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H Pylori protects against oesophageal cancer
Newsdesk H Pylori protects against oesophageal cancer Helicobacter pylori infection may confer protection against oesophageal adenocarcinoma, according to the results of a study from Stanford University School of Medicine, CA, USA. Catherine de Martel and Augusto Llosa analysed records from around 130 000 patients who had been followed since the 1960s. 52 of this group had developed oesophageal adenocarcinoma. The researchers examined blood-sampling data from the individuals with oesophageal cancer for signs of H pylori infection; they subsequently compared these results with samples from 551 individuals who had not developed cancer. Those infected with H pylori had a risk of developing oesophageal adenocarcinoma that was around 70% lower than the uninfected group. This finding was not altered by adjustment for other risk factors such
as age, gender, obesity, and history of smoking. The conclusions from this study are consistent with previous reports, says Richard Peek, Vanderbilt University, TN, USA. “Colonisation with H pylori, particularly strains possessing the cag pathogenicity island, is associated with a decreased risk for gastroesophageal reflux disease (GERD) and its complications, which include oesophageal adenocarcinoma”, he says. de Martel suggests that H pylori confers its protective activity by interfering with gastric-acid secretion, which is responsible for GERD, a condition that often precedes oesophageal adenocarcinoma. Peek agrees: “H pylori may induce inflammation within the acid-secreting gastric corpus. This is supported by data showing that severity of gastric inflammation in the corpus is inversely proportional to the
prevalence of GERD.” The role of cag is currently being investigated by de Martel’s group. Considering other research connecting H pylori and cancer, de Martel’s findings are perplexing. This bacterium has been implicated in development of stomach ulcers and cancer. Therefore, although eradicating H pylori would help alleviate these conditions, this course of action may actually increase the risk of another cancer. However, as de Martel points out, “This study does not address the question of eradication. The H pylori-negative individuals included in the study had not been treated for infection, they had never got the bacteria in the first place.” She also emphasises that these results are preliminary and more work is required to establish the exact role of H pylori in oesophageal cancer. Cathel Kerr
Hormone hypersensitivity link to familial breast cancer
THE LANCET Oncology Vol 4 July 2003
stronger with younger age at menarche. In pairs where only one twin had cancer, there was no correlation between early puberty and risk. Intriguingly, in double-cancer twins the researchers found no association between increased risk and later events
Rights were not granted to include this image in electronic media. Please refer to the printed journal. Twins with breast cancer are a genetically high-risk group.
in adulthood, such as parity and menopause, indicating that the association with early puberty may not simply be a consequence of extending the woman’s exposure to menstruation. Instead, Hamilton proposes, “This may indicate some kind of damage to immature breast cells that makes them vulnerable to developing breast cancer later in life”. Although previous studies have
Robert Harding Photo Library
A study of identical twins has shown that development of some types of hereditary breast cancer may be a result of hypersensitivity to hormones—not cumulative exposure as previously thought. “BRCA1 and 2 do not explain the majority of hereditary breast cancers”, says Ann Hamilton, University of Southern California, CA, USA, who, with colleague Thomas Mack, carried out the study. Substantial evidence links long-term hormone exposure to risk of breast cancer, but Hamilton and Mack have identified another pathway linking reproductive hormones and cancer. “The hormone sensitivity of immature breast cells during puberty is crucial”, explains Hamilton. The team set out to investigate whether risk factors for breast cancer differ according to genetic susceptibility. “We determined that identical twins who both have breast cancer represent the subset with the highest susceptibility”, Hamilton recalls. The only factor that seemed to influence development of breast cancer in the first twin was early onset of puberty. Furthermore, the effect seemed to be
shown that early menarche increases risk of breast cancer, Hamilton suggests that this may reflect an averaging effect of a high risk in a genetically susceptible subgroup. “The risk of early menarche for these individuals may actually be much higher”, she says. “We found risk increased five times.” “This work challenges the assumption that reproductive or hormonal risk factors such as age at first pregnancy, number of children, and late menopause, apply equally to the development of all breast cancers”, says Graham Colditz, Harvard Medical School, MA, USA. Previous studies of hereditary breast cancer suggested that familial cases may not be affected by reproductive risk factors. But, says Colditz, “these studies relied on self-reporting and were far less able to untangle the genetic risk”. In Hamilton’s study, however, “clear evidence points to different pathways for breast cancer causation”, he adds. Hamilton and Colditz agree that future application of this work may lead to new approaches to therapy or prevention. Hannah Brown
http://oncology.thelancet.com
For personal use. Only reproduce with permission from The Lancet.
