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At least 253 records · Page 14Linked to original sources
PubMed2003

Outcome of clinical versus genetic family screening in hypertrophic cardiomyopathy with focus on cardiac beta-myosin gene mutations.

OBJECTIVE: Familial hypertrophic cardiomyopathy (FHC) is caused by mutations in genes encoding cardiac sarcomere proteins. Although available, genetic analyses are generally not used clinically. In the present study, we evaluated the outcome of clinical vs. genetic screening of family members with specific focus on mutations in the cardiac beta-myosin heavy chain (MYH7) gene. METHODS: A consecutive cohort of 68 FHC probands and their families (395 persons) of Danish origin was evaluated including patient- and family histories, physical examinations, electrocardiogram and echocardiography. Mutation screening was performed by a combination of single strand conformation/heteroduplex analysis and direct sequencing. RESULTS: Eight different MYH7 gene mutations were identified in nine (13%) families (96 persons). In eight (89%) of the families, major cardiac events had occurred. Myectomy or percutaneous septal alcohol ablation had been performed in a higher number of MYH7 probands i.e. in five of nine (56%) as compared to 10 of 59 (17%) (P<0.05) non-MYH7 mutation probands. Neither echocardiographic nor ECG findings were useful to distinguish MYH7 from non-MYH7 probands. Between adult MYH7 mutation-carriers (n=38) and their non-carrier relatives (n=39), low sensitivity and specificity of the clinical diagnostic criteria tested were observed and minor clinical diagnostic criteria alone were not useful for identification of mutation carriers. By genetic screening of relatives with no or only minor hypertrophy on echocardiography, i.e. a priori possible mutation-carriers normally recommended clinical follow-up-the diagnosis was excluded in 52 (83%) persons. In addition, six relatives with secondary hypertrophy were identified as non-carriers. CONCLUSION: Neither echocardiographic nor ECG findings were useful to distinguish MYH7 from non-MYH7 probands. Extension of screening to include genetic analyses offered a marked diagnostic advantage as compared to clinical screening alone in FHC families.

Adolescent↗
PubMed2006

Microsatellite instability and novel mismatch repair gene mutations in northern Chinese population with hereditary non-polyposis colorectal cancer.

OBJECTIVE: Hereditary non-polyposis colorectal cancer (HNPCC) syndrome is the most common cause of hereditary colorectal cancer with an early age of onset. Microsatellite instability (MSI) and germline mutation in one of the DNA mismatch repair (MMR) genes are found in the majority of HNPCC families and provide an opportunity for genetic diagnosis and prophylactic screening. The MMR gene mutation spectrum may vary across different populations and be influenced by founder mutations that prevail in specific ethnic groups. China is a big and ancient nation with enormous genetic diversity, which is especially notable between the northern and southern Chinese populations. A MMR gene mutation database for the southern Chinese population based in Hong Kong has been previously established. This study compares the MMR gene mutation spectrum and the MSI of HNPCC between the northern and southern Chinese populations. METHODS: Twenty-five HNPCC families from northern China were systematically analyzed. The MSI analysis was performed using five loci in the USA National Cancer Institute (NCI) panel (D2S123, D5S346, BAT-25, BAT-26 and BAT-40) by PCR from the tumor and normal tissue. MSH2, MSH6 and MLH1 were performed using immunohistochemical staining. Two founder mutations of MSH2 and MLH1 were examined by PCR base analyses using primers flanking the two deletion sites (c.1452_1455delAATG in MSH2 and 1.8 kb deletion involving exon 11 of MLH1). RESULTS: Of the 25 families collected, 19 met Bethesda guideline (BG) 1 and six met BG3. Twenty-two (15.7%) were extra-colonic cancers with gastric cancer (in seven patients) being the most common cancer type. Of the 25 tumors analyzed, 21 (84%) were high level microsatellite instability (MSI-H) and four (16%) were microsatellite stable (MSS). Eighteen (86%) of the 21 MSI-H tumors showed loss of either the MLH1 or the MSH2 protein. Three MSI-H tumors and all four MSS tumors showed no loss of expression of the three MMR proteins. Out of the 21 patients with MSI-H tumors, 12 (57%) showed pathogenic germline mutations in either MLH1 (n = 8) or MSH2 (n = 4). Overall, three novel mutations (in patients H22, H17 and H29) have been identified. One of them, c.503_4insA, caused a frameshift mutation in the MLH1 gene. The other two were found in the MSH2 gene, including a frameshift (c.899_890insAT) and a splice junction (IVS7-1G-->A, SA of Exon 8) mutation. CONCLUSIONS: The results suggest a distinctly different mutation spectrum of MMR genes between northern and southern Chinese populations and call for a systematic, nationwide study to facilitate the design of a MMR gene mutation detection strategy tailored for individual populations in China.

