Andrew P. South, PhD

Associate Professor

Andrew P. South, PhD

Contact

233 South Tenth Street
BLSB 406
Philadelphia, PA 19107

Andrew.South@jefferson.edu

215-955-1934
215-503-5788 fax

Andrew P. South, PhD

Associate Professor

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, COL7A1COL7A1 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.

Publications

Most Recent Peer-Reviewed Publications

 

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