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That Pilsner May Be Good For You

  1. Top of page
  2. That Pilsner May Be Good For You
  3. Not Just Estrogens Alone
  4. On the Tracks of Helicobacter Pylori
  5. To CHEK or not to CHEK

The consumption of vegetables and fruits is thought to lower the risk of colon cancer and natural components from plant sources have shown inhibitory effects in experimental colon carcinogenesis models. Although beer contains several phytochemicals that display antioxidative, anti-mutagenic, cytotoxic and anti-tumor promotion activity in vitro, the cancer-preventive potential of dietary beer intake has remained ambiguous at best. Previous research has even implicated alcohol as a potential risk factor for the development of colorectal cancer. In this issue, Nozawa et al. report that daily, moderate consumption of beer reduces the incidence of azoxymethane-induced adenomas and adenocarcinomas in the colon of rats (pages 404–411). Rats that were fed beer or malt extract for 2 weeks suffered significantly less DNA damage in their colonocytes after a single injection of azoxymethane (AOM). In addition, beer consuming rats developed 35% fewer aberrant crypt foci (ACF) when injected with AOM twice weekly over the course of 5 weeks than controls. Freeze-dried beer and hot water extracts of malt also lowered the number of ACF, suggesting that the observed effect was not due to alcohol as assumed earlier. A long-term experiment stretching over 42 weeks indicated that the intake of beer decreased tumor incidence by 22% and decreased the number of neoplastic lesions, including adenomas and adenocarcinomas, by 44%. The results suggest that moderate consumption of beer may reduce the risk of colon cancer susceptibility. The efficacy varied widely with the brand of beer and the components responsible haven't been pinned down yet1.

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Illustration 1. Effects of beer, malt extract and hops extract on DNA damage in the rat colonocyte induced by AOM.

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Not Just Estrogens Alone

  1. Top of page
  2. That Pilsner May Be Good For You
  3. Not Just Estrogens Alone
  4. On the Tracks of Helicobacter Pylori
  5. To CHEK or not to CHEK

The leading hypothesis about endometrial tumorigenesis postulates that exposure to estrogens not opposed by progesterone raises the odds of developing endometrial cancer whereas androgens do not seem to have a directly stimulatory effect on endometrial cell proliferation. One theory, however, holds that after menopause, when the ovarian production of estrogen ceases, abnormal endometrial cells could aromatize androstenedione from the plasma pool into estrogens and thus gain a growth advantage independent of circulating estrogens. A prospective multicenter study, which included 124 postmenopausal patients with invasive endometrial cancer, found evidence in favor of this hypothesis (pages 425–432). Lukanova et al. matched each case with 2 controls and calculated the odds ratios of endometrial cancer with regard to increasing hormone concentrations. They found a strong direct association of circulating estrogens and androgens, albeit a lesser one for the latter and an inverse association of sex-hormone binding globulin (SHBG) with endometrial cancer in postmenopausal women. Although they could not exclude an independent effect of androgens, the effect of elevated androstenedione and testosterone levels on disease risk seems to be mediated mainly through their conversion to estrogens. This fits nicely with the finding that endometrial tumor tissues possess aromatase activity.

On the Tracks of Helicobacter Pylori

  1. Top of page
  2. That Pilsner May Be Good For You
  3. Not Just Estrogens Alone
  4. On the Tracks of Helicobacter Pylori
  5. To CHEK or not to CHEK

Half of the world's population is colonized with Helicobacter pylori. Most people have few symptoms—some gastric inflammation, perhaps —before an apparently harmonious relationship sets in that can last for decades. However, 10 to 20 % of infected individuals are not so lucky. Some suffer from duodenal ulcers (DU), while others develop a progressive inflammation of the stomach, which leads to the loss of acid-producing cells and increases their risk for stomach cancer. Naturally, a diagnostic test able to distinguish between infected persons likely to develop one of these serious clinical symptoms and harmlessly infected individuals would be of great benefit. Using sera from gastric cancer and duodenal ulcer patients, Krah et al. identified more than a dozen candidate antigens that might serve as markers to spot Helicobacter pylori-infected people at risk of developing gastric carcinoma (GC) (pages 456–463). They compared high-resolution immunoblots of H. pylori strain 26695 stained with sera from patients with duodenal ulcers (n=30) and gastric cancers (n=30). Despite strongly varying antigen recognition patterns, 14 antigens showed significant differences between sera from GC and DU patients. Particular protein species of GroEL, HyuA, GroES and AtpA appeared to be potentially useful surrogate markers for the detection of GC. Further experiments will show whether these antigens also have prognostic value and could be used in diagnostic tests to identify people at increased cancer risk2.

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Illustration 2. Immunoblot master image with spot intensities of the 14 differentially recognized spots.

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To CHEK or not to CHEK

  1. Top of page
  2. That Pilsner May Be Good For You
  3. Not Just Estrogens Alone
  4. On the Tracks of Helicobacter Pylori
  5. To CHEK or not to CHEK

The genetic risk factors for male breast cancer are poorly understood. To date, few genes other than BRCA1 and BRCA2 have been implicated in conferring male breast cancer susceptibility. Considerable interest was generated when a frameshift mutation in CHEK2 that abrogates the kinase activity was found to confer a 2-fold increase of breast cancer risk in women and a 10-fold increase in men. But three independent studies in this issue indicate that the relative risk of breast cancer in male carriers of CHEK2*delC is likely to be considerably smaller than previously suggested and that it does not explain the familial aggregation of breast cancer in families of male cases (pages 475–476, 477–478, and 479–480). A study in Finland by Syrjäkoski et al. detected the 1100delC mutation in 2 out of 114 male breast cancer (MBC) patients. The frequency (1.8%) was similar to the mutation frequency in the Finnish control population (1.4%) and did not differ substantially from the one reported in the original study (18/1620, 1.1%). Ohayon et al. studied 54 Israeli MBC patients, none of whom carried the mutation. Among 146 unaffected control samples no carriers were detected and a single carrier was found in 219 BRCA1/2 carriers. According to the pooled results, the overall Ashkenazi population frequency of 1100delC in Israel was estimated to be only 0.3 %. None of the 188 MBC patients Neuhausen et al. recruited in the US and the UK carried the mutation whereas the frequency in the control population (21/3887) was 0.5%. While the high frequency of 1100delC mutations among MBC patients in the original study may be due to chance, it seems more likely that the conferred risk has been overestimated.