Patients with CLL responding to initial chemotherapy with fludarabine alone (F) or in combination with cyclophosphamide (FC) were randomized for treatment with alemtuzumab (30 mg i.v. TIW, 12 weeks) or observation. Of 21 evaluable patients, 11 were randomized to alemtuzumab before the study was stopped due to severe infections in seven of 11 patients. These infections (one life-threatening pulmonary aspergillosis IV; four CMV reactivations III requiring i.v. ganciclovir; one pulmonary tuberculosis III; one herpes zoster III) were successfully treated and not associated with cumulative dose of alemtuzumab. In the observation arm, one herpes zoster infection II and one sinusitis I were documented. At 6 months after randomization, two patients in the alemtuzumab arm converted to CR, while three patients in the observation arm progressed. After alemtuzumab treatment, five of six patients achieved a molecular remission in peripheral blood while all patients in the observation arm remained MRD-positive (P ¼ 0.048). At 21.4 months median follow-up, patients receiving alemtuzumab showed a significant longer progression-free survival (no progression vs mean 24.7 months; P ¼ 0.036). In conclusion, a consolidation therapy with alemtuzumab is able to achieve molecular remissions and longer survival in CLL, but a safe treatment regimen needs to be determined.

Summary We studied 228 consecutive stem cell transplant recipients, screened for reactivation of human herpesvirus‐6 (HHV‐6) in peripheral blood and other specimens as clinically indicated by means of qualitative polymerase chain reaction. Among them, 197 received an allograft and 31 autograft. Ninety‐six of 228 patients (42·1%) showed HHV‐6 reactivation in peripheral blood and 129 of 228 (56·6%) demonstrated HHV‐6 in at least one of the specimens tested. 41·9% of patients were asymptomatic when HHV‐6 was identified. Clinical features, noted when HHV‐6 was detected, included interstitial or alveolar pneumonia, gastroduodenal and colorectal disease, bone marrow suppression and liver disease. However, based on clinical and histopathological criteria, HHV‐6 was considered a causal agent in only a minority of patients, in particular, those suffering from bone marrow suppression (n = 11), gastroduodenitis (five), colitis (three), interstitial/alveolar pneumonia (five), skin rash (one), pericarditis (two) and encephalitis (one). HHV‐6 reactivation was significantly associated with the occurrence of graft‐versus‐host disease [odds ratio (OR) 5·31], Epstein–Barr virus coinfection (OR 8·89) and unrelated donor transplantation (OR 5·67) indicating an increased stage of immunosuppression.

The proteomic approach is a valuable tool to detect and identify proteins that are associated with cancer. In previous investigations on experimentally induced rat hepatomas, we detected aldose reductase-like protein (ARLP) as a highly significant marker protein. Our present study was intended to look for the presence of similar tumor-associated marker proteins on human hepatocellular carcinomas (HCC). We found several novel tumorassociated protein variants that represent members of the aldo-keto reductase (AKR) superfamily. Human aldose reductase-like protein-1 (hARLP-1) was the most prominent tumorassociated AKR member detected in HCC by 2-dimensional electrophoresis (2-DE) and identified by mass spectrometric fingerprinting. The enzyme was found in 4 distinct forms H uman hepatocellular carcinoma (HCC) ranks fifth in worldwide cancer incidence and is an important component of public health. Many HCC risk factors are known, including hepatitis B or C (HBV or HCV) infection, ingestion of aflatoxin-contaminated food, and alcohol. 1,2 The development of HCC is associated with multiple changes at the messenger RNA (mRNA) and/or protein level, some of them serving as tumor markers, e.g., ␣-fetoprotein, 3 or, less specifically, cyclin D1 or the proliferating cell nuclear antigen. 4 Misprogramming of genetic information in cancer is reflected by quantitative and/or qualitative protein alterations. These protein alterations might represent tumor markers that are useful in the diagnosis of human tumors and may also help the understanding of mechanisms of tumor induction and development. Proteome analysis of liver proteins and HCC were predominantly performed using either chemically induced hepatomas in animals (predominantly the rat 5-10 ) or human HCC cell lines, such as HepG2 and Huh7 cells, 11 BEL-7404 cells, 12 or HCC-M cells. 2,13,14 Numerous so-called tumor-associated or cancer-related proteins were identified; these provide valuable information for the establishment of HCC protein databases. 2,[11][12][13][14] Comparative analysis of liver tissue and hepatocellular carcinomas might give additional insights into the induction or repression of tumor-associ-

No abstract

HCMV infection status in transplant patients detects patients with increased risk for transplant failure caused by TVP.