Adaptor Proteins, Signal Transducing↗
PubMed2004

[Detection of FLT3 gene and FLT3/ITD gene mutation in chronic myeloid leukemia and its significance].

BACKGROUND & OBJECTIVE: Fms-like tyrosine kinase 3 (FLT3)gene abnormal expression could be detected in most of acute myeloid leukemia (AML)patients, and 20%-30% of them have FLT3/ITD gene mutation which indicate poor prognosis. This study was to detect FLT3 gene expression, and FLT3/ITD gene mutation in chronic myeloid leukemia (CML)patients, and analyze their relationships with prognosis. METHODS: Polymerase chain reaction (PCR)was used to detect FLT3 gene expression, and FLT3/ITD gene mutation in 53 CML patients of chronic phase,and 34 CML patients of accelerated phase or blast crisis. RESULTS: FLT3 gene was detected in 5.7%(3/53)CML patients of chronic phase, and in 55.9% (19/34)CML patients of accelerated phase or blast crisis,the difference of FLT3 gene positive rate between these 2 groups was significant (P< 0.001). Only 2 of 87 CML patients (2.3%)were found with FLT3/ITD mutation. CONCLUSIONS: FTL3 gene expresses mainly in CML patients of accelerated phase or blast crisis. FTL3/ITD gene mutation was seldom involved in CML patients. The CML patients with FLT3 gene expression and FTL3/ITD gene mutation may have poor prognosis.

Adult↗
PubMed1995

Amplification of the dihydrofolate reductase gene is a mechanism of acquired resistance to methotrexate in patients with acute lymphoblastic leukemia and is correlated with p53 gene mutations.

Although dihydrofolate reductase (DHFR) gene amplification is a common mechanism of resistance to methotrexate (MTX) in tumor cell lines, with the exception of a few case reports, the incidence of this phenomenon as a mechanism of MTX resistance in the clinic has not been reported. We studied 38 untreated patients and 29 patients in relapse with acute lymphoblastic leukemia (ALL) for gene amplification and p53 gene mutations. Three patients were studied both at diagnosis and at each of two relapses after treatment with MTX. Nine of 29 relapsed patients (31%) had low-level DHFR gene amplification (two to four gene copies) associated with increased levels of DHFR mRNA and enzyme activity. Of significance was a correlation of gene amplification with p53 mutations in seven of nine relapsed patients (P < .001). Low-level DHFR gene amplification may be an important cause of MTX resistance in ALL and strengthens the concept that mutations in the p53 gene may lead to gene amplification as a consequence of defective cell cycle control.

Adolescent↗
PubMed2006

Targeted gene mutation in Phytophthora spp.

The genus Phytophthora belongs to the oomycetes and is composed of plant pathogens. Currently, there are no strategies to mutate specific genes for members of this genus. Whole genome sequences are available or being prepared for Phytophthora sojae, P. ramorum, P. infestans, and P. capsici and the development of molecular biological techniques for functional genomics is encouraged. This article describes the adaptation of the reverse-genetic strategy of targeting induced local lesions in genomes (TILLING) to isolate gene-specific mutants in Phytophthora spp. A genomic library of 2,400 ethylnitrosourea (ENU) mutants of P. sojae was created and screened for induced point mutations in the genes encoding a necrosisinducing protein (PsojNIP) and a Phytophthora-specific phospholipase D (PsPXTM-PLD). Mutations were detected in single individuals and included silent, missense, and nonsense changes. Homozygous mutant isolates carrying a potentially deleterious missense mutation in PsojNIP and a premature stop codon in PsPXTM-PLD were identified. No phenotypic effect has yet been found for the homozygous mutant of PsojNIP. For those of PsPXTM-PLD, a reduction in growth rate and an appressed mycelial growth was observed. This demonstrates the feasibility of target-selected gene disruption for Phytophthora spp. and adds an important tool for functional genomic investigation.

