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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We histologically compared 3 types of adenoma and cancer of the large intestine using 620 adenoma specimens (509 Is type lesions, 83 Ip type lesions, and 28 flat type lesions) and 113 specimens of early stage cancer (51 Is type lesions, 39 Ip type lesions, and 23 flat type lesions) obtained during the past 5-year period at our department. More than 90% of the Is and Ip type polyps were adenoma or carcinoma in adenoma while 25.5% of the flat elevations were m or sm carcinoma. Flat elevations even less than 10 mm in diameter were frequently carcinomas (26.3%) compared with the other types (both Is and Ip types, 6.7%), and all of those 10 mm or more in size were carcinomas. The distribution of the flat type early cancers in the large intestine was similar to that of advanced cancer with high percentages of carcinoma at each site compared with the other types. These results suggest that the carcinogenesis and progression of flat type early stage cancer differ from those of the other types.
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PMID:[Clinico-pathological studies on Is, Ip polyps and flat elevations in the large intestine]. 238 82

Fundamental aberrations in carbohydrate metabolism have been previously demonstrated in focal hepatic lesions emerging early during hepatocarcinogenesis induced in rat liver by limited oral administration (stop model) of N-nitrosomorpholine. Using this experimental approach, we have now investigated quantitatively the activity of pyruvate kinase (PK), a key enzyme of glycolysis and gluconeogenesis, in individual preneoplastic and neoplastic hepatic lesions, particularly in glycogen storage foci, mixed cell foci, basophilic cell foci, hepatocellular adenomas and carcinomas and in a specific type of preneoplastic hepatic lesion designated as an enzymatically hyperactive focus (EHF). The focal lesions were dissected from freeze-dried tissue sections with a laser microdissection device. This permits the excision of very small foci and the measurement of enzyme activities in serial sections of the same focus with different substrate concentrations, thus enabling possible changes in the isoenzyme pattern to be detected. On average, PK activity was increased in glycogen storage foci. Mixed cell foci showed a nearly normal or slightly decreased enzyme activity. However, a pronounced reduction in PK activity was observed in low glycogen basophilic foci and in basophilic hepatic tumors. An exceptionally high PK activity was found in one glycogenotic adenoma. An increased activity was also observed in EHF. The results suggest that a reduction in PK activity is a relatively late event during the sequence of cellular changes leading from glycogenotic foci to hepatocellular carcinomas. A drastic decrease in the enzyme activity occurs only when low glycogen basophilic cell populations develop from the glycogenotic foci in later stages of hepatocarcinogenesis.
Carcinogenesis 1990 Aug
PMID:Biochemical microanalysis of pyruvate kinase activity in preneoplastic and neoplastic liver lesions induced in rats by N-nitrosomorpholine. 238 24

Enzyme-histochemical investigation of pancreatic carcinogenesis in male Wistar rats treated at the age of 19 days by a single dose of 30 mg azaserine/kg body wt led to the detection of a new 'marker' for the recognition of foci of atypical acinar cells: the Mg2+-dependent ATPase. The two well-known populations of pancreatic atypical acinar cell foci, classified histologically as basophilic and acidophilic foci, showed a decreased and strongly increased ATPase reaction, respectively. The enhanced enzyme activity of the acidophilic foci has been characterized as unspecific nucleoside polyphosphatase. To validate the new marker, comparative quantitative evaluation was performed on haematoxylin and eosin-stained paraffin sections and ATPase-stained cryostat sections of the same pancreata of 25 azaserine-treated rats. Evaluation of basophilic ATPase-deficient foci of small diameter was more reproducible in haematoxylin and eosin-stained sections, while small acidophilic strongly ATPase-positive foci could be detected more reliably by the ATPase staining technique. The number of foci/cm3 pancreas was similar for both staining techniques above a focus diameter of about 100 microns for basophilic foci and 200 micronfor acidophilic foci. There were more acidophilic than basophilic foci/cm3 pancreas, and the acidophilic foci had significantly larger mean focal diameters than the basophilic foci. Together with the strong acidophilic staining of the latter emerging adenoma, this suggests that the acidophilic foci represent a neoplastic cell population progressing eventually to pancreatic carcinoma. The new 'marker' enzyme ATPase may greatly facilitate further investigations into the role of these putative preneoplastic lesions in pancreatic carcinogenesis.
Carcinogenesis 1986 Mar
PMID:Adenosine triphosphatase, a new marker for the differentiation of putative precancerous foci induced in rat pancreas by azaserine. 241 8

