ผู้ช่วยศาสตราจารย์ ดร.ทนพญ.ศิริพร จิตแก้ว

Assistant Professor Siriporn Jitkaew, MT, Ph.D.

Research Interest

Dr. Siriporn Jitkaew received her B.Sc. (Medical Technology, First Class Honors) in 2002 and her Ph.D. (Biochemistry) in 2009 from Mahidol University, Bangkok, Thailand. From 2009 to 2014, Dr. Siriporn continued her research training as a postdoctoral visiting fellow at the National Cancer Institute, National Institutes of Health (NIH) in the United States. Currently, Dr. Siriporn is a faculty member in the Department of Clinical Chemistry at the Faculty of Allied Health Sciences. Her primary research focus is the study of inflammation and novel cell death pathways, with a particular emphasis on necroptosis, ferroptosis, senescence, and Immunogenic Cancer Cell Death (ICD). She explores their roles in shaping the tumor microenvironment (TME), influencing tumorigenesis, and driving cancer progression. Additionally, she investigates the translational implications of her findings in cancer immunotherapy, cancer precision medicine, and other age-related inflammatory diseases and aging. Dr. Siriporn’s ultimate research goal is to translate these novel discoveries into innovative biomarkers for prevention, diagnosis, and prognosis, as well as to develop novel therapeutic strategies. Her research employs a combination of 2D and 3D in vitro cell culture models and in vivo studies, including animal models and patients. She integrates bioinformatics, multi-omics, functional genomics approaches, including CRISPR/Cas genome editing, into her work. Dr. Siriporn collaborates extensively with both national and international research partners.

Education

2004-2009 Ph.D. (Biochemistry), Mahidol University, Thailand 1998-2002 B.Sc. (Medical Technology), First Class Honors, Mahidol University, Thailand

Training

2009-2014 Postdoctoral visiting fellow, National Cancer Institute, National Institute of Health, United States of America 2006-2008 Registered visiting Ph.D. student, Karolinska Institutet, Stockholm, Sweden

Publications

  1. Lomphithak T, Sae-Fung S, Tampieri A, Sprio S, Jitkaew S*, Fadeel B*. Exploiting the ferroaddiction of pancreatic cancer cells using Fe-doped nanoparticles. Nanomedicine: Nanotechnology, Biology, and Medicine. 2023 Oct: 102714 (SJR Q1; Cite Score Tier 1; JCR IF = 5.400) *These authors contributed equally to this work.
  2. Lomphithak T, Jaikla P, Sae-Fung A, Sonkaew S, Jitkaew S. Natural Flavonoids Quercetin and Kaempferol Targeting G2/M Cell Cycle-Related Genes and Synergize with Smac Mimetic LCL-161 to Induce Necroptosis in Cholangiocarcinoma Cells. Nutrients. 2023 Jul 10;15(14):3090. (SJR Tier1; JCR IF = 5.215)
  3. Sae-Fung A, Mutirangura A, Jitkaew S. Identification and validation of a novel ferroptosis-related gene signature for prognosis and potential therapeutic target prediction in cholangiocarcinoma. Front Immunol. 2023 Jan 17;13:1051273. (SJR Q1; JCR IF = 5.215)
  4. Lomphithak T, Akara-Amornthum P, Murakami K, Hashimoto M, Usubuchi H, Iwabuchi E, Unno M, Cai Z, Sasano H, Jitkaew S. Tumor necroptosis is correlated with a favorable immune cell signature and programmed death-ligand 1 expression in cholangiocarcinoma. Scientific Reports. 2021 Jun 3;11(1):11743. (SJR Tier1; JCR IF = 4.997)
  5. Lomphithak T, Choksi S, Mutirangura A, Tohtong R, Tencomnao T, Usubuchi H, Unno M, Sasano H, Jitkaew S. Receptor-interacting protein kinase 1 is a key mediator in TLR3 ligand and Smac mimetic-induced cell death and suppresses TLR3 ligand-promoted invasion in cholangiocarcinoma. Cell Commun Signal. 2020 Oct 9;18(1):161. (SJR Q1; JCR IF = 5.712)
  6. Akara-Amornthum P, Lomphithak T, Choksi S, Tohtong R, Jitkaew S. Key necroptotic proteins are required for Smac mimetic-mediated sensitization of cholangiocarcinoma cells to TNF-α and chemotherapeutic gemcitabine-induced necroptosis. PLoS One. 2020 Jan 8;15(1): e0227454. (SJR Tier1; JCR IF = 3.240)
  7. Xu Q*, Jitkaew S*, Choksi S, Kadigamuwa C, Qu J, Choe M, Jang J, Liu C, Liu ZG. The cytoplasmic nuclear receptor RARγ controls RIP1 initiated cell death when cIAP activity is inhibited. Nat Commun. 2017 Sep 4;8(1):425. *These authors contributed equally to this work. (SJR Tier1; JCR IF= 12.353)
  8. Cai Z*, Jitkaew S*, Zhao J*, Chiang HC, Choksi S, Liu J, Ward Y, Wu LG, Liu ZG. Plasma membrane translocation of trimerized MLKL is required for TNF-induced necroptosis. Nat Cell Biol. 2014, 16(1):55-65. *These authors contributed equally to this work. (SJR Tier1; JCR = 20.761)
  9. Zhao J*, Jitkaew S*, Cai Z*, Choksi S, Li Q, Luo J, and Liu ZG. MLKL is a key receptor interacting protein 3 downstream component of TNF-induced necrosis. Proc Natl Acad Sci U S A. 2012, 109(14): 5322-7. * These authors contributed equally to this work. (SJR Tier1; JCR IF = 9.737)
  10. Jitkaew S, Trebinska A, Grzybowska E, Carlsson G, Nordström A, Lehtiö J, Fröjmark AS, Dahl N, Fadeel B. Nα-tosyl-L-phenylalanine chloromethyl ketone induces caspase-dependent apoptosis in transformed human B cell lines with transcriptional down-regulation of anti-apoptotic HS1-associated protein X-1. J Biol Chem 2009, 284(41): 27827-37 (SJR Q1, JCR IF = 4.651)
  11. Jitkaew S*, Witasp E*, Zhang S, Kagan VE, and Fadeel B. Induction of caspase- and reactive oxygen species-independent phosphatidylserine externalization in primary human neutrophils: role in macrophage recognition and engulfment. J Leukoc Biol 2009, 85(3): 427-37 (SJR Q1; JCR IF = 4.568) * These authors contributed equally to this work.