A photo of Tanya V. Kalin.

Tanya V. Kalin, MD, PhD

  • Professor, UC Department of Pediatrics



My lab is interested in understanding the molecular and cellular mechanisms of lung injury, inflammation, repair and pulmonary fibrosis. Using normal cells, clinical tissue samples and animal models of lung diseases, we investigate the signaling networks that regulate functions of epithelial and stromal cells in the lung.

Our research areas include:

  • Endothelial cell and pericyte biology during lung injury and regeneration. This includes blood vessel maturation and stabilization and targeting pulmonary vasculature for drug delivery.
  • Tumor microenvironment in cancer progression and metastasis. We’re studying normalization of tumor-associated vessels to enhance anti-cancer therapy, and the combination of proton radiation treatment with immune-checkpoint inhibitors in anti-cancer therapy.
  • Development of novel cell-based and nanoparticle-based therapies for treatment of chronic interstitial lung diseases.
  • Efficacy of proton radiation treatment in lung diseases and prevention of radiation-induced injury of normal lung tissue.

The primary focus of my laboratory is to understand the critical regulatory interactions responsible for the cross-talk between lung epithelial and stromal cells. My lab generated multiple transgenic and knockout mouse models to study several transcription factors and their roles in different cell populations, including lung epithelial cells, macrophages, fibroblasts, pericytes and endothelial cells. We identified multiple signaling pathways involved in these cellular interactions as well as several transcription factors regulating these signaling pathways.

Our laboratory is actively involved in developing new therapeutic approaches to target different cell types in the lung interstitial microenvironment. In addition, we have developed several biomarkers to predict tumor responses to chemotherapy and assess lung toxicity and fibrotic responses after thoracic irradiation. Our long-term goal is to develop new therapies to treat chronic fibrosing lung diseases and metastatic lung cancers.

Our work has been published by multiple journals and recognized by the scientific and medical community. Some of our groundbreaking discoveries include:

  • Identifying the role of pulmonary epithelium in lung fibrosis and lung inflammation. For over a decade, my laboratory has been focused on transcriptional mechanisms driving lung inflammation and fibrosis. Using novel transgenic mouse models generated in my laboratory, we uncovered essential roles for transcription factors of Forkhead Box (Fox) family in lung regeneration, cellular proliferation, epithelial-to-mesenchymal transition and recruitment of inflammatory cells to the lung tissue. We were first to show the pro-fibrotic role of FOXM1 transcription factor during radiation-induced and bleomycin-mediated pulmonary fibrosis and to identify FOXM1- and FOXF1-regulated enhancers in promoter regions of several pro-inflammatory genes. Our long-term goal is to develop new therapeutic agents targeting transcription factors involved in lung fibrogenesis.
  • Uncovering epithelial-stromal interactions in lung cancer and chronic lung diseases. We’ve made seminal contributions in uncovering a cross-talk between pulmonary epithelial cells and their microenvironment, including inflammatory cells, fibroblasts and endothelium during lung morphogenesis and lung injury/repair. We found that this cross-talk is regulated by multiple transcription factors — including SPDEF, FOXM1, FOXF1, FOXF2 and SNAIL — that induce transcription of genes critical for cellular proliferation, migration and survival. We are interested in understanding how disruption of these regulatory cascades contributes to the pathogenesis of congenital and acquired pulmonary diseases.
  • Discovering novel regulators that drive re-programming of quiescent lung endothelial cells into tumor-associated endothelial cells. Cancer cells re-program normal lung endothelial cells (EC) into tumor-associated endothelial cells (TEC) that form leaky vessels supporting carcinogenesis. We recently identified Forkhead box F1 (FOXF1) transcription factor as a critical regulator of EC-to-TEC transition. FOXF1 is highly expressed in normal lung vasculature but is decreased in TEC within human and mouse non-small cell lung cancers. Using transgenic mice with endothelial-specific deletion or over-expression of FOXF1, we found that FOXF1 induces pericyte coverage, decreases vessel permeability and inhibits lung tumor growth and metastasis. FOXF1 promotes tumor vessel stability and inhibits lung cancer progression by stimulating FZD1/ Wnt/β-catenin signaling in endothelial cells.
  • Discovering molecular mechanisms of fibroblast activation during fibrotic lung remodeling. Idiopathic pulmonary fibrosis (IPF) is characterized by aberrant accumulation of collagen-secreting myofibroblasts. Development of effective IPF therapies is limited due to incomplete understanding of molecular mechanisms regulating myofibroblast expansion. Utilizing comprehensive analysis of human IPF genomics data, lung biopsies and transgenic mice, we recently identified multiple transcriptional regulators of lung remodeling and fibrogenesis. For example, we demonstrated that FOXF1 transcription factor inhibits pulmonary fibrosis, decreases myofibroblast invasion and collagen secretion, and prevents a switch from N-cadherin (CDH2) to Cadherin-11 (CDH11), which is a critical step in acquisition of pro-fibrotic phenotype. Our studies showed that stimulation of FOXF1 signaling can be beneficial for treatment of lung fibrosis.
  • Discovering novel non-nuclear function of transcription factors. We are interested in subcellular localization of nuclear transcription factors (TF) and their non-nuclear role. For example, we demonstrated that nuclear TF FOXM1 can localize to mitochondria, where it regulates mitochondrial mass, membrane potential, respiration and electron transport chain (ETC) activity. In mitochondria, this TF directly binds to and increases the pentatricopeptide repeat domain 1 (PTCD1) protein, a mitochondrial leucine-specific tRNA binding protein that inhibits leucine-rich ETC complexes. While we identified a new paradigm (that nuclear transcription factor regulated mitochondrial homeostasis in a process independent of nuclear transcription), the importance of this phenomenon is unknown for the disease states.

