Axillary ultrasonography for early-stage invasive breast cancer.

BACKGROUND: Among women with early invasive breast cancer and 1-2 positive sentinel nodes, sentinel lymph node biopsy (SLNB) is non-inferior to axillary lymph node dissection (ALND).1-3 However, preoperative axillary ultrasonography (AxUS) may not be sensitive enough to discriminate burden of nodal metastasis in these patients, potentially leading to overtreatment.4-6 This study compares axillary operation rates in patients who did and did not receive preoperative AxUS, assessing its utility and risks for overtreatment. METHODS: This is a retrospective cohort study of patients with clinical T1/T2 breast tumors who were clinically node negative and underwent an axillary operation. RESULTS: Patients who had preoperative AxUS received more ALND compared to patients who did not (5.6% vs. 1.4%, p â€‹< â€‹0.001). There was no significant difference in the number of additional axillary operations following SLNB (2.1% vs. 2.3%, p â€‹= â€‹0.77). CONCLUSION: Eliminating preoperative AxUS is associated with fewer invasive ALND procedures, without increased rate of axillary reoperations.

A conserved SREBP-1/phosphatidylcholine feedback circuit regulates lipogenesis in metazoans.

Sterol regulatory element-binding proteins (SREBPs) activate genes involved in the synthesis and trafficking of cholesterol and other lipids and are critical for maintaining lipid homeostasis. Aberrant SREBP activity, however, can contribute to obesity, fatty liver disease, and insulin resistance, hallmarks of metabolic syndrome. Our studies identify a conserved regulatory circuit in which SREBP-1 controls genes in the one-carbon cycle, which produces the methyl donor S-adenosylmethionine (SAMe). Methylation is critical for the synthesis of phosphatidylcholine (PC), a major membrane component, and we find that blocking SAMe or PC synthesis in C. elegans, mouse liver, and human cells causes elevated SREBP-1-dependent transcription and lipid droplet accumulation. Distinct from negative regulation of SREBP-2 by cholesterol, our data suggest a feedback mechanism whereby maturation of nuclear, transcriptionally active SREBP-1 is controlled by levels of PC. Thus, nutritional or genetic conditions limiting SAMe or PC production may activate SREBP-1, contributing to human metabolic disorders.