Alkoholkonsum und Krebsrisiko

2019 ◽  
Vol 144 (19) ◽  
pp. 1354-1360
Author(s):  
Hans Scherübl
Keyword(s):  
Alcohol Use ◽  
Cancer Risk ◽  
Squamous Cell Cancer ◽  
Cell Cancer ◽  
Modifiable Risk Factors ◽  
Increase Cancer Risk ◽  
Risky Alcohol ◽  
Alcohol Cessation ◽  
Risk Of Cancer

AbstractAlcohol use is one of the most important and potentially modifiable risk factors for cancer in Germany. The more and the longer a person drinks, the higher the risk of cancer. Even modest use of alcohol may increase cancer risk. Statistically, every German drinks more than 100 gram of alcohol per week; this amount is currently considered to be the limit of low-risk use. Alcohol is causally associated with oropharyngeal and larynx cancer, esophageal squamous cell cancer, hepatocellular carcinoma, breast cancer, and colorectal cancer. People with long-term risky alcohol use should be encouraged to join programs of cancer screening. Alcohol cessation appears to be effective in reducing the alcohol-induced, increased cancer risk.

Prognostic factors in microinvasive cervical squamous cell cancer: long-term results

2005 ◽  
Vol 15 (1) ◽  
pp. 88-93 ◽  
Author(s):  
F. Raspagliesi ◽  
A. Ditto ◽  
P. Quattrone ◽  
E. Solima ◽  
R. Fontanelli ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Squamous Cell ◽  
Squamous Cell Cancer ◽  
Cell Cancer ◽  
Long Term Results

Long-term use of oral nucleos(t)ide analogues for chronic hepatitis B does not increase cancer risk - a cohort study of 44 494 subjects

2017 ◽  
Vol 45 (9) ◽  
pp. 1213-1224 ◽  
Author(s):  
G. L.-H. Wong ◽  
Y.-K. Tse ◽  
T. C.-F. Yip ◽  
H. L.-Y. Chan ◽  
K. K.-F. Tsoi ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Cohort Study ◽  
Hepatitis B ◽  
Cancer Risk ◽  
Chronic Hepatitis B ◽  
Increase Cancer Risk

scholarly journals Genetically-proxied therapeutic inhibition of antihypertensive drug targets and risk of common cancers

2021 ◽  
Author(s):  
James Yarmolinsky ◽  
Virginia Díez-Obrero ◽  
Tom G Richardson ◽  
Marie Pigeyre ◽  
Jennifer Sjaarda ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Blood Pressure ◽  
Cancer Risk ◽  
Systolic Blood Pressure ◽  
Antihypertensive Drug ◽  
Drug Targets ◽  
Mendelian Randomization ◽  
Ace Inhibition ◽  
Risk Of Cancer

AbstractBackgroundEpidemiological studies have reported conflicting findings on the potential adverse effects of long-term antihypertensive medication use on cancer risk. Naturally occurring variation in genes encoding antihypertensive drug targets can be used as proxies for these targets to examine the effect of their long-term therapeutic inhibition on disease outcomes.MethodsSingle-nucleotide polymorphisms (SNPs) in ACE, ADRB1, and SLC12A3 associated (P < 5.0 x 10-8) with systolic blood pressure in genome-wide association studies (GWAS) were used to proxy inhibition of angiotensin-converting enzyme (ACE), β-1 adrenergic receptor (ADRB1), and sodium-chloride symporter (NCC), respectively. Summary genetic association estimates for these SNPs were obtained from GWAS consortia for the following cancers: breast (122,977 cases, 105,974 controls), colorectal (58,221 cases, 67,694 controls), lung (29,266 cases, 56,450 controls), and prostate (79,148 cases, 61,106 controls). Replication analyses were performed in the FinnGen consortium (1,573 colorectal cancer cases, 120,006 controls). Inverse-variance weighted random- effects models were used to examine associations between genetically-proxied inhibition of these drug targets and risk of cancer. Multivariable Mendelian randomization and colocalisation analyses were employed to examine robustness of findings to violations of Mendelian randomization assumptions.ResultsGenetically-proxied ACE inhibition equivalent to a 1 mmHg reduction in systolic blood pressure was associated with increased odds of colorectal cancer (OR 1.13, 95% CI 1.06-1.22; P = 3.6 x 10-4). This finding was replicated in the FinnGen consortium (OR 1.40, 95% CI 1.02-1.92; P = 0.035). There was little evidence of association of genetically-proxied ACE inhibition with risk of breast cancer (OR 0.98, 95% CI 0.94-1.02, P = 0.35), lung cancer (OR 1.01, 95% CI 0.92-1.10; P = 0.93), or prostate cancer (OR 1.06, 95% CI 0.99-1.13; P = 0.08). Genetically-proxied inhibition of ADRB1 and NCC were not associated with risk of these cancers.ConclusionGenetically-proxied long-term ACE inhibition was associated with an increased risk of colorectal cancer, warranting comprehensive evaluation of the safety profiles of ACE inhibitors in clinical trials with adequate follow-up. There was little evidence to support associations across other drug target-cancer risk analyses, consistent with findings from short-term randomised controlled trials for these medications.

scholarly journals Long-term regional control in the observed neck following definitive chemoradiation for node-positive oropharyngeal squamous cell cancer

2013 ◽  
Vol 133 (5) ◽  
pp. 1214-1221 ◽  
Author(s):  
Anuj Goenka ◽  
Luc G.T. Morris ◽  
Shyam S. Rao ◽  
Suzanne L. Wolden ◽  
Richard J. Wong ◽  
...  
Keyword(s):  
Squamous Cell ◽  
Squamous Cell Cancer ◽  
Cell Cancer ◽  
Node Positive ◽  
Regional Control ◽  
Definitive Chemoradiation

scholarly journals Enhanced risk of cancer in companion animals as a response to the longevity

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Moeko Tanaka ◽  
Sachi Yamaguchi ◽  
Yoh Iwasa
Keyword(s):  
Cancer Risk ◽  
Cancer Progression ◽  
Companion Animals ◽  
Replication Error ◽  
Companion Dogs ◽  
Long Run ◽  
Step Model ◽  
Positive Rate ◽  
Risk Of Cancer

Abstract Cancer is caused by the lifetime accumulation of multiple somatic deformations of the genome and epigenome. At a very low rate, mistakes occur during genomic replication (e.g., mutations or modified epigenetic marks). Long-lived species, such as elephants, are suggested to have evolved mechanisms to slow down the cancer progression. Recently, the life span of companion dogs has increased considerably than before, owing to the improvement of their environment, which has led to an increase in the fraction of companion dogs developing cancer. These findings suggest that short-term responses of cancer risk to longevity differ from long-term responses. In this study, to clarify the situation, we used a simple multi-step model for cancer. The rates of events leading to malignant cancer are assumed to be proportional to those of genomic replication error. Perfect removal of replication error requires a large cost, resulting in the evolution of a positive rate of genomic replication error. The analysis of the model revealed: that, when the environment suddenly becomes benign, the relative importance of cancer enhances, although the age-dependent cancer risk remains unchanged. However, in the long run, the genomic error rate evolves to become smaller and mitigates the cancer risk.

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