Obtaining co-morbidity data for patients may assist in understanding these findings. We have previously demonstrated that our sentinel network adequately describes ILI activity in Victoria. However, we know that ILI patients from whom a nose and throat swab are taken, are not representative of all ILI patients or of all patients notified with influenza. Children were underrepresented in patients from whom a swab was collected in the sentinel practices. Despite its limitations, we have demonstrated that the Victorian sentinel surveillance network is able to provide estimates of influenza VE. We have further compared VE estimates with vaccine and circulating strain matches and, while there were no significant differences in VE across the years, there was some suggestion that VE may be lower in years when the influenza A/ H3N2 subtype is mismatched, perhaps reflecting the fact that infection with the H3N2 subtype is generally more severe in adults. Routine monitoring data of this type will be further interrogated to add value to Thiamine hydrochloride the sentinel surveillance of influenza. Our study is the first to demonstrate that recurrent genetic mutations occur in cervical cancer. An earlier study that examined this question did not identify LKB1 mutations in sporadic cervical cancers, but only minimal deviation adenocarcinomas were analyzed, as the goal of the study was to ascertain LKB1 mutation frequencies in gynecologic malignancies known to be associated with PJS. However, this earlier study, performed prior to the advent of MLPA, identified LOH of the LKB1 19p13.3 region in 3/8 cases, suggesting that LKB1 deletions may have been present. Another study where 26 cervical tumors were analyzed by single-strand conformational polymorphism analysis identified LKB1 mutations in only one case. The discovery of a homozygous LKB1 deletion in HeLa is noteworthy because of the historical significance of this cell line to biomedical research. HeLa was derived in 1951 from a cervical adenocarcinoma. As the first immortalized human cell line isolated and successfully perpetuated in vitro, HeLa greatly accelerated the progress of biomedical research in the second half of the 20th century. HeLa cells were unusual in growing so rapidly in culture,Pyridoxine but the primary tumor was also aggressive. The primary tumor was confined to the cervix at the time of diagnosis, but it metastasized early and widely despite aggressive therapy including radiation treatment, leading to the patient’s death just six months after the initial diagnosis. Our results suggest that the homozygous deletion we have documented within LKB1 contributed to this aggressive growth phenotype, rationalizing some of the unusual features of the HeLa primary tumor and cell line. Consistent with this idea, enforced expression of LKB1 cDNA into HeLa and other HeLa-deficient cell lines induces growth arrest. This is also the first report that LKB1 mutations confer a worse prognosis for a particular human cancer. However, this observations is in line with genetically-engineered mouse models of LKB1 deficiency that have consistently found that Lkb1 loss promotes invasive/metastatic growth. In K-ras driven mouse models of lung cancer, Lkb1 inactivation provided the strongest cooperation in terms of tumor latency and frequency of metastasis.