BACKGROUND Circulating tumor DNA (ctDNA) carries information on tumor burden. However, the mutation spectrum is different among tumors. This study was designed to examine the utility of ctDNA for monitoring tumor burden based on an individual mutation profile. METHODOLOGY DNA was extracted from a total of 176 samples, including pre- and post-operational plasma, primary tumors, and peripheral ...

OBJECTIVES Results from the phase 3 Metastatic Pancreatic Adenocarcinoma Clinical Trial (MPACT) led to approval of nab-paclitaxel plus gemcitabine for first-line treatment of metastatic pancreatic cancer. The current analysis evaluated the effects of nab-paclitaxel plus gemcitabine versus gemcitabine on primary pancreatic and metastatic lesions. METHODS In this analysis of the previously desc...

The only therapy with the potential for complete cure of patients with gastroenteropancreatic neuroendocrine tumors is complete surgical excision. Surgical options per se are often dictated by the tumor's site of origin, degree of tumor burden, and overall health or debility of the individual patient. This article considers different options based on the type of tumor and site of origin.

larger tumor burden leads to higher serum ca-125 levels and the ability to perform optimal tumor cytoreduction of advanced ovarian cancer is also a function of tumor bulk. the purpose of this study was to identify the ability of preoperative serum ca-125 to predict possibility of optimal primary tumor cytoreduction in epithelial ovarian carcinoma (eoc). a total of 90 patients with eoc were eval...

Survival from cancer depends primarily on reduction of tumor burden through surgery chemotherapy and radiotherapy. But other factors such as energy levels, immunity and will to live have long been known to play a part. Some of these factors are best provided by complementary therapy. Our program, educational in nature, attempts to make these modalities available to the patient.

BRAF mutations in aggressive melanomas result in kinase activation. BRAF inhibitors reduce BRAF(V600E) tumors, but rapid resistance follows. In this issue of the JCI, Ma and colleagues report that vemurafenib activates ER stress and autophagy in BRAF(V600E) melanoma cells, through sequestration of the ER chaperone GRP78 by the mutant BRAF and subsequent PERK activation. In preclinical studies, ...