Algal Proteins↗
PubMed2006

Association of rare SPINK1 gene mutation with another base substitution in chronic pancreatitis patients.

AIM: To verify and expand the known spectrum of serine protease inhibitor Kazal type 1 (SPINK1) gene mutations in chronic pancreatitis. METHODS: DNA extracted from 172 chronic pancreatitis patients was assayed for SPINK1 gene mutations by PCR and DNA sequencing. A control cohort of 90 unrelated healthy individuals was analysed by the same methods for presence of common populational polymorphisms, and frequency of five-loci haplotypes was calculated. Linkages of gene aberrations in single SPINK1 gene copies were analysed by long-distance PCR followed by allele-specific PCR and DNA sequencing. RESULTS: The most frequent SPINK1 gene mutation N34S was found at a frequency of 6%. Furthermore, we detected the heterozygous intervening sequence (IVS) 3 + 2 T > C mutated gene in 2 German patients and 1 Macedonian chronic pancreatitis patient. In all three SPINK1 gene copies an additional rare base substitution was found: 5'untranslated region (UTR)-215 G > A. Polymorphism analysis revealed that all three affected genes carried the same five-loci haplotype. DNA sequencing of another chronic pancreatitis-related gene PRSS1 (cationic trypsinogen) did not reveal any mutations in these 3 patients. CONCLUSION: We found in 3 (2%) of 172 chronic pancreatitis patients an IVS3 + 2 T > C SPINK1 gene mutation and a base substitution 5'UTR-215 G > A in the same gene copy. Most probably the 5'UTR-215 G > A represents a rare polymorphism and not a mutation as previously concluded. Haplotype analysis suggests a common origin of the IVS3 + 2 T > C mutation in these patients.

5' Untranslated Regions↗
PubMed1992

[Tumor suppressor genes: mutations in RB and p53 genes are significant carcinogenic factors].

The RB and p53 tumour suppressor genes encode nuclear proteins that exert an inhibitive effect on cell growth. A large variety of human tumour types manifest loss or mutation of the RB or p53 genes, and p53 mutation is the commonest genetic alteration found in tumour cells. In addition, the RB and p53 proteins may be inactivated by complex formation with viral oncoproteins--for instance, in the case of cervical carcinoma carrying human papilloma virus. In vivo introduction of an intact RB or p53 gene into malignant cells lacking the respective gene results in suppression of the neoplastic phenotype and thus of tumourigenicity, p53 being the more potent of the two in this respect. Further elucidation of tumour suppressor genes may well result in future improvement in the diagnosis and treatment of cancer.

Genes, Retinoblastoma↗
PubMedDate not supplied

[Do viruses participate in the origin of group outbursts of gene mutations occurring in natural Drosophila populations?].

It has been experimentally shown that different viruses apathogenic for Drosophila and unable to reproduce in it, and also highly polymerized DNA isolated from these viruses, act as effective mutagens when injected into the hemolymph of this insect. They induce numerous lethal and visible stable gene mutations. Some of them can be present in Drosophila natural populations. But these virus induced gene mutations or those induced by virus DNA never take part in the origin of group outbursts of gene mutation which are observed in Drosophila melanogaster natural populations. These mutability outbursts include only gene mutations induced by transpositions of mobile genetic elements. These mutations are usually unstable: they are apt to be converted to other allelic mutant states which are phenotypically differently expressed. Viruses which are endemic for Drosophila melanogaster and can reproduce in it take no part in the outbursts of gene mutations. They can only induce a small number of lethal and visible gene mutations which are stable and arise very infrequently. It seems probable that group outbursts of gene mutations in natural populations of Drosophila melanogaster are a result of various environmental stresses which cause a rise in the frequency of transpositions of mobile genetic elements, this leading to the mutability outbursts of gene mutations.

Animals↗
PubMed1997

[Identification of G6PD gene mutations in several nationalities from Yunnan province].

