Shioko  Kimura, Ph.D.

Shioko Kimura, Ph.D.

  • Center for Cancer Research
  • National Cancer Institute
Cancer Innovation Laboratory


Dr. Kimura’s research focuses on understanding the role of homeodomain transcription factor NKX2-1, a marker for lung adenocarcinoma in humans, and its downstream target, a novel cytokine-like immunomodulatory protein, secretoglobin (SCGB) 3A2, in development, function, homeostasis, and physiology of the thyroid and lung, and pathogenesis of diseases, including cancers of these organs. Dr. Kimura uses cell culture and mouse models with various genetically engineered mouse lines to investigate these problems.

Areas of Expertise

Genetically Engineered Mice and Mouse Models


Selected Recent Publications

Secretoglobin 3A2 eliminates human cancer cells through pyroptosis

Yokoyama S, Nakayama S, Xu L., Pilon AL, and Kimura S.
Cell Death Discovery. 7: 12, 2021. [ Journal Article ]

A novel pathway of LPS uptake through syndecan-1 leading to pyroptotic cell death

Yokoyama S, Cai Y, Murata M, Tomita T, Yoneda M, Xu L, Pilon AL, Cachau RE, Kimura S.
Elife. 7: e37854, 2018. [ Journal Article ]

An in vivo model for thyroid regeneration and folliculogenesis

Iwadate M, Takizawa Y, Shirai YT, Kimura S.
Lab Invest. 98(9): 1126-1132, 2018. [ Journal Article ]

Preclinical evaluation of human secretoglobin 3A2 in mouse models of lung development and fibrosis

Cai Y, Winn ME, Zehmer JK, Gillette WK, Lubkowski JT, Pilon AL, Kimura S.
Am J Physiol Lung Cell Mol Physiol. 306: L10-L22, 2014. [ Journal Article ]

Nkx2-1 represses a latent gastric differentiation program in lung adenocarcinoma

Snyder EL, Watanabe H, Magendantz M, Hoersch S, Chen TA, Wang DG, Crowley D, Whittaker CA, Meyerson M, Kimura S, and Jacks T.
Mol. Cell . 50: 1-15, 2013. [ Journal Article ]

Job Vacancies

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Postdoctoral Fellow (Visiting)
Henrique Dias, Ph.D.
Postdoctoral Fellow (Visiting)
Atsumi Tamura, M.D., Ph.D.
Research Fellow
Yo-Taro Shirai, Ph.D.
postbaccalaureate fellow
Victoria Alfano
Laboratory Technician/Biologist
Nabanita Kundu, Ph.D.


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Journal of Cancer - October 2016

Co-expression of Achaete-Scute Homologue-I and Calcitonin Gene-Related Peptide during NNK-Induced Pulmonary Neuroendocrine Hyperplasia and Carcinogenesis in Hamsters

Published Date

Cover:  Co-expression of Achaete-Scute Homologue-I and Calcitonin Gene-Related Peptide during NNK-Induced Pulmonary Neuroendocrine Hyperplasia and Carcinogenesis in Hamsters

Abstract:  Achaete-scute homologue-1 or ASCL1 (MASH1, hASH1) plays roles in neural development and pulmonary neuroendocrine (NE) differentiation, and it is expressed in certain lung cancers. This study was aimed to assess whether and/or how ASCL1 plays a role in 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced pulmonary NE hyperplasia and carcinogenesis in hamsters. Hamsters were injected 3 times weekly with either NNK or solvent alone (control) for treatment periods of 6 and 24 weeks, both without and with 6-week recovery. Immunohistochemical analysis was carried out to examine the expressions of ASCL1, CGRP (calcitonin gene-related peptide), secretoglobin SCGB1A1 (club [Clara] cell specific 10 kD protein, CC10, CCSP), synaptophysin (SYP), and PCNA (proliferating cell nuclear antigen). The number of ASCL1-expressing NE foci per airway increased from 0.8 in controls to 1.6 and 2.0 during NNK exposure for 6 and 24 weeks, respectively, and the number of cells per foci doubled after NNK exposure. Most ASCL1-expressing cells in NEBs (neuroepithelial bodies) were also CGRP immunoreactive; NNK enhanced this co-expression with CGRP, a NE marker with known proliferation-promoting properties. NNK also increased PCNA expression within NE foci. NNK-induced tumors showed no immunoreactivity for NE markers. This study confirms ASCL1 as an excellent marker for pulmonary NE cells and demonstrates CGRP co-expression in ASCL1-positive NEB cells participating in NNK-induced NE hyperplasia.