Oncologist use of the Adjuvant! model for risk communication: a pilot study examining patient knowledge of 10-year prognosis

<p>Abstract</p> <p>Background</p> <p>Our purpose was to collect preliminary data on newly diagnosed breast cancer patient knowledge of prognosis before and after oncology visits. Many oncologists use a validated prognostic software model, Adjuvant!, to estimate 10-year recurrence and mortality outcomes for breast cancer local and adjuvant therapy. Some oncologists are printing Adjuvant! screens to use as visual aids during consultations. No study has reported how such use of Adjuvant! printouts affects patient knowledge of prognosis. We hypothesized that Adjuvant! printouts would be associated with significant changes in the proportion of patients with accurate understanding of local therapy prognosis.</p> <p>Methods</p> <p>We recruited a convenience sample of 20 patients seen by 2 senior oncologists using Adjuvant! printouts of recurrence and mortality screens in our academic medical center. We asked patients for their estimates of local therapy recurrence and mortality risks and counted the number of patients whose estimates were within ± 5% of Adjuvant! before and after the oncology visit, testing whether pre/post changes were significant using McNemar's two-sided test at a significance level of 5%.</p> <p>Results</p> <p>Two patients (10%) accurately estimated local therapy recurrence and mortality risks before the oncology visit, while seven out of twenty (35%) were accurate afterwards (p = 0.125).</p> <p>Conclusion</p> <p>A majority of patients in our sample were inaccurate in estimating their local therapy recurrence and mortality risks, even after being shown printouts summarizing these risks during their oncology visits. Larger studies are needed to replicate or repudiate these preliminary findings, and test alternative methods of presenting risk estimates. Meanwhile, oncologists should be wary of relying exclusively on Adjuvant! printouts to communicate local therapy recurrence and mortality estimates to patients, as they may leave a majority of patients misinformed.</p

Antiangiogenic therapy for breast cancer

Angiogenesis is an important component of cancer growth, invasion and metastasis. Therefore, inhibition of angiogenesis is an attractive strategy for treatment of cancer. We describe existing clinical trials of antiangiogenic agents and the challenges facing the clinical development and optimal use of these agents for the treatment of breast cancer. Currently, the most promising approach has been the use of bevacizumab, a humanized monoclonal antibody directed against the most potent pro-angiogenic factor, vascular endothelial growth factor (VEGF). Small molecular inhibitors of VEGF tyrosine kinase activity, such as sorafenib, appear promising. While, the role of sunitinib and inhibitors of mammalian target of rapamycin (mTOR) in breast cancer has to be defined. Several unanswered questions remain, such as choice of drug(s), optimal duration of therapy and patient selection criteria

Vascular Targeted Agents for the Treatment of Angiosarcoma

Background: Angiogenesis is the process of new blood vessel formation, and is regulated by angiogenic growth factors including vascular endothelial growth factor (VEGF). Angiosarcomas are rare, aggressive vascular tumours. Studies were performed to investigate the expression of angiogenic growth factors in angiosarcoma, and to assess vascular targeted agents for the treatment of angiosarcoma. Methods: In vitro studies compared two human cutaneous angiosarcoma cell lines (ASM and ISO-HAS) with human dermal microvascular endothelial cells (HuDMECs). The cell lines were compared in functional assays, including cell viability, cell differentiaiton and cell migration assays, and protein expression profiled using antibody arrays. Cell responses to vascular targeted agents were compared, including response to bevacizumab an anti-VEGF antibody, axitinib a VEGF receptor (VEGFR) tyrosine kinase inhibitor, selumetinib a MEK inhibitor, and DMXAA a vascular disrupting agent. Immunohistochemistry studies measured the expression of angiogenic growth factors in angiosarcoma tumour specimens using benign vascular lesions for comparison, and assessed canine angiosarcoma as a model of human angiosarcoma. Results: ASM and ISO-HAS demonstrated accelerated growth kinetics, chaotic tubule formation, and increased cell migration compared to HuDMECs. ASM and ISO-HAS expressed significantly increased VEGF compared to HuDMECs. Only minor responses were observed to VEGF targeted agents in functional assays despite western blot studies that showed target inhibition of VEGFR2 phosphorylation,. Striking responses were seen however to selumetinib and DMXAA. Immunohistochemistry studies demonstrated benign and malignant vascular tumours expressed a range of pro-angiogenic growth factors, however analysis did not distinguish malignant from benign vascular tumours. The morphology of canine angiosarcoma was similar to human angiosarcoma. VEGF and VEGFR2 expression was significantly increased in canine angiosarcoma compared to benign vascular lesions. Conclusion: These studies predict limited in vivo angiosarcoma tumour response to VEGF targeted agents. Selumetinib and DMXAA are suggested for further study. Canine angiosarcomas represent a potential model of human angiosarcoma to be explored in future studies