Cancer Institute A national cancer institute
designated cancer center
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Russell K Pachynski, MD

Academic Appointments

Key Documents

Contact Information

  • Clinical Offices
    Medical Oncology 875 Blake Wilbur Dr Clinic E MC 5820 Stanford, CA 94305
    Tel Work (650) 498-6000 Fax (650) 725-9113
  • Academic Offices
    Personal Information
    Not for medical emergencies or patient use

Professional Overview

Clinical Focus

  • Cancer> Urologic Oncology
  • Genitourinary Cancer
  • Immunotherapy
  • Prostate Cancer
  • Medical Oncology

Honors and Awards

  • Pilot Award, Stanford Translational Medicine Program (TRAM) (2012)
  • Fellowship Award, California Breast Cancer Research Program (2009-2010)
  • ASCO Young Investigator Award, American Society of Clinical Oncology (2009)
  • ASCO/AACR Workshop: Methods in Clinical Cancer Research, American Society of Clinical Oncology (2009)
  • NCCN Fellows Recognition Program, National Comprehensive Cancer Network (2007)
  • American Medical Association Seed Grant Award, American Medical Association (2002)
View All 9honors and awards of Russell Pachynski

Professional Education

Fellowship: Stanford University - CAPS CA (2009)
Residency: Stanford University - CAPS CA (2005)
Medical Education: Univ Of Ws Sch Of Med-Madison WI (2003)
Board Certification: Internal Medicine, American Board of Internal Medicine (2007)

Scientific Focus

Current Research and Scholarly Interests

Infiltration of specialized immune cells regulates the growth and survival of neoplasia. In a survey of leukocyte chemoattractant expression in public whole genome expression datasets, we found that the gene for chemerin is downregulated during tumorigenesis in animal models and in many human cancers. Low or absent chemerin expression predicted inferior outcomes in melanoma, and tumor-expressed chemerin inhibited in vivo growth of mouse melanoma and breast adenocarcinoma models. Growth inhibition was associated with an altered host response, and was abrogated by NK cell depletion. Intratumoral injection of chemerin also inhibited tumors, suggesting the potential for therapeutic application. We conclude that chemerin is an endogenous tumor suppressive chemoattractant cytokine whose downregulation in neoplasia contributes to immune evasion and tumor growth.


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Publication Topics

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