Dr. Nikitski is a member of the Division of Molecular Genomic Pathology.
Education & Training
PhD - Nagasaki University, Nagasaki, Japan, 2016
MD - Belarussian State Medical University, Minsk, Belarus, 2011
Research Interests
Dr. Nikitski's research is focused on thyroid cancer genetics as well as mechanisms of chromosomal rearrangements and other mutations induced by ionizing radiation in thyroid cells and other cell types.
Representative Publications
- Panebianco F, Nikitski AV, Nikiforova M, Kaya C, Yip L, Condello V, et al. Characterization of Thyroid Cancer Driven by Known and Novel ALK Fusions. Endocr Relat Cancer. 2019 Nov;26(11):803-814.
- Malik N, Nikitski AV, Klam E, Hunt J, Witt B, Chadwick B, et al. Molecular Profile and Clinical Outcomes in Differentiated Thyroid Cancer Patients Presenting with Bone Metastasis. Endocr Pract. 2019 Dec;25(12):1255-1262
- Nikitski AV, Rominski SL, Condello V, Kaya C, Wankhede M, Panebianco F, et al. Mouse Model of Thyroid Cancer Progression and Dedifferentiation Driven by STRN-ALK Expression and Loss of p53: Evidence for the Existence of Two Types of Poorly Differentiated Carcinoma. Thyroid: official journal of the American Thyroid Association. 2019;29(10):1425-37.
- Panebianco F, Nikitski AV, Nikiforova MN, Nikiforov YE. Spectrum of TERT promoter mutations and mechanisms of activation in thyroid cancer. Cancer Med. 2019;8(13):5831-9.
- Nikiforova MN, Nikitski AV, Panebianco F, Kaya C, Yip L, Williams M, et al. GLIS Rearrangement is a Genomic Hallmark of Hyalinizing Trabecular Tumor of the Thyroid Gland. Thyroid : official journal of the American Thyroid Association. 2019;29(2):161-73.
- Nikitski AV, Rominski SL, Wankhede M, Kelly LM, Panebianco F, Barila G, et al. Mouse Model of Poorly Differentiated Thyroid Carcinoma Driven by STRN-ALK Fusion. Am J Pathol. 2018;188(11):2653-61.
- Evdokimova VN, Gandhi M, Nikitski AV, Bakkenist CJ, Nikiforov YE. Nuclear myosin/actin-motored contact between homologous chromosomes is initiated by ATM kinase and homology-directed repair proteins at double-strand DNA breaks to suppress chromosome rearrangements. Oncotarget. 2018;9(17):13612-22.
- Nikitski AV, Rogounovitch TI, Bychkov A, Takahashi M, Yoshiura KI, Mitsutake N, et al. Genotype Analyses in the Japanese and Belarusian Populations Reveal Independent Effects of rs965513 and rs1867277 but Do Not Support the Role of FOXE1 Polyalanine Tract Length in Conferring Risk for Papillary Thyroid Carcinoma. Thyroid : official journal of the American Thyroid Association. 2017;27(2):224-35.
- Nikitski A, Saenko V, Shimamura M, Nakashima M, Matsuse M, Suzuki K, et al. Targeted Foxe1 Overexpression in Mouse Thyroid Causes the Development of Multinodular Goiter But Does Not Promote Carcinogenesis. Endocrinology. 2016;157(5):2182-95.
- Rogounovitch TI, Bychkov A, Takahashi M, Mitsutake N, Nakashima M, Nikitski AV, et al. The common genetic variant rs944289 on chromosome 14q13.3 associates with risk of both malignant and benign thyroid tumors in the Japanese population. Thyroid : official journal of the American Thyroid Association. 2015;25(3):333-40.
- Bychkov A, Saenko V, Nakashima M, Mitsutake N, Rogounovitch T, Nikitski A, et al. Patterns of FOXE1 expression in papillary thyroid carcinoma by immunohistochemistry. Thyroid : official journal of the American Thyroid Association. 2013;23(7):817-28.