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    • Cancer epidemiology studies have shown relationships

    2018-10-30

    Cancer epidemiology studies have shown relationships with short LTL, but differences by cancer site and study design were noted. In a meta-analysis of 27 reports (), short LTL was associated with cancer risk, primarily in case–control studies (OR=2.9 in case–control studies vs. 1.2 in prospective studies). This suggests that short LTL is a disease marker rather than a risk factor. Recently, a large study linked long LTL to melanoma risk (). The spectrum of cancers associated with long LTL is not clear yet, but suggested to include lung and Non-Hodgkin\'s lymphoma (NHL). It is of interest that cutaneous melanoma and possibly NHL are the main cancers associated with excess risk in PCBs exposed individuals (), suggesting a possible contribution of LTL in PCB-related carcinogenesis. The large sample size, the national representation, and the wealth of collected information NHANES offers are among the strengths of this study. On the other hand, the cross-sectional design restricted its ability to establish a causal inference between LTL, PCB exposure, and cancer risk. The one-time measurement of PCB blood level and LTL may not reflect the full spectrum of the association. Information on the duration and dose of exposure to PCBs would have been useful (reviewed in ) Short-term exposure to ambient particulate matter was associated with long LTL, while longer exposures were associated with short LTL. Exposure dose in relation to LTL was noted in other environmental exposures. For example, exposure to low dose of arsenic resulted in telomerase overexpression and telomere LY2584702 in cord blood cells, while exposure at large doses suppressed telomerase, shortened telomeres, and induced apoptosis. A recent study () evaluating the association between LTL and pesticide exposure suggested a differential effect on LTL in long-term versus recent exposures for certain pesticides. While LTL may present a good surrogate for telomere length in other tissues, it is not clear how good of a surrogate it is for tissues affected by chemical exposures. Measuring telomere length in organs directly affected by PCB exposure, and comparing this to LTL may explain the role telomeres may play in PCB-related carcinogenesis. Also, LTL measurement obtained by quantitative polymerase chain reaction (qPCR) assay may be affected by the cell composition of the sample since telomere length differs by peripheral blood cell subtype. Using a leukocyte cell-type specific TL measurement assay such as flow FISH may provide better insights into such association. Important considerations in epidemiological studies of telomere length are discussed in details elsewhere ().
    In this issue of , Pandharipande and colleagues report important data that may well assist the decision-making process when screening families at risk for pancreatic ductal adenocarcinoma (PDAC) (). The aim of the study was to compare, using a simulation model, the effectiveness of different screening strategies in -mutation carriers. Hereditary factors play a role in the development of PDAC in about 5% of all cases (). Individuals at increased risk of developing PDAC can be subdivided into those with an underlying gene defect such as , /, and -mutations and those individuals with a significant family history of PDAC (Familial pancreatic cancer (FPC)). Carriers of a mutation constitute the largest group of mutation carriers at risk for PDAC. The risk of developing PDAC in this group is between 5–10%, depending on the number of patients with PDAC in the family ().
    Alcohol misuse is a global health problem that includes the digestive diseases. However, compared to the liver diseases, much less attention has been paid to alcoholic pancreatic disorders. Alcohol misuse is the most common cause of chronic pancreatitis (CP) and is the second-most common cause of acute pancreatitis (AP) after gallstones (). In Japan, for example, alcohol is the leading cause of both AP and CP (), accounting for 33.5% and 69.7% of such cases, respectively. One reason for the insufficient awareness of alcohol misuse as an important risk factor of pancreatitis is that only 2–5% of heavy drinkers develop pancreatitis (), a number much lower than that for chronic liver diseases. Some individuals may develop alcoholic pancreatitis with alcohol intake as low as 20g/day, whereas most individuals do not develop pancreatitis no matter how much they drink or how long. It has been suggested that an additional insult is required to precipitate pancreatitis (). However, detailed mechanisms remain largely unknown.