and conduct related research was assembled to consider opportunities to optimize the use of pediatric-inspired ALL regimens in these adult patients. Following 2 systematic biomedical literature searches from April 2009 through April 2024, a modified Delphi method was used to distill expert opinion into clinical statements that met a standardized definition of consensus. After 2 iterative Delphi method surveys, 23 statements met the standardized definition of consensus, whereas 19 statements did not. Five statements were merged to avoid redundancy. The clinical statements were grouped into 5 distinct categories: 1) hepatotoxicity; 2) hypersensitivity reactions; 3) thromboembolic and coagulopathy complications; 4) pancreatitis and metabolic complications; and 5) dosing. The intent of these statements is to provide health care providers with information that will help them mitigate, monitor for, and manage the most common and/or unique ASNase-induced AE in adult ALL patients, allowing these patients to receive more or all the planned ASNase doses and thereby improve outcomes.

  PublisherOA PDFDOI

• Figure S4 from FLT3/CD99 Bispecific Antibody–Based Nanoparticles for Acute Myeloid Leukemia

  2025-03-28

  preprintOpen accessSenior author

  &lt;p&gt;Figure S4 – qPCR analysis results for CDC25A, E2F1, CDKN2B, CDC20, and MYC in MV4-11 cells treated with with FLT3-A192, CD99-A192 and Co-Assembled CD99-A192 and FLT3-A192.&lt;/p&gt;

  PublisherDOI

• Figure S3 from FLT3/CD99 Bispecific Antibody–Based Nanoparticles for Acute Myeloid Leukemia

  2024-10-03

  preprintOpen accessSenior author

  &lt;p&gt;Figure S3 – Western Blot data from USC100 following treatment with FLT3-A192, CD99-A192 and Co-Assembled CD99-A192 and FLT3-A192.&lt;/p&gt;

  PublisherDOI

Recent grants

• Developing robust and scalable genomics tools and databases to analyze immune receptor repertoires across broad populations

  NIH · $2.5M · 2023–2029

Frequent coauthors

• Vijaya Vaikari

  63 shared

• Yiting Meng

  57 shared

• J. Andrew MacKay

  57 shared

• Atham Ali

  55 shared

• Mateusz Pospiech

  49 shared

• Ryan Chu

  47 shared

• Alvin Phan

  47 shared

• Mincheol Park

  47 shared