TIN+/-V still represents a very major concern for patients. Uncontrolled TIN+/-V often results in significant appetite and weight loss, leading to increased risk for malnutrition. Malnutrition and weight loss, in turn, are associated with poorer prognosis, treatment tolerance and response, performance status, QoL and survival. Consequently, a multiple symptom intervention approach focusing on N&V as core symptoms is recommended. Clinicians should genuinely consider combining essential antiemetic therapies with other evidence-based pharmacological (e.g. nausea: psychotropics, such as olanzapine) and non-pharmacological approaches (e.g. N&V: relaxation) in attempts to not only improve prevention and control of N&V for their patients, but also reduce the synergistic impact of cluster symptoms (e.g. N&V, appetite loss) as a whole and resultant QoL impairment likewise. Where associated symptoms are not adequately controlled by these antiemetic-based interventions, targeted evidence-based strategies should be supplemented.

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Understanding the unmet needs of cancer patients is important for developing and refining services to address the identified gaps in cancer care. In order to describe the psychological and practical support needs of Western Australians with cancer, the Western Australian Cancer Registry was used to identify a sample of individuals with cancer. These individuals were then invited to complete the Supportive Care Needs Survey (SCNS-LF59) and a demographic questionnaire. Data from participants who completed and returned both questionnaires were analysed using descriptive statistics, chi-square tests and one-way anova. Of the 1770 participants identified and contacted, a total of 829 individuals (47% response) completed the SCNS-LF59 alone, and 786 (94.8%) completed both questionnaires. Overall, a substantial minority of Western Australian cancer patients reported unmet needs, primarily in the psychological and physical and daily living domains. Disease-specific needs were also identified for the five most common cancer groups in Australia; for example, prostate cancer patients had unmet needs relating to sexuality, and melanoma patients had unmet informational needs. Cancer services need to look at how best to tailor resources and interventions to meet these needs of specific cancer subpopulations.

We showed earlier that routine screening for microsatellite instability (MSI) and loss of mismatch repair (MMR) protein expression in colorectal cancer (CRC) led to the identification of previously unrecognized cases of Lynch syndrome (LS). We report here the results of screening for LS in Western Australia (WA) during 1994-2012. Immunohistochemistry (IHC) for loss of MMR protein expression was performed in routine pathology laboratories, while MSI was detected in a reference molecular pathology laboratory. Information on germline mutations in MMR genes was obtained from the state's single familial cancer registry. Prior to the introduction of routine laboratory-based screening, an average of 2-3 cases of LS were diagnosed each year amongst WA CRC patients. Following the implementation of IHC and/or MSI screening for all younger (<60 years) CRC patients, this has increased to an average of 8 LS cases diagnosed annually. Based on our experience in WA, we propose three key elements for successful population-based screening of LS. First, for all younger CRC patients, reflex IHC testing should be carried out in accredited pathology services with ongoing quality control. Second, a state-or region-wide reference laboratory for MSI testing should be established to confirm abnormal or suspicious IHC test results and to exclude sporadic cases by carrying out BRAF mutation or MLH1 methylation testing. Finally, a state or regional LS coordinator is essential to ensure that all appropriate cases identified by laboratory testing are referred to and attend a Familial Cancer Clinic for followup and germline testing.Lynch syndrome (LS), formerly known as hereditary nonpolyposis colorectal cancer (HNPCC), is an autosomal dominant condition caused by germline mutations in DNA mismatch repair (MMR) genes, most commonly MLH1, MSH2, MSH6, and PMS2.1,2 Tumours from LS cases have a defective DNA mismatch repair system, leading to ubiquitous small deletions and insertions in DNA repeat regions (microsatellites) resulting in microsatellite instability (MSI). MSI is almost always accompanied by the loss of expression of MMR proteins that can be readily detected using immunohistochemical (IHC) methods. These two molecular features are also observed in approximately 10% of sporadic (nonhereditary) colorectal cancer (CRC), meaning they are not completely specific markers for the presence of LS. However, sporadic microsatellite-unstable (MSI1) CRC contains mutations in the BRAF oncogene and often shows methylation of the MLH1 gene promoter, whereas MSI1 CRC from LS patients does not.3,4 Hence, the BRAF mutation and MLH1 methylation tests can be used to distinguish sporadic from LS-associated MSI1 CRC.In addition to CRC, LS is also associated with an increased risk of endometrial, small bowel, urothelial, gastric, ovarian, and other cancer types. Although some authors have reported that LS may be responsible for up to 3% of CRC, 5,6 population data derived from MSI screening suggested this

Adding stage to routinely collected information in a cancer registry is possible for many cancer types, particularly if the assumptions regarding missing data are found to be acceptable or if the guidelines for MX = M0 assumptions are clarified. These findings should be generalizable to most cancer registries in developed countries, if hospital-based cancer registries or other specialized databases are accessible.