CLINICAL ONCOLOGY JOHN E. NIEDERHUBER, MD Executive Vice President, Inova Health System President and CEO, Genomics and Bioinformatics Research Institute Fairfax, Virginia; Professor, Department of Public Health Sciences Member, Center for Public Health Genomics University of Virginia School of Medicine Charlottesville, Virginia; Adjunct Professor, Oncology and Surgery The Johns Hopkins University School of Medicine Deputy Director Johns Hopkins Clinical Research Network Baltimore, Maryland
JAMES O. ARMITAGE, MD Joe Shapiro Professor of Medicine University of Nebraska Medical Center Omaha, Nebraska MICHAEL B. KASTAN, MD, PhD Executive Director, Duke Cancer Institute William and Jane Shingleton Professor, Pharmacology and Cancer Biology Professor of Pediatrics Duke University School of Medicine Durham, North Carolina
Notices Abeloff’s Clinical Oncology 2020 6th Edition pdf
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Part I: Science Science and Clinical Clinical Oncology
different protein fused to the activation domain of a transcriptional activator (prey) are expressed together in yeast cells. If the bait and prey interact, transcription of a reported gene is induced and detected typically by a color reaction that reflects the transactivation of the reporter gene, and by proxy, the interaction of the two test proteins. The method can also be used for large-scale protein interactions, determination of RNA-protein interactions, and proteinligand binding. As a complementary proteomics tool, mass spectrometry (MS) is an accurate mass measurement of charged peptides isolated by twodimensional gel electrophoresis, producing a mass-to-charge ratio of charged samples under vacuum that can be used to determine the sequence identity of peptides. Combined with a specific proteolytic cleavage step, mass spectroscopy can be used for peptide mass mapping. Automation of this process has made mass spectroscopy the analytic tool of choice for many proteomics projects. For diagnostic purposes, liquid chromatography and mass spectrometry (LC-MS/MS) have been combined to detect not only a single–amino acid change in the whole proteome, but also posttranslational protein modification such
Part II: Problems Problems Common to Cancer and Therapy
MANAGEMENT OF COLORECTAL METASTASES Liver metastases develop in half of patients with colorectal cancer. Unfortunately, approximately 80% of these patients have unresectable disease at the time of presentation.8,40 If no further treatment is offered, the median survival for patients with unresectable liver metastases from colorectal cancer is generally poor, with roughly a 30% 1-year survival rate and a 0% to 5% 5-year survival rate (Table 58.2).8,41,42 Several studies have demonstrated that patients with resectable liver metastases who do not undergo surgery fare slightly better, with 1-year survival rates ranging between 20% and 80% and median survival rates ranging from 10.6 to 21 months. A retrospective analysis of 484 patients with untreated colorectal liver metastases identified six independent determinants of survival at multivariable analysis. The strongest predictive factor was percentage of metastatic liver tumor burden. The remaining significant factors were primary tumor grade, extrahepatic disease, mesenteric lymph node involvement, serum carcinoembryonic antigen (CEA) level, and age.41 Survival is significantly improved in patients with resectable liver metastases who do undergo surgery and should be discussed with all patients; this will be further detailed in subsequent sections. Survival Rate Prediction Survival for patients with metastatic colorectal cancer has significantly improved in the past decade with the advent of improved local and systemic treatment options and the increased use of resection. As surgical management of liver metastases has become more aggressive, long-term survival and even cure are now possible. Over the past two decades, in series of patients who have undergone resection of colorectal liver metastases, 5-year survival rates of 25% to