Lung cancer is the leading cause of cancer deaths in the United States and worldwide. Biomarker testing is critical to personalized therapy in lung adenocarcinoma and has been extensively investigated in whites and Asians. However, little information addresses the underlying genetic changes among Caribbean and African Caribbean patients. In this study, we identified targetable biomarkers in Caribbean patients with lung adenocarcinoma. DNA extracted from lung adenocarcinoma specimens collected from 157 patients in whom primary lung adenocarcinoma was diagnosed from 2013 to 2015 in the University Hospital of Martinique was tested for mutation of the epidermal growth factor receptor gene (EGFR), Kirsten rat sarcoma viral oncogene homolog gene (KRAS), B-Raf proto-oncogene, serine/threonine kinase gene (BRAF), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha gene (PIK3CA), ROS proto-oncogene 1, receptor tyrosine kinase gene (ROS), and MMNG HOS Transforming gene (MET). Clinical characteristics of our patients have been retrospectively gathered and correlated with mutational status. Mutations in EGFR were identified in 57 cases (36%). Women accounted for 68% of patients with mutations versus 38% of those without mutations (p < 0.001). Eighteen percent of patients with mutations were smokers versus 62% of patients without mutations (p < 0.001). Sex, smoking habit, and age were significantly associated with differences in mutational status in univariate analysis, and the difference remained statistically significant in multivariate analysis (p = 0.0411, p = 0.001, and p = 0.0483, respectively). After the analysis was restricted to patients born in the French West Indies, the mutation rates reached 41%. Patients in Martinique, and specifically those of African descent, show very high levels of EGFR mutation as opposed to what can be found in mainland France or in African Americans. These findings may be ascribed to low tobacco consumption as well as to genetic factors. Systematic screening in patients of African Caribbean origin should be prescribed.
Monitoring and controlling respiratory motion is a challenge for the accuracy and safety of therapeutic irradiation of thoracic tumors. Various commercial systems based on the monitoring of internal or external surrogates have been developed but remain costly. In this article we describe and validate Madibreast, an in‐house‐made respiratory monitoring and processing device based on optical tracking of external markers. We designed an optical apparatus to ensure real‐time submillimetric image resolution at 4 m. Using OpenCv libraries, we optically tracked high‐contrast markers set on patients' breasts. Validation of spatial and time accuracy was performed on a mechanical phantom and on human breast. Madibreast was able to track motion of markers up to a 5 cm/s speed, at a frame rate of 30 fps, with submillimetric accuracy on mechanical phantom and human breasts. Latency was below 100 ms. Concomitant monitoring of three different locations on the breast showed discrepancies in axial motion up to 4 mm for deep‐breathing patterns. This low‐cost, computer‐vision system for real‐time motion monitoring of the irradiation of breast cancer patients showed submillimetric accuracy and acceptable latency. It allowed the authors to highlight differences in surface motion that may be correlated to tumor motion.PACS number(s): 87.55.km
We reinvestigate the relationship between axillary lymph node involvement in breast cancer and the overall risk of death. Patients were women from the Surveillance, Epidemiology, and End Results (SEER) program, aged between 50 and 65 years, presenting a first primary T1-T2 (tumor size ≤5 cm), node-positive, non-metastasized unilateral breast carcinoma, diagnosed from 1988 to 1997, treated with mastectomy without radiotherapy. Hazard ratios (HRs) were computed at each percentage of involved nodes using the proportional hazards model, adjusting for the patient's demographic and tumor characteristics. The pattern of the hazard ratios was examined using serial correlations. Significance testing used the "portmanteau" test. Based on 4,387 records available for analysis, the relation between adjusted mortality and axillary lymph node involvement was modeled as Ht - Ht-1 = μ + at, where t is the percentage of involved nodes, Ht is the mortality hazard ratio at the percentage t, μ is a constant, and at is white noise. The constant μ was estimated at 0.020, corresponding to a 2% increment in the mortality hazard ratio per 1% increase in the percentage of positive nodes. The model was considered acceptable by the "portmanteau" test (P=0.205). We conclude that the effect of the tumor burden might be expressed as a random walk difference model, relating the mortality hazard ratio with the percentage of involved nodes. We will use the model to explore how treatments affect the course of the disease.