391
as age, gender, obesity, and history of smoking. The conclusions from this study are consistent with previous reports, says Richard Peek, Vanderbilt University, TN, USA. “Colonisation with H pylori, particularly strains possessing the cag pathogenicity island, is associated with a decreased risk for gastroesophageal reflux disease (GERD) and its complications, which include oesophageal adenocarcinoma”, he says. de Martel suggests that H pylori confers its protective activity by interfering with gastric-acid secretion, which is responsible for GERD, a condition that often precedes oesophageal adenocarcinoma. Peek agrees: “H pylori may induce inflammation within the acid-secreting gastric corpus. This is supported by data showing that severity of gastric inflammation in the corpus is inversely proportional to the
prevalence of GERD.” The role of cag is currently being investigated by de Martel’s group. Considering other research connecting H pylori and cancer, de Martel’s findings are perplexing. This bacterium has been implicated in development of stomach ulcers and cancer. Therefore, although eradicating H pylori would help alleviate these conditions, this course of action may actually increase the risk of another cancer. However, as de Martel points out, “This study does not address the question of eradication. The H pylori-negative individuals included in the study had not been treated for infection, they had never got the bacteria in the first place.” She also emphasises that these results are preliminary and more work is required to establish the exact role of H pylori in oesophageal cancer. Cathel Kerr
Hormone hypersensitivity link to familial breast cancer
THE LANCET Oncology Vol 4 July 2003
stronger with younger age at menarche. In pairs where only one twin had cancer, there was no correlation between early puberty and risk. Intriguingly, in double-cancer twins the researchers found no association between increased risk and later events
Rights were not granted to include this image in electronic media. Please refer to the printed journal. Twins with breast cancer are a genetically high-risk group.
in adulthood, such as parity and menopause, indicating that the association with early puberty may not simply be a consequence of extending the woman’s exposure to menstruation. Instead, Hamilton proposes, “This may indicate some kind of damage to immature breast cells that makes them vulnerable to developing breast cancer later in life”. Although previous studies have
Robert Harding Photo Library
A study of identical twins has shown that development of some types of hereditary breast cancer may be a result of hypersensitivity to hormones—not cumulative exposure as previously thought. “BRCA1 and 2 do not explain the majority of hereditary breast cancers”, says Ann Hamilton, University of Southern California, CA, USA, who, with colleague Thomas Mack, carried out the study. Substantial evidence links long-term hormone exposure to risk of breast cancer, but Hamilton and Mack have identified another pathway linking reproductive hormones and cancer. “The hormone sensitivity of immature breast cells during puberty is crucial”, explains Hamilton. The team set out to investigate whether risk factors for breast cancer differ according to genetic susceptibility. “We determined that identical twins who both have breast cancer represent the subset with the highest susceptibility”, Hamilton recalls. The only factor that seemed to influence development of breast cancer in the first twin was early onset of puberty. Furthermore, the effect seemed to be
shown that early menarche increases risk of breast cancer, Hamilton suggests that this may reflect an averaging effect of a high risk in a genetically susceptible subgroup. “The risk of early menarche for these individuals may actually be much higher”, she says. “We found risk increased five times.” “This work challenges the assumption that reproductive or hormonal risk factors such as age at first pregnancy, number of children, and late menopause, apply equally to the development of all breast cancers”, says Graham Colditz, Harvard Medical School, MA, USA. Previous studies of hereditary breast cancer suggested that familial cases may not be affected by reproductive risk factors. But, says Colditz, “these studies relied on self-reporting and were far less able to untangle the genetic risk”. In Hamilton’s study, however, “clear evidence points to different pathways for breast cancer causation”, he adds. Hamilton and Colditz agree that future application of this work may lead to new approaches to therapy or prevention. Hannah Brown
http://oncology.thelancet.com
For personal use. Only reproduce with permission from The Lancet.
391