Emilian Racila, MD

Assistant Professor, Department of Laboratory Medicine and Pathology

Emilian Racila

Contact Info

evracila@umn.edu

Office Phone 612-273-5976

Mailing Address:
MMC 76 Mayo
8076A (Campus Delivery Code)
420 Delaware St. SE
Minneapolis, MN 55455

MD, University of Medicine and Pharmacy “Carol Davila”, Bucharest, Romania, 1982-1988

University of Iowa Hospitals and Clinics (AP/CP Pathology), 2009-2013

UT Southwestern Medical Center (Multidisciplinary NIH Training Fellowship-Immunology), 1996-1997

UT Southwestern Medical Center (Multidisciplinary NIH Training Fellowship - Surgery/Oncology), 1997-1999

Roswell Park Cancer Institute/SUNY, Buffalo NY (Surgical Pathology Fellowship/Clinical Fellowship in Oncologic Pathology), 2013-2014

Brigham and Women’s Hospital/Harvard Medical School (Thoracic Pathology), 2014-2015

Summary

Research

Research Summary/Interests

Dr. Racila is an anatomic and clinical pathologist and associate director of the residency program.  His research interests in cancer immunology, genetics and vaccine development; circulating tumor cells; genetic variants in the complement system associated with tumor response to therapy; the molecular genetics of metastatic mesothelioma; and the use of mutational signatures to differentiate primary from metastatic squamous cell carcinoma to the lung. The focus of much of his early research was in the isolation and characterization of circulating tumor cells in systemic and metastatic disease, including breast, colon, and prostate carcinomas. They devised new strategies and methodologies for isolating and characterizing circulating tumor cells from the peripheral blood of patients with these diseases. Their work formed the basis of a widely used commercial technology called CellSearch that can determine the number of circulating tumor cells in these patients.

More recently, Racila’s research focus shifted to the complement cascade and the role of mutations in complement genes to treatment response. Complement is a part of the immune system that helps or complements the ability of antibodies to kill the tumor cells, or phagocytic cells to remove pathogens from the body. The complement system, which is part of the innate immune system, consists of a number of complex proteins that circulate in the blood. Racila and his colleagues have found that single nucleotide polymorphisms in certain complement genes such as C1q are correlated with treatment response and metastasis in breast cancer and lymphoma. C1q plays a role in angiogenesis and also binds to apoptotic bodies from dying cells, including tumor cells, coating these bodies to facilitate engulfment and removal by macrophages to prevent an autoimmune response. In cancer, an autoimmune response against tumor cells is desirable, yet tumor cells employ mechanisms for suppressing the immune cell response. Racila found that lower levels of C1q are actually associated with less propensity to develop metastatic disease in breast carcinoma, possibly because more apoptotic bodies from tumor cells escape engulfment and become available for processing and antigen presentation, therefore eliciting a stronger immune response. Bettering understanding of the complement system, a more primitive ancestor of cellular and humoral immunity, can shed light on possible mechanisms for strengthening the host response to cancer.

Racila and his fellow researchers also usednext-generation DNA sequencing (NGS) technology to investigate the molecular heterogeneity of malignant mesothelioma.They looked at the overall number and type of nucleotide substitutions as well as chromosome copy number variation of various genes. They hypothesized that the mutational frequency differences observed between the epithelioid, sarcomatoid and biphasic types of malignant mesothelioma may affect tumor behavior, response to treatment and clinical outcome. Also, identification of a method to reliably differentiate between primary and metastatic squamous cell carcinoma to the lung has direct implications for the therapy and prognosis of these tumors. Currently, this differentiation cannot be done by the use of morphologic features alone. Racila and his colleagues found that these lung neoplasms can be distinguished by the specific mutational signatures they carry and an algorithm can be developed that will assist pathologists in identifying the origin of these lung tumors.

Publications

  • Vahidi S, Stewart J, Amin K, Racila E, Li F. Metastatic medullary thyroid carcinoma or calcitonin-secreting carcinoid tumor of lung? A diagnostic dilemma in a patient with lung mass and thyroid nodule. Diagnostic Cytopathology. 10 Nov 2017, DOI: 10.1002/dc 23852 http://onlinelibrary.wiley.com/doi/10.1002/dc.23852/full
  • Spratt JR, Racila E, Shumway SJ. Acute interstitial pneumonitis requiring extracorporeal membrane oxygenation and lung transplantation in an adolescent patient. J Thorac Cardiovasc Surg. 2017 Aug 24. pii: S0022-5223(17)31788-9. doi: 10.1016/j.jtcvs.2017.08.027. [Epub ahead of print] http://www.jtcvsonline.org/article/S0022-5223(17)31788-9/fulltext
  • Xia H, Gilbertsen A, Herrera J, Racila E, Smith K, Peterson M, Griffin T, Benyumov A, Yang L, Bitterman PB, Henke CA. Calcium-binding protein S100A4 confers mesenchymal progenitor cell fibrogenicity in idiopathic pulmonary fibrosis.  J Clin Invest. 2017 May 22. pii: 90832. doi: 10.1172/JCI90832. [Epub ahead of print]
  • Sontheimer RD, Racila E., Racila DM. 2005. C1q: its functions within the innate and adaptive immune responses and its role in lupus autoimmunity. J Invest Dermatol. 125(1):14-23.
  • Racila E., Racila DM, Ritchie JM, Taylor C, Dahle C, Weiner GJ. 2006. The pattern of clinical breast cancer metastasis correlates with a single nucleotide polymorphism in the C1qA component of complement. Immunogenetics.58: 1-8.
  • Siao-Yi Wang, E. Racila, RP Taylor, GJ Weiner. 2008. NK cell activation and antibody dependent cellular cytotoxicity induced by rituximab-coated target cells is inhibited by the C3b component of complement. Blood 111:1456-63.
  • Racila E., LinkBK, WengWK, WitzigTE, AnsellS, MaurerMJ, HuangJ, DahleC, HalwaniA, LevyR, and Weiner GJ. 2008. A Polymorphism in the Complement Component C1qA Correlates with Prolonged Response Following Rituximab Therapy of Follicular Lymphoma. Clin. Cancer. Res. 14(20): 6697-703.
  • Wang SY., Veeramani S., Racila E., Cagley J, Fritzinger DC., Vogel CW., St John W., Weiner GJ. 2009. Depletion of the C3 component of complement enhances the ability of rituximab-coated target cells to activate human NK cells and improves the efficacy of monoclonal antibody therapy in an in vivo model. Blood 114(26):5322-30.

Clinical

Board Certifications

Anatomic Pathology, Clinical Pathology