Abstract. Although infrequent, shark attacks attract a high level of public and media interest, and often have serious consequences for those attacked. Data from the Australian Shark Attack File were examined to determine trends in unprovoked shark attacks since 1900, particularly over the past two decades. The way people use the ocean has changed over time. The rise in Australian shark attacks, from an average of 6.5 incidents per year in 1990-2000, to 15 incidents per year over the past decade, coincides with an increasing human population, more people visiting beaches, a rise in the popularity of water-based fitness and recreational activities and people accessing previously isolated coastal areas. There is no evidence of increasing shark numbers that would influence the rise of attacks in Australian waters. The risk of a fatality from shark attack in Australia remains low, with an average of 1.1 fatalities year À1 over the past 20 years. The increase in shark attacks over the past two decades is consistent with international statistics of shark attacks increasing annually because of the greater numbers of people in the water.

Approximately 100 cases of angiosarcoma following breast-conserving therapy have been reported. The prevalence of angiosarcoma following breast conservation has not been accurately established and optimal treatment has not been defined. The goal of this article is to clarify both issues. The Fisher's exact test was used to compare the prevalence of postirradiation angiosarcoma seen in our private practice to the prevalence reported from the two largest national database studies. A literature review was performed to determine optimal treatment guidelines. The results of the comparison indicated that the prevalence of postirradiation angiosarcoma seen in our practice was significantly higher than that reported in the two national database studies at p-values of 0.0124 and 0.0080. Also, results from the literature review suggest that early detection and aggressive treatment lead to improved outcomes. The data are insufficient to draw firm conclusions, but suggest that the current literature underestimates the prevalence of angiosarcoma following breast-conserving therapy. Since elderly women derive less benefit from radiation and may be more prone to develop postirradiation angiosarcoma, confirmation of our findings could lead to a reappraisal of the management of elderly patients with early stage breast cancer.

Breast cancer risk has been hypothesized to increase with exposure to heterocyclic aromatic amines (HAAs) formed from cooking meat at high temperature. HAAs require enzymatic activation to bind to DNA and initiate carcinogenesis. N-acetyltransferase 2 (NAT2) enzyme activity may play a role, its rate determined by a polymorphic gene. We examined the effect of NAT2 genetic polymorphisms on breast cancer risk from exposure to meat by cooking method, doneness and estimated HAA [2-amino-1-methyl-6-phenylimidazole[4,5-b]pyridine (PhIP), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx)] intake. Women were recruited with suspicious breast masses and questionnaire data were collected prior to biopsy to blind subjects and interviewers to diagnoses. For 114 cases with breast cancer and 280 controls with benign breast disease, NAT2 genotype was determined using allele-specific PCR amplification to detect slow acetylator mutations. HAAs were estimated from interview data on meat type, cooking method and doneness, combined with a quantitative HAA database. Logistic regression models controlled for known risk factors, first including all controls, then 108 with no or low risk (normal breast or no hyperplasia) and finally 149 with high risk (hyperplasia, atypical hyperplasia, complex fibroadenomas). Meat effects were examined within NAT2 strata to assess interactions. We found no association between NAT2 and breast cancer. These Californian women ate more white than red meat (control median 46 versus 8 g/day). There were no significant associations of breast cancer with red meat for any doneness. White meat was significantly protective (>67 versus <26 g/day, OR 0.46, 95% CI 0.23-0.94, P for trend = 0.02), as was chicken, including well done, pan fried and barbecued chicken. MeIQx and DiMeIQx were not associated with breast cancer. A protective effect of PhIP was confounded after controlling for well done chicken. Results were unchanged using low or high risk controls or dropping 30 in situ cases. There was no interaction between NAT2 and HAAs. These findings do not support a role for HAAs from meat or NAT2 in the etiology of breast cancer. Further research is needed to explain the white meat association.

Multigene panel testing detects pathogenic BRCA1/2 mutations at equivalent rates as limited testing and increases the diagnostic yield. Panel testing increases the VUS rate, mainly as a result of non-BRCA genes. Patients at risk for hereditary breast cancer can safely benefit from up-front, more efficient, multigene panel testing.

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The relationship of breast cancer to cigarette smoking is inconsistent in the literature, possibly due in part to heterogeneity in carcinogen metabolism. N-acetyltransferase 2 (NAT2) enzyme activity is believed to play a role in the activation of tobacco smoke carcinogens. We examined the effect of NAT2 genetic polymorphisms on risk of breast cancer from active and passive smoking. Women were recruited from those who had suspicious breast masses detected clinically and/or mammographically. Questionnaire data were collected prior to biopsy diagnosis to blind subjects and interviewers. Histopathology showed 113 cases with mammary carcinoma (30 carcinoma in situ) and 278 controls with benign breast disease. NAT2 genotype was determined using allele-specific polymerase chain reaction amplification to detect slow acetylator mutations. Effects of passive and active tobacco smoke and of NAT2 genotype on breast cancer risk were examined with logistic regression controlling for known risk factors. Models first included all controls, and subsequently 107 with no or low risk (normal breast or no hyperplasia), and finally 148 with high risk (hyperplasia, atypical hyperplasia, complex fibroadenomas). Referents had no active or passive smoke exposure. We found no association between breast cancer risk and NAT2, smoking status (never, former, current), smoking duration, or cigarettes per day. There were no effects of passive exposure among never-smokers. Models were unchanged across control groups. There were no statistical interactions between tobacco smoke exposure and NAT2. The results were similar when restricting the analysis to invasive cancers. These findings do not support the hypothesis that NAT2 is a risk factor for breast cancer or that it alters susceptibility to tobacco smoke.

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