Sun protection and sunbathing practices among at-risk family members of patients with melanoma

<p>Abstract</p> <p>Background</p> <p>Despite the increased level of familial risk, research indicates that family members of patients with melanoma engage in relatively low levels of sun protection and high levels of sun exposure. The goal of this study was to evaluate a broad range of demographic, medical, psychological, knowledge, and social influence correlates of sun protection and sunbathing practices among first-degree relatives (FDRs) of melanoma patients and to determine if correlates of sun protection and sunbathing were unique.</p> <p>Methods</p> <p>We evaluated correlates of sun protection and sunbathing among FDRs of melanoma patients who were at increased disease risk due to low compliance with sun protection and skin surveillance behaviors. Participants (<it>N </it>= 545) completed a phone survey.</p> <p>Results</p> <p>FDRs who reported higher sun protection had a higher education level, lower benefits of sunbathing, greater sunscreen self-efficacy, greater concerns about photo-aging and greater sun protection norms. FDRs who reported higher sunbathing were younger, more likely to be female, endorsed fewer sunscreen barriers, perceived more benefits of sunbathing, had lower image norms for tanness, and endorsed higher sunbathing norms.</p> <p>Conclusion</p> <p>Interventions for family members at risk for melanoma might benefit from improving sun protection self-efficacy, reducing perceived sunbathing benefits, and targeting normative influences to sunbathe.</p

A New Nail in the CTCL Coffin

The impact of immunotherapy on the natural progression of cutaneous T-cell lymphoma (CTCL), particularly the mycosis fungoides and Sézary syndrome variants, has been based on our evolving understanding of the disease's immunobiology

Granuloma annulare with a mycosis fungoides-like distribution and palisaded granulomas of CD68-positive histiocytes.

We describe 3 unusual cases of granuloma annulare with multiple macular lesions in a distribution that simulated mycosis fungoides in patients with no associated underlying diseases. Repeated biopsies showed typical well-formed palisading granulomas and no evidence of an atypical lymphocytic infiltrate. There was no vasculitis, neutrophilic, eosinophilic, or interstitial infiltrate. The patients had no associated underlying diseases. Most of the histiocytes in the palisading granulomas were strongly positive for CD68. The lymphocytes were a minor component of the granulomatous inflammation and were predominantly CD8(+) T-cells. The findings in these cases add to the spectrum of previously defined granulomatous eruptions of the skin

Molecular Diagnosis of Cutaneous T-Cell Lymphoma: Polymerase Chain Reaction Amplification of T-Cell Antigen Receptor β-Chain Gene Rearrangements

The goal of our study was to molecularly diagnose CTCL, by cloning the T-cell antigen receptor beta chain (TCR-β) gene rearrangement from the malignant T cells of a patient with Sézary syndrome, in order to generate a specific oligonucleotide probe capable of detecting CTCL cells through polymerase chain reaction (PCR) amplification. Total RNA isolated from peripheral blood lymphocytes was reverse transcribed and resultant first strand cDNA was PCR amplified utilizing a concensus primer to the TCR-β variable region (Vβ) and a 3' primer to the TCR-β constant region (Cβ). PCR reaction products were subcloned into a plasmid vector and sequenced. Sequence analysis revealed that the patient's in-frame TCR-β gene rearrangement utilized Vβ6.4, Dβ1.1, Jβ2.2, and Cβ2.1 gene segments. Oligo-primers to Vβ6.4 and Jβ2.2 were utilized to PCR amplify genomic DNA taken from the patient's blood and involved skin. Screening the amplified DNA with an oligoprobe specific for the patient's V-D-J junctional sequences resulted in the detection of the patient- specific sequences. No sequences were detected from DNA from other malignant or benign infiltrates. Thus, we have defined a “molecular fingerprint” specific for a patient's malignant T-cells and can molecularly diagnose CTCL through PCR amplification