Mycosis fungoides and sezary syndrome: An update

Kim, Ellen J.; Lin, Julie; Junkins‐Hopkins, Jacqueline M.; Vittorio, Carmela C.; Rook, Alain H.

doi:10.1007/s11912-006-0061-1

Cited by 43 publications

(39 citation statements)

References 67 publications

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“…12 There are many therapeutic options available for the management of CTCL, including MF/SS. 7,13 The choice of treatment is often determined by physician or patient preference, or institutional experience, particularly as there is a paucity of data from phase III trials and a lack of consensus concerning treatment for later stages of MF/SS. 3,[14][15][16] However, a number of authors have published recommendations or reviews on the management of CTCL, 1,3,7,15,17 , and guidelines have been published jointly by the British Association of Dermatologists and the UK Cutaneous Lymphoma Group.…”

Section: Introductionmentioning

confidence: 99%

EORTC consensus recommendations for the treatment of mycosis fungoides/Sézary syndrome

Trautinger

Knobler

Willemze

et al. 2006

European Journal of Cancer

391

308

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Section: Introductionmentioning

confidence: 99%

EORTC consensus recommendations for the treatment of mycosis fungoides/Sézary syndrome

Trautinger

Knobler

Willemze

et al. 2006

European Journal of Cancer

391

308

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“…27 Importantly, loss of CD7 expression is a hallmark of neoplastic T cells in MF. [28][29][30] Prior work demonstrated that loss of CD7 expression by MF cells in primary patient samples correlated with resistance to galectin-1-induced death. 30 However, we found that HH, a CD7 ϩ T-cell line derived from a patient with cutaneous T-cell lymphoma, was also resistant to galectin-1-induced cell death.…”

Section: Introductionmentioning

confidence: 99%

Haploinsufficiency of C2GnT-I glycosyltransferase renders T lymphoma cells resistant to cell death

Cabrera

Amano

Mitoma

et al. 2006

Blood

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Neoplastic T cells in mycosis fungoides (MF)are resistant to apoptotic agents, including galectin-1 that is abundant in skin. Although MF cells are typically CD7 ؊ , and thus galectin-1 resistant, CD7 ؉ HH cells, derived from a patient with MF, were also resistant to galectin-1. HH cells demonstrate altered cell surface glycosylation, with loss of core 2 Oglycan ligands for galectin-1 created by core 2 ␤1,6-N-acetylglucosaminyltransferase (C2GnT-I). Loss of core 2 O-glycans on tumor cells was also seen in primary CD7 ؉ MF lesions. Surprisingly, HH cells are heterozygous for a C2GnT-I point mutation, yet this mutation resulted in a dramatic reduction in cellular glycosyltransferase activity. Expression of wild-type C2GnT-I in human HH cells, or murine lymphoma cells that lack C2GnT-I, restored core 2 O-glycan expression and susceptibility to galectin-1, whereas mutant enzyme lacked activity and did not restore core 2 O-glycan expression or susceptibility to galectin-1. Mutant enzyme did not have a dominant negative effect by affecting dimerization or activity of wild-type enzyme; rather, C2GnT-I haploinsufficiency is sufficient for loss of core 2 O-glycan expression and galectin-1 resistance. Thus, glycosyltransferase haploinsufficiency results in altered cellular glycosylation and resistance to cell death, identifying a new survival mechanism for T-lymphoma cells.

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“…11,26 Canine epitheliotropic lymphoma is a similar disease of older dogs that typically affects skin or mucus membranes and may have relatively slow (1-4 years) clinical progression. 16,20 The neoplastic cells are typically composed of CD8…”

mentioning

confidence: 99%

Perforin Expression in Feline Epitheliotropic Cutaneous Lymphoma

2008

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Abstract. Cutaneous lymphomas are uncommon in people and companion animals. The tumors can be broadly categorized into epitheliotropic and nonepitheliotropic forms, which appear to have different biological behaviors. The present case describes a feline cutaneous epitheliotropic lymphoma. Masses in a 9-year-old cat were first identified on the tail. The cat was treated with chemotherapy, but additional skin masses developed on the flank, face, and ears. Local radiation induced transient tumor regression, but eventual dissemination prompted euthanasia 13 months after initial tumor appearance. Granular lymphocytes were consistently detected on blood smears, and histologically, the tumor involved the skin and superficial subcutis. Tumor lymphocytes expressed cluster of differentiation 3 (CD3) and perforin molecules, suggestive of a cytotoxic phenotype. Location, histopathological features, and perforin expression were similar to a distinct entity in human medicine designated primary cutaneous, CD8-positive, epidermotropic, cytotoxic, T-cell lymphoma.

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Mycosis fungoides and sezary syndrome: An update

Cited by 43 publications

References 67 publications

EORTC consensus recommendations for the treatment of mycosis fungoides/Sézary syndrome

EORTC consensus recommendations for the treatment of mycosis fungoides/Sézary syndrome

Haploinsufficiency of C2GnT-I glycosyltransferase renders T lymphoma cells resistant to cell death

Perforin Expression in Feline Epitheliotropic Cutaneous Lymphoma

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