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1.
Appetite ; 23(1): 43-55, 1994 Aug.
Article in English | MEDLINE | ID: mdl-7826056

ABSTRACT

Past laboratory and field studies show that the effort necessary to obtain food acts as a determinant of food selection and consumption. Two studies examined the impact of increasing the effort needed to obtain candy or potato chips on selection in a normal lunch setting. In the first study, food selection, acceptance and intake were obtained during the first week baseline and under the effort manipulation during the second week. With increased effort, candy selection dropped dramatically in week 2. Subjects substituted items from the desert, fruit and accessory food groups. In the second study, food selection and acceptance were measured during a 2-week baseline, a 3-week effort period, and a 3-week recovery period. With increased effort, potato chip selection dropped dramatically and only partially recovered in the last phase. Subjects substituted items from the starch food group. These results demonstrate that changes in the effort needed to obtain food can have a nutritional impact in an actual eating situation and could be an important part of a healthy eating strategy.


Subject(s)
Diet , Food Preferences , Adolescent , Candy , Food Services , Food Supply , Humans , Nutritional Physiological Phenomena , Universities
2.
Gastroenterology ; 102(1): 230-6, 1992 Jan.
Article in English | MEDLINE | ID: mdl-1309358

ABSTRACT

Activation of the Ki-ras oncogene by specific point mutations at codon 12 occurs at a remarkably high frequency in pancreatic ductal adenocarcinoma and is likely to be an important event in the pathogenesis of this cancer. To determine whether ras activation also occurs in noninvasive proliferative lesions of the pancreas, a series of cases of ductal papillary hyperplasia, intraductal papillary neoplasia, and intraduct extensions of ductal adenocarcinoma were examined for activating mutations of Ki-ras at codons 12, 13, and 61 using polymerase chain reaction amplification. Specific mutations at Ki-ras codon 12 were found in 5 of 6 cases (83%) of intraduct extensions of carcinomas and in 12 of 16 (75%) invasive carcinomas. In cases with both intraductal and invasive components, the same mutation was identified in each. No mutations were found in 5 intraductal papillary neoplasms and 9 cases of ductal papillary hyperplasia. The authors conclude that Ki-ras activation at codon 12 is important in the tumorigenesis of ductal adenocarcinoma of the pancreas but is not required in the pathogenesis of ductal papillary hyperplasia or intraductal papillary neoplasm.


Subject(s)
Carcinoma, Intraductal, Noninfiltrating/genetics , Gene Expression Regulation, Neoplastic , Genes, ras/physiology , Oncogenes/physiology , Pancreatic Neoplasms/genetics , Adult , Aged , Carcinoma, Intraductal, Noninfiltrating/pathology , Female , Humans , Hyperplasia , Male , Middle Aged , Mutation , Neoplasm Invasiveness , Pancreatic Ducts/pathology , Pancreatic Neoplasms/pathology
3.
Br J Cancer ; 64(6): 1076-82, 1991 Dec.
Article in English | MEDLINE | ID: mdl-1764370

ABSTRACT

The tumour suppressor gene p53 has been found to be mutated or inactivated at high frequency in several common human tumours. We have examined a series of exocrine pancreatic carcinomas for over-expression of mutant forms of p53 by immunohistochemistry with a panel of specific antibodies. We found immunodetectable p53 in 13 of 22 (60%) frozen pancreatic cancers and seven of 13 pancreatic cell lines. One of the antibodies, CM1, recognises p53 in formalin-fixed, paraffin-embedded archival material and using this reagent we found immunodetectable p53 in 28 of 124 (23%) pancreatic cancers. We have successfully demonstrated the presence of point mutations by direct sequencing of genomic DNA extracted from archival tissue showing CM1 immunoreactivity. We conclude that p53 activation is an important event in human pancreatic tumorigenesis and that the CM1 antibody can detect a proportion of cases of overexpression of mutant p53 in archival pathological material.


Subject(s)
Genes, Tumor Suppressor , Genes, p53 , Pancreatic Neoplasms/genetics , Tumor Suppressor Protein p53/genetics , Antibodies, Monoclonal , Base Sequence , Blotting, Western , DNA Mutational Analysis , Genes , Humans , Molecular Sequence Data , Oligodeoxyribonucleotides/chemistry , Precipitin Tests , Tumor Cells, Cultured , Tumor Suppressor Protein p53/immunology
4.
Br J Cancer ; 63(2): 227-33, 1991 Feb.
Article in English | MEDLINE | ID: mdl-1671751

ABSTRACT

The expression of the EGF receptor, c-erbB-2 and PDGF receptor proteins has been studied in a series of human brain tumour biopsies and cell lines. Western blotting was used to determine the amount of protein present and their intrinsic and ligand promoted enzyme activities were studied by immunoprecipitation followed by autophosphorylation. EGF receptors were found to be expressed at very high levels in 40% of primary tumour biopsies, but at uniformly low levels in tumour derived cell lines. The c-erbB-2 protein was not detected in tumour biopsies, but was present at variable, but low levels in extracts of tumour cell lines. PDGF receptors were also found at moderate to low levels in both primary tumours and cell lines. The EGF receptor gene was amplified in four out of 14 primary tumours and this generally correlated with high levels of protein expression. The c-erbB-2 gene was not amplified. Employing the polymerase chain reaction and sequence specific oligonucleotides as probes there was no evidence of mutations in the c-erbB-2 gene transmembrane region. These results suggest that alterations of expression of the EGF receptor may play a role in human brain tumours. There was however no evidence for aberrant expression of the c-erbB-2 protein. Additional experiments are required to assess the influence of PDGF receptor expression in brain tumour cells.


