ABSTRACT
Recent research conducted in Australia shows that many oncologists withhold information about expensive unfunded drugs in what the authors of the study suggest is unacceptable medical paternalism. Surprised by the Australian results, we ran a version of the study in New Zealand and received very different results. While the percentages of clinicians who would prescribe the drugs described in the scenarios were very similar (73-99% in New Zealand and 72-94% in Australia depending on the scenario) the percentage who would not discuss expensive unfunded drugs was substantially lower in New Zealand (6.4-11.1%) than it was in Australia (28-41%). This seems surprising given the substantial similarities between the two countries, and the extensive interaction between their medical professions. We use the contrast between the two studies to examine the generalisability of the Australian results, to identify influences on clinicians' decisions about what treatment information to give patients, and so the tendency towards medical paternalism and, more pragmatically, about how such decisions might be influenced.
Subject(s)
Antineoplastic Agents/economics , Attitude of Health Personnel , Drug Costs , Medical Oncology/ethics , Paternalism , Antibodies, Monoclonal/economics , Antibodies, Monoclonal, Humanized , Antibodies, Monoclonal, Murine-Derived , Antineoplastic Agents/supply & distribution , Bevacizumab , Dacarbazine/analogs & derivatives , Dacarbazine/economics , Female , Health Services Accessibility , Humans , Male , New Zealand , Patient Education as Topic , Rituximab , TemozolomideSubject(s)
Cost of Illness , Melanoma/prevention & control , Skin Neoplasms/prevention & control , Causality , Comorbidity , Early Diagnosis , Humans , Incidence , Melanoma/diagnosis , Melanoma/epidemiology , New Zealand , Population Surveillance/methods , Skin Neoplasms/diagnosis , Skin Neoplasms/epidemiology , Sunburn/epidemiology , Sunburn/prevention & controlABSTRACT
Hereditary diffuse gastric cancer (HDGC) is a recently defined cancer syndrome caused by inactivating, heterozygous germline mutations in the gene for the cell-to-cell adhesion protein E-cadherin (CDH1). Here, we describe the search for CDH1 mutations in 10 newly identified gastric cancer families. Seven of 10 families met the clinical criteria for HDGC. Germline mutations were identified in four of these seven families and one family that was borderline for the clinical criteria. Of the mutations identified in the five new families, four were previously unreported and consisted of two frameshift and two donor splice site mutations. One splice site mutation occurred at the 100% conserved +1 position. The second splice site mutation occurred at the +5 position and was shown to lead to abnormal splicing. Additional CDH1 variants detected include the heterozygous -160 C-->A promoter polymorphism, which has previously been reported to be associated with decreased CDH1 transcription. We, however, found this polymorphism to be common in a control population, suggesting that a major role for this polymorphism in gastric cancer susceptibility is unlikely.
