Immune and Gene Therapy Laboratory, Cancer Centre Karolinska, Karolinska University Hospital Solna, Stockholm, Sweden.

Immunotherapy is being increasingly utilized for adjuvant treatment for breast cancer (BC). We have previously described immune functions during primary therapy for BC. The present study describes immune recovery patterns during long-term, unmaintained follow-up after completion of adjuvant therapy.A group of patients with primary BC had been treated with adjuvant radio-chemotherapy (RT + CT) 5-fluorouracil, epirubicin and cyclophosphamide (FEC) (n = 21) and another group with radiotherapy (RT) (n = 20) alone. Immunological testing of NK and T-cell functions was performed initially at the end of adjuvant treatment and repeated after 2, 6 and 12 months. NK cell cytotoxicity was significantly higher (P < 0.05) at all time-points in patients than in age-matched controls and did not differ between the two treatments groups during one year observation. In contrast, lower numbers of CD4 T-cells and lower expression of CD28 on T-cells was observed particularly in RT + CT patients and did not normalize during the observation period. The numbers of T(reg) cells (CD4(+)CD25(high)) were low in the RT + CT group during follow-up, as well as expression of TCRxi, Zap70, p56(lck), P59(fyn) and PI3 k in CD4(+) cells. In contrast, expression of intracellular cytokines (IFN-gamma, IL-2, IL-4) in CD4 and CD8 T cells were significantly higher in RT + CT patients than in the RT group and the difference increased during follow-up. In conclusion, NK-cell cytotoxicity increased during unmaintained long-term follow-up whereas CD4 and regulatory T cells as well as signal transduction molecules remained low following adjuvant radio-chemotherapy.

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Public Health Sciences Division, Fred Hutchinson Cancer Research Center and Department of Epidemiology, University of Washington, 1100 Fairview Avenue N, M4-B874, Seattle, WA, 98109-1024, USA, aderoos@fhcrc.org.

OBJECTIVE: Myelodysplastic syndromes (MDS) following treatment with chemotherapy or irradiation are termed ’secondary’ MDS. Clinical observations suggest a worse prognosis for secondary than for primary MDS, but differences in survival have not been studied in a general population sample. METHODS: We analyzed data from the Surveillance, Epidemiology, and End Results (SEER) program to describe survival in MDS patients according to previous cancer diagnosis. Our study included 3,938 MDS cases diagnosed in 2001-2004 and reported by registries which have participated in SEER since the 1970s. RESULTS: A previous cancer diagnosis (26% of MDS cases) was associated with 13% increased risk of death from any cause among MDS cases (hazard ratio [HR]=1.13, 95% confidence interval [CI]: 1.02-1.25). Radiation treatment for a previous cancer was associated with 52% increased risk of death (95% CI: 1.15-2.02). Shortened survival was most pronounced if the latency between the previous cancer and MDS was less than five years, including lung cancer diagnosed in the year preceding MDS (HR = 3.43, 95% CI: 1.93-6.10) and lymphohematopoietic cancer 1-5 years before MDS (HR = 2.11; 95% CI: 1.33-3.36). CONCLUSIONS: Our results confirm a more severe prognosis for secondary MDS than for primary MDS, associated with certain types and treatments of previous cancer.

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Cisplatin (cis-diamminedichloroplatinum II) is one of the most effective chemotherapeutic agents used in the treatment of a variety of human solid tumors. However, its clinical use is limited due to severe toxicity. The pathogenesis of liver damage caused by cisplatin is generally considered to be oxidative damage. The aim of this study was to evaluate the protective effect of the ethanol extract of Prunus persica flesh (PPFE) against cisplatin-induced hepatotoxicity in animal models. In a xenograft model with the repeated administration of a low-dose cisplatin (5 mg/kg body weight) for 15 days, and in an acute toxicity model with a single administration of a high-dose cisplatin (45 mg/kg body weight) over a 16 h period, the consecutive administration of PPFE in combination with and prior to the cisplatin injection reversed the cisplatin-induced decrease in the liver weight as a percentage of total body weight, and the cisplatin-induced increases in the serum alanine aminotransferase and aspartate aminotransferase levels caused by liver damage. Moreover, the oral administration of PPFE significantly recovered the reduced glutathione level and inhibited lipid peroxidation in the cisplatin-treated mice. These results demonstrate that supplementation with PPFE might protect against cisplatin-induced toxicity in cancer patients. Copyright (c) 2007 John Wiley & Sons, Ltd.

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