I am honored to have received many awards and appointments for my work, including:

  • American Cancer Society Institutional Research Award from the University of Cincinnati (2007)
  • Scholar award from Ohio Cancer Research Associates (2008)
  • Research Scholar Award from the American Cancer Society (Ohio Division) (2008)
  • Conquer Cancer Now Award from the Concern Foundation (2008)
  • Department of Defense (DoD) New Investigator Award (2009)
  • Early Career Woman Faculty Professional Development Award from the Association of American Medical Colleges (AAMC) (2010)
  • New Investigator Award from the National Cancer Institute (2010)
  • Research Scholar Award from the American Cancer Society (National) (2013)
  • Review panel member, DoD Peer Reviewed Cancer Research Program (PRCRP) (2013)
  • National Institutes of Health National Cancer Institute (NIH/NCI) tumor-microenvironment (TME) study section (2014)
  • Mentoring Achievement Award from Cincinnati Children’s (2014)
  • Review panel member, Lung Cancer Research Program (LCRP) for the Department of Defense Congressionally Directed Medical Research Programs (CDMRP) Panel (2014 to present)
  • Research Award from the National American Cancer Society (2015)
  • National Cancer Institute, Special Emphasis Panel study section (2015)
  • Cambridge Foundation Award for lung cancer research (2016)
  • Standing member, NIH/NCI study section member, Transition to Independence – Subcommittee I
  • Cincinnati Children’s Innovation Award for identification of anti-cancer small molecule compound RCM-1 (2018)



Loss of FOXM1 in macrophages promotes pulmonary fibrosis by activating p38 MAPK signaling pathway. Goda, C; Balli, D; Black, M; Milewski, D; Le, T; Ustiyan, V; Ren, X; Kalinichenko, VV; Kalin, TV. PLoS Genetics. 2020; 16.


The FOXM1 Inhibitor RCM-1 Decreases Carcinogenesis and Nuclear β-Catenin. Shukla, S; Milewski, D; Pradhan, A; Rama, N; Rice, K; Le, T; Flick, MJ; Vaz, S; Zhao, X; Setchell, KD; et al. Molecular Cancer Therapeutics. 2019; 18:1217-1229.


FOXF1 Inhibits Pulmonary Fibrosis by Preventing CDH2-CDH11 Cadherin Switch in Myofibroblasts. Black, M; Milewski, D; Le, T; Ren, X; Xu, Y; Kalinichenko, VV; Kalin, TV. Cell Reports. 2018; 23:442-458.


FOXM1 activates AGR2 and causes progression of lung adenomas into invasive mucinous adenocarcinomas. Milewski, D; Balli, D; Ustiyan, V; Le, T; Dienemann, H; Warth, A; Breuhahn, K; Whitsett, JA; Kalinichenko, VV; Kalin, TV. PLoS Genetics. 2017; 13.


FoxF1 and FoxF2 transcription factors synergistically promote rhabdomyosarcoma carcinogenesis by repressing transcription of p21Cip1 CDK inhibitor. Milewski, D; Pradhan, A; Wang, X; Cai, Y; Le, T; Turpin, B; Kalinichenko, VV; Kalin, TV. Oncogene. 2017; 36:850-862.


SPDEF inhibits prostate carcinogenesis by disrupting a positive feedback loop in regulation of the Foxm1 oncogene. Cheng, X; Black, M; Ustiyan, V; Le, T; Fulford, L; Sridharan, A; Medvedovic, M; Kalinichenko, VV; Whitsett, JA; Kalin, TV. PLoS Genetics. 2014; 10.


Foxm1 expression in prostate epithelial cells is essential for prostate carcinogenesis. Cai, Y; Balli, D; Ustiyan, V; Fulford, L; Hiller, A; Misetic, V; Zhang, Y; Paluch, AM; Waltz, SE; Kasper, S; et al. Journal of Biological Chemistry. 2013; 288:22527-22541.


Foxm1 transcription factor is required for lung fibrosis and epithelial-to-mesenchymal transition. Balli, D; Ustiyan, V; Zhang, Y; Wang, I; Masino, AJ; Ren, X; Whitsett, JA; Kalinichenko, VV; Kalin, TV. EMBO Journal. 2013; 32:231-244.


Foxm1 transcription factor is required for macrophage migration during lung inflammation and tumor formation. Balli, D; Ren, X; Chou, F; Cross, E; Zhang, Y; Kalinichenko, VV; Kalin, TV. Oncogene. 2012; 31:3875-3888.


Endothelial cell-specific deletion of transcription factor FoxM1 increases urethane-induced lung carcinogenesis. Balli, D; Zhang, Y; Snyder, J; Kalinichenko, VV; Kalin, TV. Cancer Research. 2011; 71:40-50.