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[HISTOSPECTROPHOTOMETRIC STUDY OF THE DNA CONTENT OF VESICAL PAPILLOMAS OF VARIOUS STAGES OF MALIGNANCY. (PRELIMINARY NOTE)].
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[ON THE POLYSACCHARIDE AND NUCLEIC ACID CONTENT IN CANCER CELLS OF THE UTERINE CERVIX].
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[ONCOGENIC-INFECTIOUS NUCLEOPROTEINS AND CERVICAL CARCINOMA. II].
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[STUDIES ON NUCLEIC ACIDS METABOLISM OF HUMAN LEUKEMIC LEUKOCYTES].
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[IMPORTANCE OF BIOCHEMICAL PROPERTIES OF THE NUCLEAR APPARATUS OF THE TUMOR CELL IN THE PATHOGENESIS OF CANCER].
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[ON THE DRY WEIGHT, THE DNA- AND HISTONE PROTEIN CONTENT OF HUMAN TUMORS].
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[STUDY OF DESOXYRIBONUCLEIC ACID IN PRE-INVASIVE AND INVASIVE CARCINOMAS, AND IN THE EPITHELIUM OF THE UTERINE CERVIX].
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[PROPOSITION ABOUT THE GENESIS OF CANCER].
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[Construction of cDNA library from human colorectal cancer cell HRT-18].
OBJECTIVE: To construct a cDNA library from human colorectal cancer cell HRT-18. METHODS: The total RNA was extracted from human CRC (colorectal cancer) cell HRT-18 and the mRNA was isolated from the total RNA by MagneSphere technique, and then the first-strand cDNA was synthesized with oligo (dT) primer containing sfi I site while the double-strand cDNA was amplified through LD-PCR (long-distance PCR) by SMART technique. The double strand cDNA was digested by sfi I ( I A & I B) restriction enzyme before cDNA size fractionation, and the double-strand cDNA fractionated was ligated into the lambdaTripIEX2 vector and then was packaged into lambda phage in vitro. RESULTS: The unamplified human CRC cell HRT-18 cDNA library consisted of 6. 5 x 10(6) independent clones, recombinants clones was more than 96%. The titer of the amplified cDNA library was 1.1 x 10(9) pfu/ml and the average insert of the recombinants was 1.1 kb. CONCLUSION: The quality of the constructed cDNA library from human CRC cell HRT-18 is excellent and it is helpful to screen CRC specific antigen.
[Diagnosis of multiple endocrine neoplasms type IIa using DNA analysis].
The gene causing MEN IIa has recently being assigned to the pericentromeric region of chromosome 10. We performed linkage analysis using DNA-markers closely related to the chromosomal locus at chromosome 10: MCK II, retinol binding protein cDNA and cTBIRBP-9. Available for the study were EDTA blood from two families. The analysis was positive in two asymptomatic offsprings in one family (B), whereas the markers were not informative in the other family (A). Genetic distance of the informative marker of family A to MEN IIa gene is 2 cM, i.e. a likelihood of 98% (95% up a confidence limit with 5%) for the gene carrier status of two children aged 11 and 7 y old. The following clinical investigation including pentagastrin test, plasma catecholamines and 24 hour urine catecholamines and parathormone was negative until now. We recommend early linkage analysis for establishing the genetic status in offspring of MEN IIa families to focus further screening to those, who are predicted to be gene carrier.
Flow cytometric analysis of cell-killing actions of 5-fluorouracil in human colorectal cancer cells.
To confirm our previous kinetic analysis of the mode of cell-killing action of 5-fluorouracil (5-FU), we carried out a flow cytometric analysis with human colorectal cancer DLD-1 cells. Cells were treated with each cytotoxic concentration of 5-FU for 1 or 72 h, and the periodic changes in flow cytometric pattern were compared with those of 5-fluorouridine (FUrd) and 5-fluoro-2'-deoxyuridine (FdUrd). When cells were cultured with 5-FU for 72 h, most of them accumulated in S phase and remained there. This pattern was the same as that seen in cells that were continuously exposed to FdUrd. In contrast, when cells were exposed to 5-FU for 1 h and cultured in drug-free medium, they ended the cell-cycle traverse in either G2/M or G1 phase after an immediate but transient accumulation in S phase. Results were identical to those observed with cells similarly treated with FUrd. These results demonstrated a good accordance with those of our kinetic analysis, and strongly suggested that the mode of cell-killing exhibited by 5-FU differs with exposure time: 5-FU acts like FUrd in short exposure conditions, and it acts similarly to FdUrd in continuous exposure conditions.