Obese mottled yellow Avy/a, lean pseudoagouti Avy/a and lean black a/a (YS X VY) F-1 hybrid female mice were fed diet containing 160 p.p.m. lindane (gamma-hexachlorocyclohexane) for 6, 12, 18 or 24 months. Clara cell hyperplasia was present in a majority of the mice after six months of lindane ingestion; however, more yellow mice (77%) than pseudoagouti (50%) or black (56%) mice had developed this lesion. Continued ingestion of lindane increased the incidence of Clara cell hyperplasia and resulted in similar prevalences in the three phenotypes. Lung tumors associated with lindane ingestion for 24 months were found only in yellow (19%) and pseudoagouti (14%) mice but not in the black mice. Prevalences of hepatocellular adenomas and carcinomas were very low (less than 10%) in untreated pseudoagouti and black mice. Lindane ingestion for 24 months resulted in an hepatocellular adenoma prevalence of 12% in pseudoagouti mice and 3% in black mice; comparable hepatocellular carcinoma prevalences were 5% and 1%. Among yellow mice fed lindane diet for 24 months, adenoma prevalence was 35% (9% among untreated controls) but carcinoma prevalence was only 17% (13% among controls). The tumorigenic responses evoked by lindane feeding in the lean pseudoagouti Avy/a mice but not in the black a/a mice indicate, for the first time, that the Avy gene itself, in the absence of obesity, sensitizes cells to transformation. The greater prevalence of hepatocellular adenomas in obese yellow Avy/a than in lean pseudoagouti Avy/a mice implicates obesity-associated factors in tumor promotion. Similarly, the increased prevalence of hepatocellular carcinomas in untreated obese yellow Avy/a mice, as compared to lean pseudoagouti mice, implicates obesity-associated factor as favoring histiotypic progression of liver tumors. Thus, the Avy gene not only sensitizes cells to respond to tumorigenic stimuli but also, by the induction of obesity, enhances promotion and progression of transformed cells.
Carcinogenesis 1987 Dec
PMID:Tumorigenic responses to lindane in mice: potentiation by a dominant mutation. 244 99

The last 20 years have witnessed dramatic technological advances in the diagnosis and treatment of colorectal polyps. These developments, in addition to an increased understanding of large bowel carcinogenesis, have shifted the risk/benefit balance toward a more aggressive approach to colorectal polyps. Mounting evidence for the adenoma-carcinoma sequence supports the position that all colorectal polyps should be removed, recovered, and evaluated. Moreover, in most cases polypectomy can be achieved endoscopically. To justify surgery today, adenomas must be too large to be removed endoscopically, located in the distal rectum, or malignant with submucosal invasion or questionable margins.
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PMID:Large bowel adenomas. 250 36

DNA extracted from familial and sporadic colorectal neoplasms was compared with constitutional DNA using a range of hypervariable locus specific probes to assess the extent of allele loss during conversion to malignancy. Chromosome 5 allele loss was observed in 23% of carcinoma samples, as previously found by others. However, we have been able to show for the first time loss of the D5S43 locus on chromosome 5 in adenomas from three patients, two of whom had the precancerous condition adenomatous polyposis coli (APC). These results suggest significant genetic changes involving chromosome 5 are occurring in benign adenomas. Probes for chromosome 1 (loci D1S7 and D1S8) and for chromosome 7 (loci D7S21 and D7S22) revealed no notable alterations in the adenoma samples. Complete loss of alleles for loci on chromosome 7 was not observed in carcinomas but reduced intensity of one parental allele was found in three specimens one of which was known to have multiple copies of this chromosome. Results using probes for chromosome 1 suggest that deletion of the D1S7 or D1S8 loci is not a common event in colorectal carcinogenesis. Loss of chromosome 5 alleles in adenomas from APC patients provides evidence in support of Knudson's hypothesis.
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PMID:Chromosome 5 allele loss in familial and sporadic colorectal adenomas. 253 77

