Cancer incidence,survival and mortality: Explaining the concepts

Cancer incidence, survival and mortality are essential population‐based indicators for public health and cancer control. Confusion and misunderstanding still surround the estimation and interpretation of these indicators. Recurring controversies over the use and misuse of population‐based cancer statistics in health policy suggests the need for further clarification. In our article, we describe the concepts that underlie the measures of incidence, survival and mortality, and illustrate the synergy between these measures of the cancer burden. We demonstrate the relationships between trends in incidence, survival and mortality, using real data for cancers of the lung and breast from England and Sweden. Finally, we discuss the importance of using all three measures in combination when interpreting overall progress in cancer control, and we offer some recommendations for their use.     

Metabolic Repair of Premutational Damage in Paramecium

The problems of experimental analysis of the post-irradiation processes leading to mutation are considered in some detail. In particular, methods for separating the effects of various modifiers on the rate of these processes from the effects on the time available for them to occur are discussed. Data are presented for recessive lethal mutations in Paramecium to show that all metabolic inhibitors tried (caffeine, iodoacetate, chloramphenicol and streptomycin) decrease the rate of loss of premutational damage and decrease mutation only because they increase the time available for loss. The results are shown to fit the hypothesis of metabolic repair of radiation-induced lesions of the chromosomes.     

Myocardial protection in reperfusion with postconditioning

Reperfusion is the definitive treatment for coronary occlusive disease. However, reperfusion carries the potential to exacerbate lethal injury, termed ‘reperfusion injury’. Studies have suggested that reperfusion injury events are triggered during the early moments of reflow, and determine, in part, the severity of downstream manifestations of postischemic injury, including endothelial dysfunction, infarction and apoptosis. The application of brief iterative episodes of reflow (reoxygenation) and reocclusion (ischemia, hypoxia) at the immediate onset of reperfusion, which has been termed ‘postconditioning’ by the authors, reduces many manifestations of postischemic injury, notably infarct size, apoptosis, coronary vascular endothelial injury and reperfusion arrhythmias. Cardioprotection with postconditioning has been reported to be comparable with that observed using the gold standard maneuver ischemic preconditioning. In contrast to preconditioning, which exerts its effects primarily during the index ischemia, postconditioning appears to exert its effects during reperfusion alone. Postconditioning modifies the early phase of reperfusion in ways that are just beginning to be understood. It appears to first: reduce the oxidant burden and consequent oxidant-induced injury; secondly, attenuate the local inflammatory response to reperfusion; and thirdly, engage end effectors and signaling pathways implicated in other cardioprotective maneuvers, such as ischemic and pharmacologic preconditioning. Postconditioning seems to trigger the upregulation of survival kinases principally known to attenuate the pathogenesis of apoptosis and possibly necrosis. The postconditioning phenomenon has been reproduced by a number of independent laboratories and has been observed in both large and small animal in vivo models, as well as in ex vivo and cell culture models. In contrast to preconditioning, postconditioning may have widespread clinical application because it can be applied during reperfusion at the point of service for angioplasty, stenting, cardiac surgery and organ transplantation.     

Serum Carcinoembryonic Antigen in Relation to Survival,DNA Ploidy Pattern,and Recurrent Disease in 406 Colorectal Carcinoma Patients

Serum carcinoembryonic antigen (CEA) levels in relation to survival, flow cytometric DNA ploidy pattern, Dukes stage, and recurrent disease was prospectively evaluated in 406 patients with colorectal carcinoma. In 246 patients (61%) the carcinomas were DNA aneuploid. Increased preoperative CEA levels (>5 μg/l) were found in 151 of 363 evaluable patients (42%). Dukes stage-B patients with preoperative CEA elevation showed significantly poorer prognosis than those with normal CEA values (p = 0.001). A weak but significant correlation was found between preoperative CEA level and Dukes stage (Kendall's α = 0.25, p < 0.01). Of 50 evaluable patients with clinical recurrence and postoperative normal or normalized CEA levels, 28 (56%) had a rise in CEA before or at the time of clinical recurrence. The sensitivity of the CEA test for primary and for recurrent disease was not significantly different in the DNA aneuploid and the DNA near-diploid groups.