Clusters, crop dusters, and myth busters: a scoping review of environmental exposures and cutaneous T-cell lymphoma

Vitamin D in Cutaneous T-Cell Lymphoma

“…The etiology of CTCL is largely unknown, and the pathogenesis is far from understood, but both genetic, epigenetic, and environmental factors are believed to be involved [ 91 , 92 , 93 , 94 , 95 , 96 ]. Disease heterogeneity is a characteristic feature of CTCL [ 93 , 97 , 98 , 99 , 100 , 101 ] even at the single-cell level [ 100 , 102 , 103 , 104 , 105 ], which has hampered the unraveling of the etiology and pathogenesis and has been a complicating factor in the development of novel therapies.…”

“…For decades, vitamin D has been suspected to play a role in the pathogenesis of CTCL [ 94 ]. Concerning the vitamin D nomenclature, it is known that it is the active form of vitamin D, 1,25(OH) 2 D, that exerts the biological effects of vitamin D. However, in the literature, the term vitamin D is generally used without discrimination between the various forms of vitamin D. We will follow the same nomenclature for vitamin D in this review if not otherwise stated.…”

“…As IL-22 is a survival factor in malignant T cells and is believed to play a role in the pathogenesis through changes in the TME [ 153 ], these findings suggest a potential anticancer effect of vitamin D both directly through the inhibition of survival signals in malignant T cells and indirectly through the modulation of the TME ( Figure 2 , left side). Mrotzek et al [ 150 ] examined the effect of vitamin D on the proliferation of an MF cell line treated with bexarotene routinely used in the treatment of CTCL patients [ 94 ] and found that vitamin D inhibited the proliferation of bexarotene-treated cells showing synergistic anticancer effects of vitamin D and bexarotene. In addition, vitamin D inhibits integrin-mediated adhesion by malignant T-cell lines and interactions with other cells in the TME [ 154 ], which are believed to promote the proliferation of malignant T cells [ 155 ].…”