The epidermal growth factor (EGF) and alpha-tumor growth factor are mitogenic proteins which bind to the EGF-receptor and may play a role in carcinogenesis or tumor progression. Our study investigated whether colorectal carcinomas and adenomas express altered levels of EGF-receptors or overproduce EGF-like activity by comparing histologically normal mucosa to carcinomas resected from the same patients. EGF-receptors were characterized by radioligand binding studies. Carcinomas contained unchanged or decreased levels of EGF-receptors in 13/16 and moderately increased levels in 3/16 patients as compared to normal mucosa. Adenomas obtained from 2 patients with familial polyposis coli and from a third patient with a coincident carcinoma had similar numbers of EGF-receptors as normal mucosa. EGF-like growth factors, in contrast, were significantly elevated in carcinoma extracts as compared to extracts from normal mucosa of the same patients. Adenomas did not contain elevated levels of EGF-like activity. We conclude that increased expression of EGF-receptors is infrequent in colonic adenocarcinomas. Increased production of EGF-like growth factors may frequently occur but seems to be associated with tumor progression rather than with premalignant lesions as represented by adenomas.
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PMID:Epidermal growth factor receptors and epidermal growth factor-like activity in colorectal mucosa, adenomas and carcinomas. 254 69

The inherited cancer disease familial polyposis coli (FPC) provides an excellent model not only for studying tumor progression in colorectal cancer but also for elucidating molecular mechanism of carcinogenesis in general. This paper reviews recent remarkable progress in the molecular mechanism of tumorigenesis in FPC. Included in this review is information on the localization of the FPC major gene and several types of genetic alterations during the development of tumors. One of these genetic alterations is activation of oncogenes such as mutated ras genes and another is inactivation of tumor suppression genes such as loss of heterozygosity. The mutated FPC gene on chromosome 5 q would be expected to be an early event to initiate the requisite hyperproliferation for adenoma formation. Adenomas will have undergone several gene or chromosome mutations before reaching the fully malignant state.
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PMID:[Carcinogenesis in familial polyposis coli]. 255 Dec 49

Familial polyposis coli (FPC) is an autosomal dominant tumorigenic disorder, the major gene of which is mapped to chromosome 5q. We searched for a gene loss in colorectal tumors from FPC patients, as related to tumorigenesis by inactivation of tumor suppression genes, using restriction fragment length polymorphism analysis. The findings were compared with those in the case of nonpolyposis colorectal carcinomas (NPCC). We examined specimens from 39 FPC patients, including 21 adenocarcinomas and 49 adenomas, and 23 colorectal carcinomas from 22 NPCC patients. For this, we used 53 polymorphic DNA markers on all autosomes. Frequent loss of heterozygosity in colorectal carcinoma from FPC patients was observed on chromosomes 5 (24%), 14 (20%), 17 (31%), 18 (40%), and 22 (35%) and also on chromosomes 5 (32%), 14 (30%), 17 (27%), 18 (20%), and 22 (19%) in NPCC. Although loss of heterozygosity in adenoma from FPC patients was observed on nine chromosomes, the frequencies were less than 7%. As we fractionated tumors only macroscopically, actual frequencies of loss of heterozygosity are probably somewhat higher. However, these results do suggest that tumor suppression genes for colorectal carcinoma may locate on chromosomes 5, 14, 17, 18, and 22 and that they may play a critical role in carcinogenesis in both FPC and NPCC patients.
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PMID:Loss of constitutional heterozygosity in colorectal tumors from patients with familial polyposis coli and those with nonpolyposis colorectal carcinoma. 256 69

Using an in vitro amplification step (polymerase chain reaction) followed by oligonucleotide dot blot analysis, DNA samples from 29 familial polyposis coli patients (75 polyp-derived and 26 'normal' colon samples with no epithelial atypia) were screened for the presence of K-, N-, and H-ras mutations. Only 5 polyps contained ras mutations (7%)--all in K-ras codon 12. In each case 'normal' colon DNA was available and found to be negative in this assay. We also report the detection of K-ras codon 12 mutations in a stably non-tumorigenic immortal adenoma-derived cell line, PC/AA, and in a tumorigenic colorectal carcinoma cell line, PC/JW. Both epithelial cell lines were derived from different FPC patients. An activated K-ras gene was also found in cell line S/AN, isolated from a sporadic villous adenoma. These results provide further evidence that there are common molecular events involved in sporadic and hereditary colorectal carcinogenesis and that K-ras mutations can precede the development of malignancy. To our knowledge PC/AA is the first reported example of a human cell line bearing a mutant ras gene that is not tumorigenic and shows that the presence of an activated ras gene even in an immortal human cell line is insufficient for malignancy.
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PMID:A study of ras gene mutations in colonic adenomas from familial polyposis coli patients. 257 69


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