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OncoImmunology Volume 5, 2016 - Issue 7
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Review

Investigating potential exogenous tumor initiating and promoting factors for Cutaneous T-Cell Lymphomas (CTCL), a rare skin malignancy

Ivan V. LitvinovDivision of Dermatology, Ottawa Hospital Research Institute, The University of Ottawa, Ottawa, ON, Canada
,
Anna ShtreisDivision of Dermatology, Ottawa Hospital Research Institute, The University of Ottawa, Ottawa, ON, Canada;Division of Dermatology, McGill University, Montréal, QC, Canada
,
Kenneth KobayashiDivision of Dermatology, Ottawa Hospital Research Institute, The University of Ottawa, Ottawa, ON, Canada
,
Steven GlassmanDivision of Dermatology, Ottawa Hospital Research Institute, The University of Ottawa, Ottawa, ON, Canada
,
Matthew TsangDivision of Dermatology, Ottawa Hospital Research Institute, The University of Ottawa, Ottawa, ON, Canada
,
Anders WoetmannDepartment of Microbiology and Immunology, The University of Copenhagen, Copenhagen, Denmark
,
Denis SassevilleDivision of Dermatology, McGill University, Montréal, QC, Canada
,
Niels ØdumDepartment of Microbiology and Immunology, The University of Copenhagen, Copenhagen, Denmark
&
Madeleine DuvicDepartment of Dermatology, The University of Texas MD Anderson Cancer Center, Houston, TX, USACorrespondence[email protected]
 show all
Article: e1175799 | Received 22 Jan 2016, Accepted 01 Apr 2016, Published online: 29 Jun 2016

Figures & data

Figure 1. Summary of proposed potential etiologic triggers/promoters for CTCL include medications, viruses, low levels of vitamin D, Mycobacterium leprae, Chlamydia pneumonia, and Staphylococcus aureus. Recent evidence documents that S. Aureus enterotoxin type A (SEA) triggers non-malignant infiltrating T cells to release IL-2 and other cytokines that upon binging to their cognate receptors on malignant T cells are able to activate STAT3 and STAT5 oncogene signaling and promote cancer progression and IL-17 secretion.

Figure 1. Summary of proposed potential etiologic triggers/promoters for CTCL include medications, viruses, low levels of vitamin D, Mycobacterium leprae, Chlamydia pneumonia, and Staphylococcus aureus. Recent evidence documents that S. Aureus enterotoxin type A (SEA) triggers non-malignant infiltrating T cells to release IL-2 and other cytokines that upon binging to their cognate receptors on malignant T cells are able to activate STAT3 and STAT5 oncogene signaling and promote cancer progression and IL-17 secretion.

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