OBJECTIVE: To analyze the G6PD gene mutations in several nationalities from Yunnan province. METHODS: G6PD gene mutation of 29 samples from G6PD deficient patients were analyzed by using common and mis-matched primering PCR followed by restriction enzyme digestion. The samples were collected from Yunnan province among several nationalities. RESULTS: In these 29 cases, 20 were of two known mutations, including 19 of 1388 (G-->A) and 1 of 1376 (G-->T) mutation. The 7 cases of national minorities, including 3 of Yi ([symbol: see text]), 2 of Bai ([symbol: see text]), 1 of Dai ([symbol: see text]), and 1 of Naxi ([symbol: see text]), were all 1388 mutations. No report of the G6PD gene 1388 mutation in these ethnic groups was published excepting for Dai. CONCLUSION: The mutation probably had been prevalent before the emergence of these national minorities. The approximate rate of G6PD gene mutations provided in Yunnan province may, in some respects, help to interpret the molecular evolution.

Asian People↗
PubMed1996

Detection of human papillomavirus DNA and p53 gene mutations in human prostate cancer.

The relationship between integration with human papillomavirus (HPV) and p53 gene mutations in tissues of prostate cancer were examined. Tissue samples analyzed were obtained by total prostatectomy (29 stage B cancer cases) and from autopsy (22 endocrine therapy-resistant metastatic disease cases). HPV DNA was detected in 8 of 51 (16%, 5 in stage B and 3 in autopsy cases) by polymerase chain reaction (PCR) using consensus primers on L1 region. Genotypes of HPV were entirely type 16. Structural abnormalities of p53 gene were detected in 7 of the 22 autopsy cases (32%) by PCR-single-strand conformation polymorphism analysis and direct sequencing. No p53 gene mutation was found in stage B cancer cases. Analysis of mutation spectra revealed clear differences between Japanese and Westerners. There was a significant difference in the mutation frequency between stage B and autopsy cases (p < 0.01, Fisher's exact test). One case showed both integration of HPV and p53 gene mutation in different cancer foci. However, the other cases revealed an inverse correlation between the presence of HPV DNA and p53 gene mutations. These data show that p53 genetic alteration is correlated with the progression of prostate cancer, in contrast to the integration of HPV that may occur in a relatively early stage. In conclusion, this study may indicate that either p53 gene mutation or the presence of HPV's oncogenic protein E6 is involved in the development of prostate cancer.

Adenocarcinoma↗
PubMed1996

[Mutator genes from Saccharomyces cerevisiae. Repair of artificial heteroduplexes in him and hsm mutants].

During recent years, genes controlling mutation in higher eukaryotes have been found to be involved actively in carcinoma regeneration in cells. In this respect, studying the genetic control of mutagenesis becomes a key direction of research into mechanisms responsible for cancer generation. The results of studying interaction of mutations in the HSM3 and HSM6 genes, controlling spontaneous and induced mutagenesis in yeasts, and mutations impairing three known pathways of DNA damage repair in this microorganism, are described in this work. It was shown that mutation rev3 completely blocks UV-induced mutagenesis in all mutants studied. On the other hand, mutation rad2 synergistically interacts with mutations him1, hsm1, hsm3, hsm6, and hsm2, thus enhancing the frequency of UV-induced mutagenesis in double mutants multiple times. Mutations him2 and him3 manifested epistatic interaction with mutation rad2. With mutation rad54, the interaction was epistatic for mutations him1 and hsm2 and was additive for mutations hsm1, him2, and him3. On the basis of the data obtained, we developed a scheme for the appearance of mismatch bases in the process of repair of UV-induced DNA damage.

DNA Damage↗
PubMed1994

Effect of non-tumor cell contamination on detection of p53 gene mutations in human gastric cancer cells by polymerase chain reaction single-strand conformation polymorphism analysis.

