Biomedical subjects

C J Lips

Publications and source records attributed to C J Lips.

148 records · Page 9Linked to original sources

PubMedDate not supplied

Calcitonin gene-related peptide in human obesity.

We studied plasma calcitonin gene-related peptide (CGRP) levels in obese women before (n = 24) and after (n = 13) weight loss, and in normal weight controls (n = 15). Furthermore, the influence of two isocaloric meals (high carbohydrate vs. high fat) on plasma CGRP concentrations was studied. The CGRP concentration in the obese group (32.26 +/- 2.01 pg/ml) was significantly (p less than 0.0001) higher than in the control group (21.64 +/- 0.15 pg/ml). After weight loss (14.3 +/- 0.72% of original weight) CGRP concentrations remained unchanged. Only the high-fat meal caused a significant (p less than 0.02) rise in CGRP levels. Our results indicate that elevated plasma CGRP levels may constitute a primary phenomenon in obese women, and that fat intake may be associated with increased CGRP secretion.

Adult↗

PubMedDate not supplied

Psychological risks of genetically testing children for a hereditary cancer syndrome.

Parents in families with a hereditary cancer syndrome are often familiar with periodical clinical testing of both themselves and their children. Genetic testing is an additional early diagnostic option that is becoming available for an increasing number of hereditary cancer syndromes. Participants in genetic counseling programs for cancer syndromes are often parents who apply for their children. If a child is identified as a carrier of a specific disease-causing gene mutation, sometimes its parents must decide on when it will be treated can treatment be postponed until expression of the disease or should the child receive presymptomatic surgery? We discuss some of the possible risks of genetically testing children: distress as a result of ambivalent feelings towards testing, preoccupation with disease-related signs, changes in family interactions, the burdening prospect of a future disease and medicalization of the carrier-child.

Child↗

PubMedDate not supplied

Screening of families predisposed to cancer development in The Netherlands.

Screening for hereditary tumours provides a basis for secondary prevention. In 1985, the Foundation for the Detection of Hereditary Tumours was established in The Netherlands to coordinate screening in families with hereditary tumours. In the initial period of four years a large number of families were collected. Registration started with families with the multiple endocrine neoplasia syndrome type 2 and familial adenomatous polyposis. Later, families with the familial dysplastic nevus syndrome, hereditary nonpolyposis colorectal cancer and the multiple endocrine neoplasia syndrome type 1 were also collected and inventoried, because expansion of the registry to include these syndromes was considered. As a general conclusion based on our studies, it may be said that screening of families with the multiple endocrine neoplasia syndrome type 2, familial adenomatous polyposis, familial dysplastic nevus syndrome, and hereditary nonpolyposis colorectal cancer leads to detection of these tumours in an earlier stage, which in turn may permit curative treatment and improvement of the prognosis and life expectancy. Screening of the MEN-1 syndrome may improve the prognosis by favouring appropriate management decisions. It is evident that a detailed family cancer history is extremely important as an indicator of a genetic basis and has implications for family screening and follow up. The doctor's task of ensuring that the necessary investigations are carried out is made easier by use of the facilities of the Foundation for the Detection of Hereditary Tumours. The registration system in particular has assured the continuation of periodic examination, because the specialist is kept informed at all times. The collection of data and the preparation of an inventory of the data of families with hereditary tumours on a national scale have contributed to both the understanding of these syndromes and the optimalization of the screening procedures. The study of hereditary tumours is important, because it can provide clues concerning carcinogenesis in general.

Adenomatous Polyposis Coli↗

PubMedDate not supplied

Oncogenesis by mutations in anti-oncogenes: a view.

Oncogenesis is the result of accumulation of specific gene mutations. Two classes of specific cancer mutations are distinguished: namely those affecting anti-oncogenes and those in which oncogenes are involved. Anti-oncogenes are thought to regulate normal growth by encoding proteins that inhibit the expression of the oncogenes. This is in line with the observation that tumor cells are often homozygous for a defect in an anti-oncogene, as this will allow the expression of an oncogene. In this paper we attempt to calculate the number of anti-oncogenes involved in the genesis of a malignant tumour cell. These calculations were initially performed using a simplified model for oncogenesis and later applied to more complicated situations. These calculations indicate that usually four mutations in anti-oncogenes are required for oncogenesis in adults. This is in contradiction to the well-known 2-hit model of oncogenesis of Knudson which predicts about 10(9) times more de novo arising tumour cells than are observed in reality. Oncogenesis is only observed in proliferating cells. Cell proliferation and growth kinetics in various organs differ greatly. Therefore the time of oncogenesis and tumour manifestation also varies in the different organs. In organs that develop in early life (e.g. retina and neurons of the brain) mitotic activity ceases soon after birth. Consequently neural and retinal tumours emerge only early in life. In contrast, the main development of the female breast occurs after puberty, and the earliest breast tumours will become apparent in young adults. The four recessive mutations in anti-oncogenes required for oncogenesis imply that probably recessive mutations are involved in two loci. It is clear that an inherited mutation in an anti-oncogene at a particular locus causes different tumour types depending on the various organs in which the tumours arise. Comparison of (a) results of calculations about the number of malignant neuroendocrine tumour cells that arise in a pancreatic islet of a patient with inherited MEN1-syndrome with (b) the pathological anatomy of such a patient, suggests that a cell with two or three oncogenic mutations has a growth advantage over normal cells. This leads to cell proliferation in a premalignant lesion until the set of four oncogenic mutations is complete. The clinically premalignant lesions have a maximal mean diameter of about 0.4 cm when the first true malignant tumour cell develops, and the pathologist will probably note malignancy when the lesion has the size of 1-2 cm.(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