Instability of microsatellites in rat colon tumors induced by heterocyclic amines.
Microsatellite instability in rat colon tumors induced by heterocyclic amines was examined by studies on the lengths of 85 microsatellite sequences, covering most of the rat chromosomes in tumors and normal tissues. Seven of eight colon tumors induced by 2-amino-1-methyl-6- phenylimidazo-[4,5-b]pyridine showed alterations at least at one locus of microsatellite sequences, whereas no mutations were observed in colon tumors induced by 2-amino-3-methylimidazo[4,5-f]quinoline. Three 2-amino-1-methyl-6-phenylimidazo-[4,5-b]pyridine-induced colon tumors had mutations in more than one microsatellite, their mutation rates being 2 of 85, 2 of 85, and 3 of 85 allele/mircrosatellite sequence, respectively. These data suggest that rat colon adenocarcinomas induced by 2-amino-1-methyl-6- phenylimidazo-[4,5-b]pyridine but not 2-amino-3-methylimidazo[4,5-f] quinoline show a trait of microsatellite instability. This is the first systematic study of microsatellite instability in experimental animal models of carcinogenesis.
A device for processing large acrylamide gels.
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A novel p53 germline alteration identified in a late onset breast cancer kindred.
Germline mutations in the p53 tumor suppressor gene are associated with the Li-Fraumeni syndrome, characterized by childhood sarcoma, leukemia and early onset breast cancer and has occasionally been found also in familial breast-ovarian cancer. Most mutations found are of missense type and located in the central region of the gene (exons 5 to 8). In the present study, a germline p53 alteration was identified in a late onset breast cancer family (kindred Lund 5; mean age 58 years) using single stranded conformation polymorphism and sequence analysis. The mutation (a CCG to CTG transition) at codon 82 in exon 4, resulting in a proline to leucine substitution, has not previously been reported and was not present in a control set of 60 healthy individuals. Three of five woman with breast cancer (45, 57 and 65 years) were carriers of the alteration. Loss of heterozygosity at the p53 locus was not seen in the primary tumors of these women, but appeared as a partial loss of the wildtype allele in subsequent recurrent lesions of two gene carriers. The family manifested no linkage to the p53 gene (a two-point LOD-score of -0.41), and has previously also been excluded for linkage to the BRCA1 and BRCA2 loci, as well as being carrier of a BRCA1 germline mutation. Although it seems unlikely that the p53 germline mutation is the major cause of disease predisposition in Lund 5, the data suggest that some p53 alteration may confer a subtle influence on breast cancer development and progression.
Microsatellite instability correlates with reduced survival and poor disease prognosis in breast cancer.
Size changes in microsatellite sequences have been detected in many types of cancer, but the influence of this form of genetic instability on disease progression remains unclear. We determined the incidence of microsatellite instability in breast cancer by comparing PCR-amplified sequences from paraffin-embedded samples of normal and tumor tissue from affected individuals. This analysis showed that at least 30% of breast cancers exhibit microsatellite instability (MI). Of importance, MI correlated with indicators commonly associated with poor disease prognosis, including lymph node status, tumor size, and advanced tumor stage. Individuals with MI+ tumors also showed significantly reduced disease-free and overall survival. These data contrast with studies showing that MI correlates with improved prognosis in colon and gastric cancers. We propose that defects resulting in MI promote disease progression and result in a poor prognosis in breast cancer.
Absence of polyomavirus JC in glial brain tumors and glioma-derived cell lines.
The human neurotropic papovavirus JC, a close relative of simian virus 40, has been associated with the formation of brain tumors in humans because of its ability to induce such tumors in other primates under experimental conditions. Here we have analyzed 30 brain tumors classified as either oligodendroglioma or astrocytoma and 22 cell lines derived from human gliomas for the presence of JC viral sequences using polymerase chain reaction with two different sets of primers. None of the tumors or cell lines contained JC viral sequences. Similarly, we failed to detect expression of JC T antigen in any of 26 human glioma lines analyzed in this study. We conclude that JC virus is not a major cause of human brain tumors.