BACKGROUND: We have previously studied p53 gene mutations in 25 primary gastric cancer tissues by polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis for exon 4-8 and immunohistochemical staining with anti-p53 antibody. In four cases, the discrepancy of the results was observed between the two methods. In one case positive by PCR-SSCP but negative by immunohistochemical staining, the mutation was silent. In three cases, the p53 gene mutations were detected only by immunohistochemical staining. This discrepancy may be due to the contamination of the samples by cells without p53 gene mutation, such as non-tumor cells. This study was conducted to investigate the sensitivity of PCR-SSCP analysis to p53 gene mutations when the sample was contaminated with non-tumor cells. METHODS: Genomic DNA was extracted by the digestion with proteinase K and phenol-chloroform-ethanol method from two human gastric adenocarcinoma cell lines, MKN-45 and KATO III. To investigate the sensitivity of PCR-SSCP, DNA extracted from cancer cells was mixed with DNA obtained from normal gastric mucosal cells at various ratios. PCR-SSCP analysis for exon 4-8 of the p53 gene was performed with the mixed DNA samples. RESULTS: In KATO III, no PCR products were generated in exon 4-8 of the p53 gene by PCR, suggesting that both alleles from exon 4-8 of the p53 gene were deleted. In MKN-45, the mobility shift was observed in exon 4. Therefore, the effect of non-tumor cell contamination on the detection of p53 gene mutations was conducted using MKN-45 and normal gastric mucosal cells. In the mixed DNA samples of MKN-45 and normal gastric mucosal cells, an extra band with the migration similar to that of MKN-45 was found in the samples of 1:8 dilution or less, while no extra band was grossly detectable in DNA of normal gastric mucosal cells and in the samples of more than 1:16 dilution. CONCLUSIONS: These results suggest that the detection of p53 mutations by PCR-SSCP analysis may be underestimated in samples contaminated by a large number of non-tumor cells.

Base Sequence↗
PubMed1999

Role of p53 gene mutation in tumor aggressiveness of intracranial meningiomas.

The mutations that occur in the p53 tumor suppressor gene have been studied in various human malignant tumors. However, little is known about this gene in meningiomas. To investigate the relationship and frequency of p53 gene mutations, the p53 polymerase chain reaction-single stranded conformational polymorphism (PCR-SSCP) and immunohistochemical study were performed on the 41 intracranial meningiomas (21 benign, 11 atypical, and 9 malignant). The higher the p53 protein expression rate, the poorer the histologic grade (9.5%, 72.7%, and 88.9% in benign, atypical and malignant meningioma, respectively) (p=0.000). The p53 protein expression rate was higher in recurrent meningioma (71.4%) than in nonrecurrent meningioma (10.5%) (p=0.002). PCR-SSCP method was performed in positive p53 protein immunoreactivity cases. p53 gene mutation rate was higher in the atypical (62.5%) and malignant (25%) meningiomas than in the benign meningioma (0%) (p=0.232). Also, the rate was higher in recurrent menigioma (20%) than in nonrecurrent meningioma (0%) (o=0.495). Among five to eight exons of the p53 gene, the mutation was observed on exon 7 more frequently. In conclusion, p53 immunoreactivity and p53 gene mutation are closely correlated with histologic grade and histologic atypia of intracranial meningiomas. p53 gene mutation would be considered as a useful marker to detect the progression of intracranial meningiomas.

Brain Neoplasms↗
PubMed1994

[Portion of certain cystic fibrosis gene mutations and linkage dysequilibrium between the CFTR-gene locus and two DNA marker loci in Russian populations].

A sample of 165 patients who were inhabitants of Russia was screened for seven CFTR gene mutations, and analysis of polymorphism frequency at two marker loci (KM19 and VNTR in intron 6 of the CFTR gene) was performed in normal and mutant chromosomes. The frequencies of mutations in 330 mutant chromosomes were distributed as follows: delta F508, 57.5%; G542X, 1.07%; and R33AW, 0.45%. Mutations G551D, R553X, R347P, and 1154insTC were not found. Alleles and haplotypes of KM19 and VNTR loci in intron 6 of the CFTR gene were characterized by a marked linkage disequilibrium with the CFTR gene. Haplotype 2-6 showed an absolute linkage disequilibrium with the delta F508 mutation.

Alleles↗
PubMed1974

Reversion of frameshift mutations by mutator genes in Escherichia coli.

The Escherichia coli mutator genes mutU4, mutS3, and mut-25 (a possible allele of mutL), previously known to induce transitional base changes, increased significantly the frequencies of reversion of lacZ frameshift mutations. mutT1, previously shown to induce only the transversion of adenine-thymine to cytosine-guanine, had no effect on the reversion of lacZ frameshift mutations. With mutator genes other than mutT1, small increases were found in the frequencies of reversion of trpA frameshift mutations.

Acridines↗
PubMed1997

A detailed analysis of the role of K-ras gene mutation in the progression of colorectal adenoma.

