27 research outputs found
Does shear wave ultrasound independently predict axillary lymph node metastasis in women with invasive breast cancer?
Shear wave elastography (SWE) shows promise as an adjunct to greyscale ultrasound examination in assessing breast masses. In breast cancer, higher lesion stiffness on SWE has been shown to be associated with features of poor prognosis. The purpose of this study was to assess whether lesion stiffness at SWE is an independent predictor of lymph node involvement. Patients with invasive breast cancer treated by primary surgery, who had undergone SWE examination were eligible. Data were retrospectively analysed from 396 consecutive patients. The mean stiffness values were obtained using the Aixplorer(®) ultrasound machine from SuperSonic Imagine Ltd. Measurements were taken from a region of interest positioned over the stiffest part of the abnormality. The average of the mean stiffness value obtained from each of two orthogonal image planes was used for analysis. Associations between lymph node involvement and mean lesion stiffness, invasive cancer size, histologic grade, tumour type, ER expression, HER-2 status and vascular invasion were assessed using univariate and multivariate logistic regression. At univariate analysis, invasive size, histologic grade, HER-2 status, vascular invasion, tumour type and mean stiffness were significantly associated with nodal involvement. Nodal involvement rates ranged from 7 % for tumours with mean stiffness <50 kPa to 41 % for tumours with a mean stiffness of >150 kPa. At multivariate analysis, invasive size, tumour type, vascular invasion, and mean stiffness maintained independent significance. Mean stiffness at SWE is an independent predictor of lymph node metastasis and thus can confer prognostic information additional to that provided by conventional preoperative tumour assessment and staging
Breast reconstruction after neoadjuvant radio chemotherapy: review and personal technique IDEAL concept
Diffuse glioma growth: a guerilla war
In contrast to almost all other brain tumors, diffuse gliomas infiltrate extensively in the neuropil. This growth pattern is a major factor in therapeutic failure. Diffuse infiltrative glioma cells show some similarities with guerilla warriors. Histopathologically, the tumor cells tend to invade individually or in small groups in between the dense network of neuronal and glial cell processes. Meanwhile, in large areas of diffuse gliomas the tumor cells abuse pre-existent “supply lines” for oxygen and nutrients rather than constructing their own. Radiological visualization of the invasive front of diffuse gliomas is difficult. Although the knowledge about migration of (tumor)cells is rapidly increasing, the exact molecular mechanisms underlying infiltration of glioma cells in the neuropil have not yet been elucidated. As the efficacy of conventional methods to fight diffuse infiltrative glioma cells is limited, a more targeted (“search & destroy”) tactic may be needed for these tumors. Hopefully, the study of original human glioma tissue and of genotypically and phenotypically relevant glioma models will soon provide information about the Achilles heel of diffuse infiltrative glioma cells that can be used for more effective therapeutic strategies
Análise dos determinantes que influenciam o tempo para o início do tratamento de mulheres com câncer de mama no Brasil
The effect of immediate breast reconstruction on the timing of adjuvant chemotherapy: a systematic review
Failure to define low back pain as a disease or an episode renders research on causality unsuitable: results of a systematic review
Opportunities for Maintenance of Certification to Better Reflect Scope of Practice Among Medical Oncologists
Abstract P1-13-05: The association between timing in adjuvant chemotherapy administration and overall survival for women with breast cancer within the National Comprehensive Cancer Network (NCCN)
Abstract
Introduction: Population based studies (eg, Hershman et al. BCRT 2006 and Lohrisch et al. JCO 2006) showed poorer survival associated with long delays in adjuvant chemotherapy (CTX) initiation following definitive surgery (DS) for women with breast cancer (BC). Delays in CTX following diagnosis (DX) have not been evaluated. The ASCO/NCCN quality measures (QMs) recommend CTX &lt;=120 days after DX for patients with stage II/III ER/PR negative disease. We sought to examine the impact of delayed CTX on survival overall and stratified by disease-specific prognostic factors.
Methods: 4,608 women with stage I-III HER2 negative breast cancer diagnosed between 2000 and 2006 at 8 NCCN centers were identified using the NCCN outcomes database. Patients with T3/4 disease or who received neoadjuvant therapy were excluded. The association between CTX timing and OS was evaluated using multivariate Cox models adjusted for CTX type, age, race, BMI, residential distance, insurance, SES, comorbidity, ER/PR, LVI, grade, T stage, and N stage. The impact of CTX timing was evaluated using a &gt;90-day (d) DS-to-CTX threshold, based on poor outcomes observed in prior studies, and a &gt;120d DX-to-CTX threshold, based on the ASCO/NCCN QMs.
Results: Median follow-up was 7.2 years and OS at 7 years was 89%. Overall, 401 (8.7%) patients received CTX &gt;120d after DX and 113 (2.4%) patients received CTX &gt;90d after DS. The DX-to-CTX interval was more strongly correlated with the DX-to-DS (r = 0.74) interval than DS-to-CTX (r = 0.54) interval. A &gt;90d DS-to-CTX interval was significantly associated with poorer survival (HR: 1.65, 95% CI 1.04–2.60, p = 0.03) in adjusted analyses. Shorter DS-to-CTX thresholds of &gt;60d (n = 636, HR: 1.13, 95% CI: 0.89–1.43, p = 0.319) or &gt;75d (n = 273, HR: 1.05, 95% CI 0.74–1.49, p = 0.76) were not associated with OS. The association between a &gt;120d DX-to-CTX interval and OS was not statistically significant (HR: 1.32, 95% CI 0.99–1.76, p = 0.06). Patients who received CTX &gt;135d (n = 231, HR 1.25, 95% CI: 0.87–1.81, p = 0.22) or &gt;150d (n = 128, HR 1.15, 95% CI: 0.59–2.24, p = 0.69) after DX did not display an increased risk of death. Excluding pathological staging factors from the model had no effect on the results. In subgroup analyses stratified by ER/PR, LVI, grade, T stage or N stage, a &gt;120d delay in CTX did not display significant associations with OS. Among ER/PR negative patients, the association between a &gt;120d delay and OS was borderline non-significant after adjusting the p-value for multiple hypothesis testing using the false discovery rate method (HR: 1.80, 95% CI: 1.16–2.79, p = 0.09).
Conclusion: Consistent with previous studies, CTX delays of &gt;90 days following surgery were associated with poorer survival. OS was not significantly compromised in patients with DX-to-CTX intervals &gt;120 days although this analysis may have limited power to detect small effects. More variation in the DX-to-CTX interval was attributed to pre-surgery time which may explain the differences observed between the DX-to-CTX and DS-to-CTX intervals. Among patients with ER/PR negative disease, a non-significant association between OS and a &gt;120 day DX-to-CTX interval was observed that warrants further examination.
Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-13-05.</jats:p
Biomechanical load evaluation by means of wearable devices in industrial environments: An inertial motion capture system and semg based protocol
Biomechanical overload is one of the main risk factors for musculoskeletal disorders among manufacturing workers and so far, it has been evaluated with observational methods. The aim of this research was to introduce a procedure for quantitative biomechanical overload risk assessment in which surface electromyography integrates with a motion capture system. The paper deals with actual test cases performed in an automotive company, using surface electromyography and a homemade inertial motion capture system. The quality of the data produced by it demonstrates that these devices can be integrated, worn in actual working conditions and are not influenced by electromagnetic interference
