Thomas Jefferson University

South, Andrew

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Andrew P. South, PhD

Andrew P. South, PhD

Contact Dr. South

233 South Tenth Street
BLSB 406
Philadelphia, PA 19107

(215) 955-1934
(215) 503-5788 fax

Research & Clinical Interests

Squamous cell carcinomas (SCC) collectively are the most common ectodermal cancers, resulting in >300,000 deaths per year. SCCs arise from renewable squamous epithelial cells that serve to create a barrier to the external environment in the skin, esophagus, lung and cervix. An early feature of squamous neoplasia is disruption of programmed differentiation, typically associated with thickening of the epithelium and increased proliferation. My laboratory focuses primarily on cutaneous SCC (cSCC) which is the most frequent skin cancer with malignant potential and contributes to greater than 1 in 4 skin cancer deaths in Caucasian populations. Patient groups with a high propensity to develop these tumors face a significant risk of mortality. One such group is the genetic skin blistering condition recessive dystrophic epidermolysis bullosa (RDEB) which is a devastating disease caused by mutations in a single gene, COL7A1. COL7A1 encodes for a protein called type VII collagen that forms connective fibrils linking the outer layer of the skin to the underlying tissue. My laboratory has a long standing interesting in trying to understand why mutations in this single gene lead to frequent and multiple life-threatening skin cancers.


Most Recent Peer-Reviewed Publications

  1. Genetic Mutations Underlying Phenotypic Plasticity in Basosquamous Carcinoma
  2. Thrombospondin-1 Is a Major Activator of TGF-β Signaling in Recessive Dystrophic Epidermolysis Bullosa Fibroblasts
  3. Identification of rigosertib for the treatment of recessive dystrophic epidermolysis bullosa–associated squamous cell carcinoma
  4. Dachshund Depletion Disrupts Mammary Gland Development and Diverts the Composition of the Mammary Gland Progenitor Pool
  5. Assessment of quality and consistency of monoclonal antibodies for CB1 and CB2 in head and neck squamous cell carcinoma
  6. Retraction: Gentamicin B1 is a minor gentamicin component with major nonsense mutation suppression activity (Proceedings of the National Academy of Sciences of the United States of America (2017) 114 (3479–3484) DOI: 10.1073/pnas.1620982114)
  7. Precision Medicine for Heritable Skin Diseases—The Paradigm of Epidermolysis Bullosa
  8. The genomic landscape of cutaneous SCC reveals drivers and a novel azathioprine associated mutational signature
  9. Reduced Microbial Diversity Is a Feature of Recessive Dystrophic Epidermolysis Bullosa-Involved Skin and Wounds
  10. Metformin clinical trial in HPV+ and HPV-head and neck squamous cell carcinoma: Impact on cancer cell apoptosis and immune infiltrate
  11. APOBEC mutation drives early-onset squamous cell carcinomas in recessive dystrophic epidermolysis bullosa
  12. The role of human papillomaviruses and polyomaviruses in BRAF-inhibitor induced cutaneous squamous cell carcinoma and benign squamoproliferative lesions
  13. First report of COL7A1 mutations in two patients with recessive dystrophic epidermolysis bullosa from Peru
  14. Seven novel COL7A1 mutations identified in patients with recessive dystrophic epidermolysis bullosa from Mexico
  15. Differential glucose requirement in skin homeostasis and injury identifies a therapeutic target for psoriasis article
  16. Extracellular Vesicles as Biomarkers for the Detection of a Tumor Marker Gene in Epidermolysis Bullosa-Associated Squamous Cell Carcinoma
  17. Preclinical comparison of proteasome and ubiquitin E1 enzyme inhibitors in cutaneous squamous cell carcinoma: The identification of mechanisms of differential sensitivity
  18. High concordance between clinical diagnosis of epidermolysis bullosa and immunofluorescence with a small, well-matched antibody panel
  19. Pro-Inflammatory Chemokines and Cytokines Dominate the Blister Fluid Molecular Signature in Patients with Epidermolysis Bullosa and Affect Leukocyte and Stem Cell Migration
  20. Amlexanox Enhances Premature Termination Codon Read-Through in COL7A1 and Expression of Full Length Type VII Collagen: Potential Therapy for Recessive Dystrophic Epidermolysis Bullosa