ABSTRACT
BACKGROUND: Insurance coverage for family planning services has been a highly controversial element of the US health care reform debate. Whether primary care providers (PCPs) support public and private health insurance coverage for family planning services is unknown. STUDY DESIGN: PCPs in three states were surveyed regarding their opinions on health plan coverage and tax dollar use for contraception and abortion services. RESULTS: Almost all PCPs supported health plan coverage for contraception (96%) and use of tax dollars to cover contraception for low-income women (94%). A smaller majority supported health plan coverage for abortions (61%) and use of tax dollars to cover abortions for low-income women (63%). In adjusted models, support of health plan coverage for abortions was associated with female gender and internal medicine specialty, and support of using tax dollars for abortions for low-income women was associated with older age and internal medicine specialty. CONCLUSION: The majority of PCPs support health insurance coverage of contraception and abortion, as well as tax dollar subsidization of contraception and abortion services for low-income women.
Subject(s)
Abortion, Legal/economics , Attitude of Health Personnel , Contraception/economics , Family Planning Services/economics , Health Care Costs , Insurance, Health, Reimbursement , Physicians, Primary Care/psychology , Age Factors , Female , Health Care Surveys , Humans , Internet , Male , Medical Assistance , National Health Insurance, United States , Oregon , Pennsylvania , Poverty , Pregnancy , Rhode Island , Sex Characteristics , United StatesABSTRACT
Cholecystokinin (CCK) and gastrin stimulate growth of pancreatic cancer. Although down-regulation of gastrin inhibits growth of pancreatic cancer, the contribution of endogenous CCK to tumor growth is unknown. The purpose of this study was to evaluate the role of endogenous CCK on autocrine growth of pancreatic cancer. Pancreatic cancer cell lines were analyzed for CCK mRNA and peptide expression by real-time RT-PCR and radioimmunoassay, respectively. The effect of endogenous CCK on growth was evaluated by treating cancer cells with CCK neutralizing antibodies and by down-regulating CCK mRNA by RNAi. Wild-type pancreatic cancer cells expressed significantly lower CCK mRNA and peptide levels than gastrin. Neither treatment of pancreatic cancer cells with CCK antibodies nor the down-regulation of CCK mRNA and peptide by shRNAs altered growth in vitro or in vivo. Conversely, when gastrin mRNA expression was down-regulated, the same cells failed to produce tumors in spite of having sustained levels of endogenous CCK. Pancreatic cancer cells produce CCK and gastrin; however, the autocrine production of gastrin is more important for stimulating tumor growth.
Subject(s)
Adenocarcinoma/pathology , Cell Proliferation , Cholecystokinin/physiology , Pancreatic Neoplasms/pathology , Adenocarcinoma/genetics , Adenocarcinoma/metabolism , Animals , Antibodies, Neutralizing/pharmacology , Autocrine Communication/drug effects , Autocrine Communication/genetics , Autocrine Communication/physiology , Cell Line, Tumor , Cell Proliferation/drug effects , Cholecystokinin/genetics , Cholecystokinin/immunology , Cholecystokinin/metabolism , Gastrins/analysis , Gastrins/genetics , Gastrins/metabolism , Gastrins/pharmacology , Gene Expression Regulation, Neoplastic/drug effects , Humans , Male , Mice , Mice, Nude , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/metabolism , RNA, Messenger/analysis , RNA, Messenger/metabolism , RNA, Small Interfering/pharmacology , Tissue Distribution , Xenograft Model Antitumor AssaysABSTRACT
The gastrointestinal peptides gastrin and cholecystokinin (CCK) stimulate growth of human pancreatic cancer by a receptor-mediated process. The purpose of this study was to investigate the molecular and functional characteristics of the receptor associated with peptide-induced pancreatic cancer proliferation. Utilizing total RNA from human pancreatic cancer cells a cDNA was cloned and sequenced by RT-PCR and rapid amplification of cDNA ends methodology. The molecular characteristics of the receptor cDNA were studied by Northern analysis and protein structure by Western analysis. An antibody raised against the novel receptor was utilized to investigate the role of the CCK-C receptor on pancreatic cancer cellular growth using in vitro technology. A spliced variant of the CCK-B receptor was identified which differed from the CCK-B receptor by the presence of intron 4. Northern analysis showed a transcript size of 3.2 Kb for the receptor mRNA in the human pancreatic cancer specimens, and Western blotting revealed binding to a 49 kDa protein in pancreatic tumors. Immunoreactivity was found in pancreatic cancer cells and tumors with localization in the cytoplasm. Treatment of BxPC-3 human cancer cells with the antibody resulted in growth inhibition. These data reveal the presence of a unique CCK receptor in human pancreatic cancer that functions in growth and is not present in normal human pancreas. The term CCK-C or 'cancer' receptor has been proposed to signify the relationship of this receptor to neoplasia.
