Philadelphia University + 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. High concordance between clinical diagnosis of epidermolysis bullosa and immunofluorescence with a small, well-matched antibody panel
  2. First report of COL7A1 mutations in two patients with recessive dystrophic epidermolysis bullosa from Peru
  3. Pro-Inflammatory Chemokines and Cytokines Dominate the Blister Fluid Molecular Signature in Patients with Epidermolysis Bullosa and Affect Leukocyte and Stem Cell Migration
  4. Amlexanox Enhances Premature Termination Codon Read-Through in COL7A1 and Expression of Full Length Type VII Collagen: Potential Therapy for Recessive Dystrophic Epidermolysis Bullosa
  5. Desmoglein 2 modulates extracellular vesicle release from squamous cell carcinoma keratinocytes
  6. Gentamicin B1 is a minor gentamicin component with major nonsense mutation suppression activity
  7. Targeted next-generation sequencing of TP53 in oral tongue carcinoma from non-smokers
  8. Cardiomyopathy diagnosed in the eldest child harbouring p.S24X mutation in JUP
  9. MEK Is a Therapeutic and Chemopreventative Target in Squamous Cell Carcinoma
  10. Inactivation of TGFβ receptors in stem cells drives cutaneous squamous cell carcinoma
  11. CREBBP mutation in human cutaneous squamous cell carcinoma
  12. Type VII Collagen Replacement Therapy in Recessive Dystrophic Epidermolysis Bullosa—How Much, How Often?
  13. Exosome-mediated transfer from the tumor microenvironment increases TGFβ signaling in squamous cell carcinoma
  14. Lysyl hydroxylase 3 localizes to epidermal basement membrane and is reduced in patients with recessive dystrophic epidermolysis bullosa
  15. Novel CARD11 Mutations in Human Cutaneous Squamous Cell Carcinoma Lead to Aberrant NF-κB Regulation
  16. Next-Generation Sequencing for Mutation Detection in Heritable Skin Diseases: The Paradigm of Pseudoxanthoma Elasticum
  17. Innate sensing of microbial products promotes wound-induced skin cancer
  18. Progress toward Treatment and Cure of Epidermolysis Bullosa: Summary of the DEBRA International Research Symposium EB2015
  19. Tissue engineering of tumor stromal microenvironment with application to cancer cell invasion
  20. BPAG1-e restricts keratinocyte migration through control of adhesion stability