Delays in time to treatment and survival impact in breast cancer.

BACKGROUND: Time interval from diagnosis of breast cancer to treatment has been promulgated as one factor that can be used to evaluate cancer care quality. It remains controversial, however, whether a delay to treatment impacts survival. The purpose of this study was to evaluate whether delays from diagnosis to initial treatment in breast cancer impacts survival. MATERIALS AND METHODS: A retrospective review of patients undergoing breast cancer treatment between August 2005 and December 2008 in a comprehensive, multidisciplinary breast oncology program was undertaken. Two hospital systems were included: a county hospital (CH) treating a primarily minority, indigent population and a university hospital (UH) treating a primarily Caucasian, insured population. Interval to treatment, calculated from date of diagnosis to surgery, chemotherapy, or radiation treatment, and overall survival was compared between the two groups. RESULTS: A total of 1337 patients were included; 634 patients were treated in the CH and 703 in the UH. Interval to treatment was longer in the CH compared with the UH (53.4 ± 2.0 vs 33.2 ± 1.2 days; mean ± standard error of the mean [SEM], P < .0001). Patients treated at the CH had overall worse survival (P = .02); however, this difference did not hold true when controlled for stage. Additionally, when time to treatment was analyzed as an individual variable for all patients, there was no impact on survival. CONCLUSIONS: Interval from diagnosis to treatment of breast cancer within the same cancer center was longer at the CH than the UH. There was, however, no effect on overall survival. Time to treatment may not be a meaningful indicator of cancer care quality.

Putative targets of CNS melanocortin receptor activity.

Chronic antagonism of hypothalamic melanocortin receptors, primarily melanocortin-4 receptor (MC4R), is the molecular basis for "agouti obesity syndrome," whereas suppression of MC4R gene activity due to genetic mutations induces obesity in both rodents and humans. However, little is known about the neurocircuitry of MC4R-mediated control of energy balance, the regulation of MC4R gene expression, or how suppression of MC4R activity leads to differential expression of potential downstream central nervous system (CNS) targets or effectors of melanocortin signaling. This paper focuses on strategies for mapping CNS melanocortin circuits using transgenic mouse models for conditional expression of MC4R and MC3R as well as progress in characterizing the murine MC4R promoter. Additionally, preliminary studies that focus on putative targets of melanocortinergic signaling will include a discussion of CD81, a gene identified using the polymerase chain reaction-based method of suppression subtractive hybridization. CD81, first described as TAPA-1 (target of antiproliferative antibody), is a member of the tetraspanin family of cell surface proteins believed to function in cell-cell adhesion, signal transduction, and possibly neuronal plasticity. Elevated expression of CD81 mRNA in hypothalamic regions of obese yellow mice suggests that loss of MC4R activity may lead to altered neuronal function via modulation of the cell surface protein CD81.