The first evidence for tumor-specific antigens came from transplantation studies of sarcomas induced by methylcholanthrene in inbred mice (1-5). Growth of a sarcoma transplant in syngeneic recipients, followed by its removal, increased resistance to subsequent challenge with the same sarcoma. The surprising feature that emerged from the study of these transplantation antigens is that they are distinct for each tumor, no two tumors having been convincingly shown to share the same antigen. Although repeated immunization with tumor cells can lead to substantial resistance to tumor challenge, antibody to the unique antigens of chemically induced sarcomas has been difficult to demonstrate in mice and, where positive results have been obtained, the analysis was not sufficiently detailed to indicate the class of surface antigen being detected. The fact that murine leukemia virus (MuLV) ~ and its antigens are often found in chemically induced sarcomas (6-8) and that normal mouse serum frequently contains naturally occurring antibody to MuLV antigens (9-11) adds a serious complication to the serological study of these tumors and makes it virtually impossible to interpret past studies where this was not taken into consideration. Apparently, MuLV-related antigens on chemically induced tumors are not effective in eliciting transplantation resistance or cross reactions between different sarcomas would have been a far more common finding.

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Hematopoietic stem cell transplant (HSCT) is a life-saving procedure for patients with several malignant and nonmalignant hematological disorders. Acute kidney injury (AKI) is a common complication after HSCT. The aim of the study was to identify the incidence and outcomes of AKI associated with HSCT in our center. Sixty-six HSCT recipients from October 2008 to March 2014 at Christian Medical College, Ludhiana, were followed up till July 31, 2014. RIFLE criteria utilizing serum creatinine was used to diagnose and stage AKI. Mortality and AKI were the primary outcomes studied. The risk of AKI in relation to conditioning regimen, type of HSCT (allogeneic and autologous), co-morbidities, graft versus host disease, drug toxicity, and veno-occlusive disease were analyzed. Sixty-five patients were included in the study. Male: Female ratio was 3.6:1 with a median age of 17 years (1.5–62). Forty-nine (75.4%) patients had AKI over 3 months, R 17 (26.2%), I 19 (29.2%), and F 13 (20%). AKI occurred at a mean of 19.4 ± 29.2 days after the HSCT. AKI was more commonly observed in patients undergoing allogeneic versus autologous HSCT (85.2% in allogeneic vs. 27.8% in autologous, P = 0.005). Mortality was seen in 20 patients (30.8%) in 3 months. AKI in the first 2 weeks (P < 0.016) was a significant risk factor for mortality. Incidence of AKI in HSCT is high and accounts for significant mortality and morbidity. RIFLE classification of AKI has prognostic significance among HSCT patients with an incremental trend in mortality.

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