Subject(s)
Brain Neoplasms/chemistry , ErbB Receptors/analysis , Brain Neoplasms/genetics , ErbB Receptors/genetics , Gene Amplification , Humans , Proto-Oncogene Proteins/analysis , Proto-Oncogenes , Receptor, ErbB-2 , Receptors, Cell Surface/analysis , Receptors, Cell Surface/genetics , Receptors, Platelet-Derived Growth Factor , Tumor Cells, Cultured/chemistry
5.
Mol Carcinog ; 4(5): 345-9, 1991.
Article in English | MEDLINE | ID: mdl-1910478

ABSTRACT

The gene for the alpha polypeptide chain (alpha s) of the heterotrimeric G protein Gs can be activated to the putative oncogene gsp by specific point mutations at codons 201 and 227. Such mutations have been reported in 40% of human growth hormone-secreting pituitary adenomas and in a single autonomously functioning thyroid adenoma. We examined an archival series of 45 differentiated human thyroid tumors by polymerase chain reaction amplification and oligonucleotide hybridization to identify point mutations at each of the affected codons. Successful amplification was achieved in 38 cases, and activating mutations were identified in 5 of 13 (38%) autonomously functioning adenomas, but in none of 16 nonfunctioning adenomas, six papillary carcinomas, or three follicular carcinomas. Our results confirm that the gsp oncogene is involved in the pathogenesis of autonomously functioning tumors but do not support a role in other thyroid tumors.


Subject(s)
Adenoma/genetics , GTP-Binding Proteins/genetics , Oncogenes , Proto-Oncogene Proteins/genetics , Thyroid Neoplasms/genetics , Alleles , Base Sequence , DNA Mutational Analysis , DNA, Neoplasm/genetics , Humans , Molecular Sequence Data , Oligonucleotide Probes/chemistry , Oligonucleotides/chemistry , Polymerase Chain Reaction
6.
J Pathol ; 161(3): 195-200, 1990 Jul.
Article in English | MEDLINE | ID: mdl-2202801

ABSTRACT

The c-erb B-2 oncogene encodes a 190 kD transmembrane growth factor receptor which is closely related to the EGF receptor and has been found to be amplified and overexpressed in a number of human adenocarcinomas, particularly of the breast. We have analysed, by immunocytochemistry using the 21N antibody, expression of c-erb B-2 in a retrospective series of pancreatic adenocarcinoma, chronic pancreatitis, and examples of histologically normal pancreas. In three cases (21 per cent) of chronic pancreatitis, there were focal areas of cytoplasmic immunoreactivity in regenerating epithelium. In 15 cases (17 per cent) of pancreatic adenocarcinoma, cytoplasmic immunoreactivity was seen, while in two cases (2 per cent) strong membrane staining of tumour cells was seen which could be blocked by peptide controls. c-erb B-2 immunoreactivity was also demonstrated using a second antibody, 20N, which recognizes another peptide sequence of the c-erb B-2 protein. There was no relationship between immunoreactivity and histological subtype or grade, but there was absolute concordance between staining in primary and metastatic deposits. Since the rat homologue (neu) of the c-erb B-2 oncogene may be activated by a specific point mutation in its transmembrane region, we have analysed 23 cases from this series for mutations by polymerase chain reaction amplification and sequence-specific oligonucleotide hybridization. We were unable to identify activity mutations in this series. These data suggest that there is abnormal expression of c-erb B-2 oncogene in nearly 20 per cent of cases although mutational activation of this gene is not seen in human pancreatic adenocarcinoma.


Subject(s)
Adenocarcinoma/genetics , Pancreatic Neoplasms/genetics , Proto-Oncogenes , Base Sequence , Humans , Immunoenzyme Techniques , Molecular Sequence Data , Mutation , Nucleic Acid Hybridization , Polymerase Chain Reaction , Proto-Oncogene Mas , Retrospective Studies
7.
Eur J Cancer ; 26(7): 777-9, 1990.
Article in English | MEDLINE | ID: mdl-2145893

ABSTRACT

The c-erbB-1 and c-erbB-2 proto-oncogenes are frequently activated by gene amplification and overexpression in a variety of human cancers. In an analysis of a large series of benign and malignant thyroid tumours, no abnormalities of structure or expression of either of c-erbB-1 or c-erbB-2 were found. Activation of these oncogenes is not a necessary event in neoplasia of this epithelial system.


Subject(s)
Proto-Oncogenes , Thyroid Neoplasms/genetics , DNA, Neoplasm/analysis , Gene Amplification , Gene Expression , Gene Rearrangement , Humans , Oligonucleotides/analysis
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