Clinical Trial Service Unit

About: Clinical Trial Service Unit is a based out in . It is known for research contribution in the topics: Population & Stroke. The organization has 428 authors who have published 1387 publications receiving 181920 citations.

Epidemiology - A human germ project?

Abstract: A few weeks ago,Nature reported the sequence of Helicobacter pylori, which is present in up to one in three people and causes peptic ulcers. But many other chronic diseases or cancers are also thought to be caused by infectious agents. Weight is now lent to this theory by two studies that link coronary heart disease to the bacterium Chlamydia pneumoniae, and the implications of these findings are discussed.

The long-term outcome of patients in the LRF CLL4 trial: the effect of salvage treatment and biological markers in those surviving 10 years.

Abstract: With 10+ years follow-up in the Leukaemia Research Fund (LRF) CLL4 trial, we report the effect of salvage therapy, and the clinical/biological features of the 10-year survivors treated for chronic lymphocytic leukaemia (CLL). Overall survival (OS) was similar in the three randomized arms. With fludarabine-plus-cyclophosphamide (FC), progression-free survival (PFS) was significantly longer (P 3 years and receiving ≤2 lines of treatment. In conclusion, clinical/biological features and salvage treatments both influence the long-term outcome. Second-line therapies that induce a CR can improve OS in CLL patients.

The mysterious steps in carcinogenesis: addendum.

Abstract: Sir, In the past 100 years, many explanations have been proposed for the process of carcinogenesis but none of them has proved to be totally persuasive. For this reason, we deliberately did not offer a modern synthesis in our review article (Brash and Cairns, 2009). However, in the last few years, thanks to certain experiments, a possible interpretation has emerged, which could be of practical importance. We now see that all cells (bacterial, yeast and mammalian cells) are more far-sighted than we had imagined. Confronted by stressful or damaging changes in their environment, populations of cells activate a programme that raises their mutation rate for several generations but temporarily masks the mutant phenotypes. This greatly increases the likelihood that some of them will be able to flourish in the new environment. Two important observations suggest that induction of this ‘stress response' might be the crucial initiating event in cancer. (1) When cells are exposed to chemical or physical initiators in vitro, every cell can be initiated so that it yields transformed descendants, which implies that initiation is the long-term activation of a programme rather than the production of mutations in certain genes (Kennedy et al, 1984). (2) Inactivation of one of the genes involved in the stress response protects mice against various experimental cancers (Dai et al, 2007). If the formation of most cancers is initiated by activation of a programme that depends on the interplay of several gene products, then defects in some of these products (although evolutionarily deleterious) might prevent most cancers; therefore, it may be useful to look for polymorphisms that protect against cancer rather than, as has become usual these days, concentrate solely on those that increase the risk. This could not easily be done with humans (whose lifetime risk of cancer is only about 50%), but could be done with mice. Even within inbred strains, mice are known to vary in susceptibility to skin cancer, and only a few generations of selective breeding can produce mice that are largely insusceptible (Boutwell, 1964). So the project would be to look for the genetic changes that accompany such selection and then, if found, study the frequency of changes in the equivalent human genes in relation to the risk of cancer, using the DNA samples that have already been collected for the many studies of genetic susceptibility.

Simple Method to Estimate Mean Heart Dose From Hodgkin Lymphoma Radiation Therapy According to Simulation X-Rays

Abstract: Purpose To describe a new method to estimate the mean heart dose for Hodgkin lymphoma patients treated several decades ago, using delineation of the heart on radiation therapy simulation X-rays. Mean heart dose is an important predictor for late cardiovascular complications after Hodgkin lymphoma (HL) treatment. For patients treated before the era of computed tomography (CT)-based radiotherapy planning, retrospective estimation of radiation dose to the heart can be labor intensive. Methods and Materials Patients for whom cardiac radiation doses had previously been estimated by reconstruction of individual treatments on representative CT data sets were selected at random from a case–control study of 5-year Hodgkin lymphoma survivors (n=289). For 42 patients, cardiac contours were outlined on each patient's simulation X-ray by 4 different raters, and the mean heart dose was estimated as the percentage of the cardiac contour within the radiation field multiplied by the prescribed mediastinal dose and divided by a correction factor obtained by comparison with individual CT-based dosimetry. Results According to the simulation X-ray method, the medians of the mean heart doses obtained from the cardiac contours outlined by the 4 raters were 30 Gy, 30 Gy, 31 Gy, and 31 Gy, respectively, following prescribed mediastinal doses of 25-42 Gy. The absolute-agreement intraclass correlation coefficient was 0.93 (95% confidence interval 0.85-0.97), indicating excellent agreement. Mean heart dose was 30.4 Gy with the simulation X-ray method, versus 30.2 Gy with the representative CT-based dosimetry, and the between-method absolute-agreement intraclass correlation coefficient was 0.87 (95% confidence interval 0.80-0.95), indicating good agreement between the two methods. Conclusion Estimating mean heart dose from radiation therapy simulation X-rays is reproducible and fast, takes individual anatomy into account, and yields results comparable to the labor-intensive representative CT-based method. This simpler method may produce a meaningful measure of mean heart dose for use in studies of late cardiac complications.