To elucidate the role of ras gene mutations during the early stage of colorectal tumour progression, K-ras gene mutations were analysed in 32 benign adenomas and 36 adenomas with focal carcinoma in the colorectum by microscraping of histologically pure regions from tissue sections, polymerase chain reaction-restriction fragment length polymorphism and in part by direct sequencing. Several regions were scraped out and analysed when an adenoma contained areas with different grades of dysplasia. The frequencies of K-ras gene mutation in mild dysplasia, moderate dysplasia and focal carcinoma were 19% (7/36), 51% (25/49) and 39% (14/36) respectively. The K-ras gene status was heterogeneous in 4 of the 11 benign adenomas from which multiple samples were obtained, and mutations were always found in the regions with more advanced dysplasia in these adenomas. Thirteen of the 36 adenomas with focal carcinoma showed heterogeneity of mutations between the adenoma region and the focal carcinoma. Seven of which had mutations only in the adenoma region. These findings indicated that the K-ras gene mutations occur during the late stage of adenoma progression and may confer a more advanced morphological phenotype of adenoma, but these mutations are not mainly involved in malignant transformation from adenoma to carcinoma.

Adenoma↗
PubMed1993

Oncogene activation: c-raf-1 gene mutations in experimental and naturally occurring tumors.

We demonstrate here consistent point mutations of the c-raf-1 proto-oncogene, within a small region of the kinase domain, in a mouse model for chemical tumor induction. This is the first demonstration of point mutated raf genes in vivo, and the first isolation of activating in vivo point mutations in the kinase domain of a proto-oncogene. The specific region where these mutations are clustered also has biological significance. This is precisely the region where 5/5 independently generated monoclonal antibodies raised against Raf-1 map to [29], and predictions based upon the crystal structure of A kinase identify this as the substrate pocket. The tumors examined show a selective specificity for Raf-1 mutations in that another family of genes, the ras proto-oncogenes which are frequently activated by point mutation in both animal and human tumors [15-21,26], is not involved. Our consistent finding of Raf-1 mutations in a mouse tumor model also has consequences for further evaluation of the role of Raf-1 in human tumor development, as it emphasizes the need to examine c-raf-1 at the sequence level. In fact preliminary screening of human lung tumors indicates point mutations at amino acid 533 (John Lyons, personal communication). Finally, the cumulative data on the critical role of Raf-1 in signal transduction and the occurrence of oncogenic Raf-1 in tumors [32-41] highlight this enzyme as an attractive target for development of novel anticancer regimens.

Animals↗
PubMed2003

Analysis of Ki-ras and p53 gene mutations in laterally spreading tumors of the colorectum.

A laterally spreading tumor (LST) is considered to be a specific subtype of superficial colorectal tumors, in view of its characteristic clinicopathological features. We attempted to compare genetic alterations found in LST (>10 mm) with those found in IIa-type adenomas (10 mm or less (small superficial elevated lesion)) and conventional polypoid adenomas (>10 mm). In addition, multiple sampling by microdissection was performed for 14 LST to examine genetic heterogeneity in the Ki-ras and p53 gene mutation patterns. Polymerase chain reaction, single-strand conformation polymorphism and direct sequencing were used to analyze Ki-ras and p53 gene mutations in 73 sporadic colorectal adenomas: 28 LST; 22 IIa-type adenomas; and 23 polypoid adenomas. Ki-ras gene mutations were found more frequently in LST (6/28 tumors) and polypoid adenomas (6/23 tumors) than in IIa-type adenomas (2/22 tumors), although this difference was not statistically significant. The frequency of p53 gene mutations in the 28 LST was 25% (7/28), which was significantly higher than that found in IIa-type adenomas (P < 0.05). However, although p53 gene mutations were found more frequently in LST than in polypoid adenomas, this difference was not statistically significant. Seven LST exhibited a combination of wild-type and mutant-type tumor cells having the p53 gene mutation pattern, whereas a pattern of different Ki-ras gene mutations was found in two of three LST that exhibited Ki-ras gene mutation heterogeneity. We suggest that the LST exhibited a characteristic pattern in terms of the Ki-ras as well as the p53 gene mutation pattern, thereby supporting the hypothesis that LST is a specific subtype of colorectal tumors.

Adenoma, Villous↗