Psychosocial distress and desire for support among inpatients with skin cancer.

BACKGROUND: Regular assessment of psychosocial distress is an important component of adequate psycho-oncological and social support in cancer patients. To date, relevant studies on skin cancer patients have primarily included individuals with melanoma. OBJECTIVES: (1) Does the need for psychosocial support vary with the type of skin cancer? (2) Do mentally distressed patients desire support? (3) From the various individuals in the treatment team, whom do patients choose as potential contact person? PATIENTS UND METHODS: Inpatients with skin cancer were asked to self-assess their psychosocial situation using the Hornheide questionnaire. In addition, they were asked about their desire for psychosocial support and the preferred potential contact person. RESULTS: The need for support among the 116 patients surveyed varied significantly depending on the diagnosis (p = 0.007). However, the direct comparison between patients with melanoma (n = 38; 32.8 %) and squamous cell carcinoma (n = 9; 7.8 %) (p = 0.724) or other types of skin cancer (n = 20; 17.2 %) (p = 0.366) revealed no such difference. The prevalence of psychosocial distress (n = 49; 42.2 %) and the desire for support (n = 20; 17.4 %) showed considerable differences. Patients primarily chose a physician (n = 14/35) or a psychologist (n = 13/35) as potential "go-to" person for their mental distress. CONCLUSIONS: Apart from psychosocial distress, the desire for support should be assessed, and patients should be provided access to additional psychosocial care options. With respect to the need for psychosocial support, it does not seem to be justified to preferentially - or even exclusively - consider melanoma patients in clinical practice and research.

Redox regulation of peptide receptivity of major histocompatibility complex class I molecules by ERp57 and tapasin.

The function of the oxidoreductase ERp57 in the major histocompatibility complex (MHC) class I peptide-loading complex has remained elusive. Here we show that in the absence of tapasin, the alpha2 disulfide bond in the MHC class I peptide-binding groove was rapidly reduced. Covalent sequestration of ERp57 by tapasin was needed to protect the alpha2 disulfide bond against reduction and thus to maintain the binding groove in a peptide-receptive state. Allelic variations in MHC class I tapasin dependency reflected their susceptibility to reduction of the alpha2 disulfide bond. In the absence of sequestration, ERp57 acted directly on the alpha2 disulfide bond. Our work provides insight into how the immune system customizes 'quality control' in the endoplasmic reticulum to fit the needs of antigen presentation.

Selective redox regulation of cytokine receptor signaling by extracellular thioredoxin-1.

The thiol-disulfide oxidoreductase thioredoxin-1 (Trx1) is known to be secreted by leukocytes and to exhibit cytokine-like properties. Extracellular effects of Trx1 require a functional active site, suggesting a redox-based mechanism of action. However, specific cell surface proteins and pathways coupling extracellular Trx1 redox activity to cellular responses have not been identified so far. Using a mechanism-based kinetic trapping technique to identify disulfide exchange interactions on the intact surface of living lymphocytes, we found that Trx1 catalytically interacts with a single principal target protein. This target protein was identified as the tumor necrosis factor receptor superfamily member 8 (TNFRSF8/CD30). We demonstrate that the redox interaction is highly specific for both Trx1 and CD30 and that the redox state of CD30 determines its ability to engage the cognate ligand and transduce signals. Furthermore, we confirm that Trx1 affects CD30-dependent changes in lymphocyte effector function. Thus, we conclude that receptor-ligand signaling interactions can be selectively regulated by an extracellular redox catalyst.