Psychosocial implications of living 5 years or more following a cancer diagnosis: a systematic review of the research evidence.

Mortality associated with cancer remains high, but more people are surviving cancer. Some people experience long-term problems associated with cancer and its treatment, and there is a need to know how to support them. This systematic literature review explores primary research for psychosocial implications of long-term survival (>or=5 years) following a cancer diagnosis and interventions designed to address psychosocial problems in the long term. A systematic search of BIDS, BNI, Cancer.gov, CINAHL, Medline, PsychINFO and Web of Science was conducted to identify research publications from 1960 to 2006. Papers were selected on the basis of pre-defined criteria and rated by three independent coders. Forty-three studies met the eligibility criteria. These indicated that most people experience few problems five or more years after their diagnosis of cancer. However, 20-30% of survivors consistently reported problems associated with cancer and its treatment including physical problems, poorer quality of life, psychological distress, sexual problems, problems with social relationships and financial concerns. Not all cancer types are represented in this review. Only two intervention studies met the eligibility criteria. Research is needed to establish appropriate interventions to support those experiencing problems in the long term to enhance well-being.

Patterns of complementary and alternative medicine use among patients undergoing cancer treatment.

This study aimed to assess the prevalence of complementary and alternative medicine (CAM) use in a representative cancer population prior to and within 6 months of diagnosis. A total of 304 newly diagnosed cancer patients from two UK cancer centres completed a postal survey. Of them, 100 patients (32.9%) used CAM before their cancer diagnosis, 59 of these CAM users continued post diagnosis. Twenty-nine individuals who had not used CAM before began to use it after their cancer diagnosis, creating a total of 88 (28.9%) CAM users in this sample. Reasons for not using CAM included lack of interest, lack of information or endorsement from professionals and satisfaction with conventional care. For those using CAM before diagnosis but not afterwards, the most common reason was a lack of expert guidance on what was safe to use. The use of CAM medicines bought from health food and other retail outlets was high. Complementary and alternative medicine use in cancer patients is common and demonstrates a complex pattern, but CAM use is not significantly greater than in the general population. Some patients purchase CAM medicines without seeking medical advice, thus risking drug interactions. Research to generate information on safety and efficacy of CAM is required.

Virus infection induces redistribution and membrane localization of the nuclear antigen La (SS-B): a possible mechanism for autoimmunity.

To investigate the possibility that anti-La (SS-B) antibodies in Sjögren's syndrome were induced by virus infection we studied the distribution of La in virus-infected human cell lines. Three monoclonal antibodies to La were used with monoclonal anti-Sm (derived from MRL/lpr lupus mice) and anti-rat immunoglobulin antibodies as controls. In uninfected cells La was predominantly in the nucleus. Twenty-four hours after infection of HEp-2 cells with adenovirus 2, the La and Sm antigens appeared to aggregate and accumulate in the periphery of the nucleus and, after 48 h, La was seen in the cytoplasm and cell membrane. No cytoplasmic or membrane expression of Sm was seen. Infection with adenovirus or cytomegalovirus caused a 2-13-fold increase in the concentration of La in three cell lines. Treatment of HE--2 cells with interferon-gamma (IFN-gamma) and infection with Epstein-Barr virus and cytomegalovirus caused cytoplasmic, but no definite membrane expression of La. The appearance of La on the surface of virally infected epithelial cells together with IFN-gamma induced class II expression could form the basis of a T cell dependent mechanism for anti-La autoantibody induction.

Titers of antibodies to RANA in rheumatoid arthritis and normal sera. Relationship to Epstein-Barr virus infection.

The disease specificity of antibodies to rheumatoid arthritis nuclear antigen (RANA) was examined by comparing anti-RANA titers in sera from 100 patients with rheumatoid arthritis (RA) with sera from 93 healthy controls. Anti-RANA antibodies were found in 86% of the RA sera and 56% of the controls. The higher titers in the RA sera were unrelated to clinical features or to measurements of circulating immune complexes or rheumatoid factors. To study the relationship of these antibodies to previous Epstein-Barr virus (EBV) infection, antibodies to the EB virus capsid antigen (VCA) were examined and found in 94% of the RA sera and 97% of the adult controls. Four of the six RA sera without anti-VCA antibodies had detectable anti-RANA antibodies, so that we might suggest anti-RANA can arise in the absence of EBV infection. From absorption experiments with non-EBV transformed extracts, we inferred that high anti-RANA titers could be due to reactions with non-Epstein-Bar virus related nuclear antigens. These data cast doubt on current speculation about a possible pathogenic role for Epstein-Barr virus in this disease.

Measurement of immunoglobulin production by peripheral blood mononuclear cells in vitro using a solid-phase immunoradiometric assay.

A simple solid-phase immunoradiometric assay for IgG and IgM is described. Supernatants from lymphocyte cultures are incubated in microtitre plates which have been precoated with anti-IgG or anti-IgM. Subsequent binding of 125I-labelled anti-immunoglobulin is measured and IgG and IgM in supernatants are estimated from the standard curve constructed for each assay. The assay is specific for human IgG and IgM, is able to detect nanogram amounts and offers advantages over other techniques for evaluating in vitro lymphocyte function.

The inhibitory effect of D-penicillamine on human lymphocyte cultures stimulated by phytohaemagglutinin, the antagonistic action of L-cysteine and synergistic inhibition by copper sulphate.

The inhibitory effects of D-penicillamine (D-Pen) on lymphocyte activation by PHA are found to be dose-dependent, showing significant effects above a concentration of 50 microgram/ml. The cells show a diminished sensitivity to D-Pen added after 24 hours in culture, although the dose-response relationship is maintained. L-cysteine is usually found to have an insignificant effect on PHA stimulation, although enhancement and inhibition are also sometimes observed. The supplementation of culture medium with L-cysteine abolishes the inhibitory effect of D-Pen, whilst copper sulphate synergistically inhibits PHA-induced transformation. The balance between the availability of naturally occurring thiols, copper ions and administered D-Pen may be critical in determining the eventual effect of the drug on the lymphoid system. Lymphocyte suppressive soluble factors appear in the sera of patients with rheumatoid arthritis and are modified by treatment with D-Pen. Although our experiments suggest possible modes of action of the drug on the immune system as a therapeutic agent as well as a potent inducer of autoimmunity in its own right, further work is required to delineate its precise mechanism of action.

Adverse reactions to Zn1-24 ACTH therapy associated with specific cellular immunity.

Lymphocyte transformation to 1-24ACTH, as assessed by the incorporation of tritiated thymidine, has been demonstrated to be associated with severe adverse reactions occurring in patients receiving a Zn-linked 1-24ACTH preparation (Tetra cosactrin depot, 'Synacthen'). Antibodies measured with an isotope-binding assay occurred commonly in all patients receiving therapy and did not correlate with adverse reactions. Lymphocyte transformation with the 1-24ACTH polypeptide, a part of the naturally occurring ACTH molecule, has not been previously recorded. The significance of antibodies and cell-mediated immunity to this polypeptide hormone is discussed.