Mariano Viapiano profile picture
315 464-7967

Mariano Viapiano, PhD

4707 Institute For Human Performance (IHP)
505 Irving Avenue
Syracuse, NY 13210
Mariano Viapiano's email address generated as an image


Associate Professor of Neuroscience and Physiology
Associate Professor of Cell and Developmental Biology
Associate Professor of Neurosurgery




Biomedical Sciences Program
Neuroscience and Physiology
Neuroscience Program


Brain cancer therapies; tumor microenvironment; tumor invasion; extracellular matrix; nano-therapeutics; immunotherapies


Cancer biology; cancer immunology; malignancies of the central nervous system


American Association for Cancer Research (AACR)
American Society for Matrix Biology
International Society of Neuroimmunology
Society for Neuro-Oncology


Additional Training: Yale University School of Medicine, 2006, Neurobiology
Additional Training: University of Sao Paulo School of Medicine, Sao Paulo, Brazil, 2001, Neuropharmacology
PhD: University of Buenos Aires, Argentina, 1998, Neuroscience
BS: University of Buenos Aires, Argentina, 1993, Molecular Biology


Brigham and Women's Hospital, 2012-2016
Harvard Medical School, 2012-2016
Ohio State University College of Medicine, 2006-2012
Yale University School of Medicine, 2001-2006



Brain Tumor Laboratory and Biorepository at SUNY Upstate

Our laboratory studies primary malignant brain cancers known as gliomas, which are highly aggressive tumors that respond poorly to conventional therapies. We analyze and target the interactions of glioma cells with other components of the tumor microenvironment, in particular neural and immune cells that can contribute to tumor growth.

The major research focus of our lab is the extracellular matrix (ECM) that forms the scaffold of neural tissue and the changes caused in this matrix by glioma cells. We investigate how ECM remodeling facilitates tumor invasion, modifies the behavior of neural cells, and even prevents the normal responses of immune cells against the tumor. Our lab currently pursues two major lines of investigation:

- Regulation of immune responses in glioma by the tumor ECM: We are investigating how gliomas change the composition of ECM molecules and how different ECM components regulate the behavior of immune cells in the tumor. In this project we are also developing novel anti-ECM reagents (including novel antibodies and engineered immune cells) to target the tumor matrix and prevent tumor invasion and growth.

- Targeting the glioma-brain communication: In this project we investigate how glioma cells respond to neural signals and release molecules that co-opt neurons and glial cells to support tumor growth. Major research in this project is focused on: 1) targeting scaffolding/polarity proteins that are needed by glioma cells to respond to pro-tumor signals from the brain; and 2) studying ECM and neuro-endocrine factors produced by "hijacked" neural cells that support the tumor cells.

Research in our Lab involves a variety of disciplines and laboratory skills, including molecular biology and genetics, bioinformatics, protein biochemistry, tumor stem cell culture, tumor organoids, and animal models of malignant glioma. In addition, we house the brain tumor bank of SUNY Upstate Medical University, with an extensive collection of tumor specimens, tumor cells, and patient blood, available for basic and translational research projects.The ultimate goal of our research is to advance novel therapeutic strategies that will improve the survival of patients with malignant brain tumors.

Intracranial gliomas

Figure 1: Intracranial gliomas treated with a control antibody or a novel monoclonal antibody ("mAb428.2") against the glioma-enriched ECM protein fibulin-3. Treatment with mAb428.2 increases the infiltration of inflammatory macrophages (IBA-1+ cells) into the tumor core and reduces tumor progression (from Nandhu et al., Clin. Cancer Res., 2018)

Spheroids from glioma stem cells

Figure 2: A) Spheroids from glioma stem cells carrying shRNA against the scaffolding protein DLG5 are grow smaller than those of control tumor cells because they cannot respond to Shh signals. B) When control and DLG5-knockdown glioma cells are introduced into new tumor spheroids the glioma cells deficient in DLG5 have less competitive fitness and eventually die out (from Kundu et al., Neuro-Oncology, 2022)


Recent Articles:

