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Liposomal doxorubicin supercharge-containing frontline treatment for diffuse large B-cell lymphoma or classical Hodgkin lymphoma: preliminary results of a phase II study Myocet™ is doxorubicin encapsulated in a non-pegylated liposomal membrane of phosphatidylcholine and cholesterol (NPLD) that spares the heart muscle from the direct cytotoxic drug. Our data suggest that the NPLD supercharge-driven strategy in high-risk DLBCL/c-HL may be a promising option to test in phase III trials, for improving negative interim-FDG-PET cases incidence. [Extracted from the article]

Abstract Objective The current methods of detection of recurrent colorectal cancer after surgical treatment are inaccurate using conventional imaging. This study set out to detect early recurrence by means of PET in patients treated surgically for colorectal cancer by curative resection. Methods Thirty-one disease-free patients were recruited and underwent FDG-PET. The results were verified by clinical, surgical and radiological follow up and/or biopsy to evaluate the accuracy for detecting recurrence. Results PET detected 6 sites of increased activity in 5 patients. Three of these underwent surgery. One was false positive with no evident tumour and two underwent an hepatic resection with removal of a homental metastasis. The sensitivity was 100% and specificity 83.3%. Clinical management was altered in two cases (6.4%). Conclusions This study demostrates that PET is more accurate than conventional imaging for the evaluation of recurrence in colorectal cancer patients. FDG-PET should be considered in the follow-up of patients after treatment for colorectal cancer in addition to other imaging methods. [ABSTRACT FROM AUTHOR]

Background Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder, caused by an increased CAG repeat size in the huntingtin gene. Apart from motor, cognitive, and psychiatric signs, other features, as dysautonomia, weight loss, sleep disturbances, and neuroendocrine disturbances may affect quality of life. Decreased bone density was shown in HD mice and in patients, according to preliminary reports. Aims Aim of this study was to evaluate bone mineral density (BMD) and whole mass body distribution by DEXA in HD patients and to correlate them to clinical and endocrine data. Patients & methods We investigated 14 consecutive patients seen at our HD Clinics. Clinical assessment of patients was performed using the Unified Huntington's Disease Rating Scale (UHDRS) motor section and the Total Function Capacity (TFC). Wide basal metabolic and endocrine investigations included serum calcium, phosphorus, alkaline phosphatase, cortisol, FSH, LH, estradiol, testosterone, androstenedione, DHEAS, insulin, growth hormone, insulin-like growth factor 1 (IGF-1). Patients and underwent dual-energy X-ray absorptiometry (DEXA) at the lumbar spine and femoral neck. Individual BMD, lean, fat and total mass values were expressed as g/cm2 and T- and Z-scores. Osteopenia and osteoporosis were diagnosed according to World Health Organization (WHO) criteria. Results Abnormal bone mineral density was present in 3/14 (21%) of patients with HD. Two patients had osteopenia and one had osteoporosis. CAG size was negative correlated with body mass index (r=−0.959, p<0.01), cortisol (r=−0.917, p<0.05), and fat mass (r=−0.999, p<0.01). Conclusions Our data, in line with data from preliminary report, show that osteoporosis may be part also of the HD phenotype, even in early disease stages. BMD values did not show any correlation with expected parameters like cortisol. Further investigations are needed to confirm this and to clarify if decreased bone mineral density could be due to a direct effect of mutant huntingtin on osteoblasts or osteoclasts in bone tissue. [ABSTRACT FROM PUBLISHER]