FDA approved treatments include the following:
(1999) Denileukin diftitox (Ontak)
(2000) Bexarotene (Targretin) a retinoid
(2006) Vorinostat (Zolinza) a hydroxymate histone deacetylase (HDAC) inhibitor
(2009) Romidepsin (Istodax) a cyclic peptide histone deacetylase (HDAC) inhibitor
(2018) Poteligeo (mogamulizumab-kpkc)Histone deacetylase (HDAC) inhibitors are shown to have antiproliferative and cytotoxic properties against CTCL.Other (off label) treatments include:

In 2010, the U.S. Food and Drug Administration granted orphan drug designation for naloxone lotion as a treatment for pruritus in cutaneous T-cell lymphoma to a pharmaceutical company called Elorac. Epidemiology
Of all cancers involving lymphocytes, 2% of cases are cutaneous T cell lymphomas. CTCL is more common in men and in African-American people. The incidence of CTCL in men is 1.6 times higher than in women.There is some evidence of a relationship with human T-lymphotropic virus (HTLV) with the adult T-cell leukemia/lymphoma subtype. No definitive link between any viral infection or environmental factor has been definitely shown with other CTCL subtypes. See also
Cutaneous B-cell lymphoma
List of cutaneous conditions

References
External links

DermNet dermal-infiltrative/cutaneous-t-cell-lymphoma
Bannayan–Riley–Ruvalcaba syndrome (BRRS) is a rare overgrowth syndrome and  hamartomatous disorder with occurrence of multiple subcutaneous lipomas, macrocephaly and hemangiomas. The disease is inherited in an autosomal dominant manner. The disease belongs to a family of hamartomatous polyposis syndromes, which also includes Peutz–Jeghers syndrome, juvenile polyposis and Cowden syndrome. Mutation of the PTEN gene underlies this syndrome, as well as Cowden syndrome, Proteus syndrome, and Proteus-like syndrome, these four syndromes are referred to as PTEN Hamartoma-Tumor Syndromes. Signs and symptoms
Bannayan–Riley–Ruvalcaba syndrome is associated with enlarged head and benign mesodermal hamartomas (multiple hemangiomas, and intestinal polyps). Dysmorphy as well as delayed neuropsychomotor development can also be present. The head enlargement does not cause widening of the ventricles or raised intracranial pressure; these individuals have a higher risk of developing tumors, as the gene involved in BRRs is phosphatase and tensin homologue.Some individuals have thyroid issues consistent with multinodular goiter, thyroid adenoma, differentiated non-medullary thyroid cancer,
most lesions are slowly growing. Visceral as well as intracranial involvement may occur in some cases, and can cause bleeding and symptomatic mechanical compression

Genetics
The genetics of the Bannayan–Riley–Ruvalcaba syndrome is determined, in the majority of cases, via the PTEN gene which presents about 30 mutations in this condition. This gene which regulates cell growth, when not working properly can lead to hamartomas. PTEN chromosomal location is 10q23.31, while the molecular location is 87,863,438 to 87,971,930  There are many syndromes that are linked to PTEN aside from Bannayan–Riley–Ruvalcaba Syndrome.The syndrome combines Bannayan–Zonana syndrome, Riley–Smith syndrome, and Ruvalcaba–Myhre–Smith syndrome.