  • Yokoda RT, Cobb WS, Yong RL, Crary JF, Viapiano MS, Walker JM, et al. CDKN2A mutations have equivalent prognostic significance to homozygous deletion in IDH-mutant astrocytoma. J Neuropathol Exp Neurol. (2023) PMID: 37550258
  • Pramio DT, Vieceli FM, Varella-Branco E, Goes CP, Kobayashi GS, Pelegrina DV, et al. DNA methylation of the promoter region at the CREB1 binding site is a mechanism for the epigenetic regulation of brain specific PKMzeta. Biochemica et Biophysica Acta - Gene Regulatory Mechanisms (2023) PMID: 36682583
  • Moncao CC, Scrideli CA, Andrade AF, Viapiano MS, Carlotti CG, et al. Indisulam reduces viability and regulates apoptotic gene expression in pediatric high-grade glioma cells. Biomedicines (2022) PMID: 36672576
  • Roshini A, Goparaju C, Kundu S, Nandhu MS, Longo SL, Longo JA, Chou J, et al. The extracellular matrix protein fibulin-3/EFEMP1 promotes pleural mesothelioma growth by activation of PI3K/Akt signaling. Front. Oncol. (2022) PMID: 36303838
  • Richardson TE, Walker JM, Abdullah KG, McBrayer SK, Viapiano MS, Mussa ZS, et al. Chromosomal instability in adult-type diffuse gliomas. Acta Neuropathol. Commun. (2022) PMID: 35978439
  • Teixeira SA, Burim RV, Viapiano MS, Bidinotto LT, Nagashi Marie SK, Fleury Malheiros SM, Oba-Shinjo SM, Andrade AF and Carlotti CG. Alpha2beta1 integrin polymorphism in diffuse astrocytoma patients. Front. Oncol. (2022) PMID: 35936750
  • Liu Y, Sathe AA, Abdullah KG, McBrayer SK, Adams SH, Brenner AJ, et al. Global DNA methylation profiling reveals chromosomal instability in IDH-mutant astrocytomas. Acta Neuropathol. Commun. (2022) PMID: 35264242
  • Kundu S, Nandhu MS, Longo SL, Longo JA, Rai S, Chin LS, et al. The scaffolding protein DLG5 promotes glioblastoma growth by controlling Sonic Hedgehog signaling in tumor stem cells. Neuro-Oncology (2022) PMID: 34984467
  • Lustig SD, Kodali SK, Longo SL, Kundu S, Viapiano MS. Ko143 reverses MDR in glioblastoma via deactivating P-Glycoprotein, sensitizing a resistant phenotype to TMZ treatment. Anticancer Res. (2022) PMID: 35093870
  • Lyon JF, Vasudevaraja F, Mirchia K, Walker JM, Corona RJ, Chin LS, et al. Spatial progression and molecular heterogeneity of IDH-Mutant glioblastoma determined by DNA methylation-based mapping. Acta Neuropathol. Commun. (2021) PMID: 34193272
  • Teixeira SA, Viapiano MS, Andrade AF, Nandhu MS, Pezuk JA, Bidinotto LT, et al. The carbonic anhydrase inhibitor E7070 sensitizes glioblastoma cells to radio and chemotherapy and reduces tumor growth. Mol. Neurobiol. (2021) PMID: 34085182
  • Richardson TE, Sathe AA, Xing C, Mirchia K, Viapiano MS, Snuderl M, et al. Molecular signatures of chromosomal instability correlate with copy number variation patterns and patient outcome in IDH-mutant and IDH-wildtype astrocytomas. J. Neuropathol. Exp. Neurol. (2021) PMID: 33755138
  • von Spreckelsen N, Fadzen CM, Hartrampf N, Ghotmi Y, Wolfe JM, Dubey S, et al. Targeting glioblastoma using a novel peptide specific to a deglycosylated isoform of brevican. Adv. Ther. (Weinh) (2021) PMID: 33997269
  • Galbraith K, Kumar A, Abdullah KG, Walker JM, Adams SH, Prior T, et al. Molecular Correlates of Long Survival in IDH-Wildtype Glioblastoma Cohorts. J. Neuropathol. Exp. Neurol. (2020) PMID: 32647886


Link to PubMed (Opens new window. Close the PubMed window to return to this page.)