T. Kinjo, K. Kamiyama, K. Chinen, T. Iwamasa, K. Kurihara, T. Hamada
{"title":"Molecular interactions hold the key to relieving bone loss","authors":"T. Kinjo, K. Kamiyama, K. Chinen, T. Iwamasa, K. Kurihara, T. Hamada","doi":"10.1136/mp.56.2.108","DOIUrl":"https://doi.org/10.1136/mp.56.2.108","url":null,"abstract":"Background/Aim: It has been reported previously in cases of adenosquamous carcinoma of the lung in Okinawa, a subtropical island 2000 km south of mainland Japan, that the squamous cell carcinoma components were positive for human papillomavirus (HPV) by non-isotopic in situ hybridisation (NISH). The adenocarcinoma cells adjacent to the squamous cell carcinoma components were enlarged and also positive for HPV. This is thought to indicate that after adenocarcinoma cells are infected with HPV, they undergo morphological changes, and that “squamous metaplasia” follows. In this present study, the effects of HPV transfection into adenocarcinoma cells were examined. The relation between the region expressing the HPV gene and squamous metaplasia was also studied. Methods: Plasmid pBR322 containing HPV type 16 (HPV-16) was transfected into cultured colonic adenocarcinoma (DLD-1) and lung adenocarcinoma (PC-14) cells using the calcium phosphate method. Neomycin was used as a selection marker. The presence of HPV E1, E2, E4, E5, E6, E7, L1, and L2 mRNAs and also transglutaminase 1, involucrin, cyclin dependent kinases (CDKs), cyclins, caspases, apoptosis inducing factor, DNase γ, Fas, and Fas ligand mRNAs in HPV transfected cells was investigated by means of reverse transcription polymerase chain reaction (RT-PCR). The G0–G1 cell population was analysed by flow cytometry. Morphological examination under light and electron microscopes was also carried out. Results: The virus transfected cells showed squamous metaplasia when they were injected into severe combined immunodeficient mice, expressing the high molecular weight keratin (Moll’s number 1 keratin) and involucrin molecules immunohistochemically, and involucrin and transglutaminase I mRNAs by RT-PCR. The squamous metaplasia was most conspicuous in the HPV transfected DLD-1 cell when compared with HPV transfected PC-14 cells. Squamous metaplasia was most clearly demonstrated in one HPV transfected DLD-1 cell clone, which expressed not only E2 but also E6–E7 fusion gene mRNA. Viral L1 mRNA expression was absent in HPV transfected cell clones, and was not related to squamous metaplasia. The growth rate of HPV transfected cells was reduced. Transfection of the virus into the cultured adenocarcinoma cells increased the G0–G1 cell population greatly, as assessed by flow cytometer analysis. Furthermore, in the virus transfected cells, apoptosis was also observed by means of the terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling method. Conclusion: HPV transfection into adenocarcinoma cells induced clear squamous metaplasia. One of the HPV transfected cell clones that expressed E2 and E6–E7 fusion gene mRNA showed the squamous metaplasia particularly clearly, and apoptosis was also demonstrated.","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 1","pages":"108 - 108"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64433501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Report on the second international workshop on the CCN family of genes.","authors":"B Perbal, D R Brigstock, L F Lau","doi":"10.1136/mp.56.2.80","DOIUrl":"https://doi.org/10.1136/mp.56.2.80","url":null,"abstract":"<p><p>For the second time, researchers from leading laboratories in the CCN field gathered in Saint-Malo, France, to participate in the Second International Workshop on the CCN family of genes. In addition to the regular research communications, meeting highlights included the inauguration of the first CCN newsletter (http://ccnnewsletter.free.fr) and the recognition of the International CCN Society (http://www.ccnsociety.jussieu.fr) as an important medium for the exchange of scientific knowledge and resources in the CCN field. Once more, the high quality of scientific communications and individual interactions set the stage for an extremely fruitful meeting.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 2","pages":"80-5"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.80","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22314689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The novel human MOST-1 (C8orf17) gene exhibits tissue specific expression, maps to chromosome 8q24.2, and is overexpressed/amplified in high grade cancers of the breast and prostate.","authors":"J M M Tan, E P C Tock, V T K Chow","doi":"10.1136/mp.56.2.109","DOIUrl":"https://doi.org/10.1136/mp.56.2.109","url":null,"abstract":"<p><strong>Aims: </strong>To elucidate genes that participate in the process of oncogenesis, primers based on the E6 genes of genital human papillomaviruses (HPVs) were used to amplify potential expressed sequence tags (ESTs) from the MOLT-4 T lymphoblastic leukaemia cell line.</p><p><strong>Methods: </strong>Using the polymerase chain reaction (PCR) with human papillomavirus E6 gene primers, an EST from the MOLT-4 T lymphoblastic leukaemia cell line was amplified. Via rapid amplification of cDNA ends (RACE) and cycle sequencing from MOLT-4 and fetal lung cDNA libraries, overlapping cDNAs of 2786 bp and 2054 bp of the corresponding novel human intronless gene designated MOST-1 (for MOLT-4 sequence tag-1) were characterised and assigned the symbol C8orf17 by the HUGO Nomenclature Committee.</p><p><strong>Results: </strong>Both cDNAs contained a potential open reading frame (ORF) of 297 bp incorporating a methionine codon with an ideal Kozak consensus sequence for translation initiation, and encoding a putative hydrophilic polypeptide of 99 amino acids. Although reverse transcription PCR (RT-PCR) demonstrated MOST-1 expression in all 19 cancer and two normal cell lines tested, differential expression was seen in only nine of 16 normal tissues tested (heart, kidney, liver, pancreas, small intestine, ovary, testis, prostate, and thymus). A 388 bp fragment was amplified from the NS-1 mouse myeloma cell line, the sequence of which was identical to that within the MOST-1 ORF. The MOST-1 gene was mapped by fluorescent in situ hybridisation to chromosome 8q24.2, a region amplified in many breast cancers and prostate cancers, which is also the candidate site of potential oncogene(s) other than c-myc located at 8q24.1. Analysis of paired biopsies of invasive ductal breast cancer and adjacent normal tissue by semiquantitative and real time RT-PCR revealed average tumour to normal ratios of MOST-1 expression that were two times greater in grade 3 cancers than in grade 1 and 2 cancers. Quantitative real time PCR of archival prostatic biopsies displayed MOST-1 DNA values that were 9.9, 7.5, 4.2, and 1.4 times higher in high grade carcinomas, intermediate grade carcinomas, low grade carcinomas, and benign hyperplasias, respectively, than in normal samples.</p><p><strong>Conclusions: </strong>These data suggest a role for MOST-1 in cellular differentiation, proliferation, and carcinogenesis.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 2","pages":"109-15"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22314693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. Maguire, J. W. Dale, T. McHugh, P. Butcher, S. Gillespie, A. Costetsos, H. Al-Ghusein, R. Holland, A. Dickens, L. Marston, P. Wilson, R. Pitman, D. Strachan, F. Drobniewski, D. Banerjee
{"title":"Molecular epidemiology of tuberculosis in London 1995–7 showing low rate of active transmission","authors":"H. Maguire, J. W. Dale, T. McHugh, P. Butcher, S. Gillespie, A. Costetsos, H. Al-Ghusein, R. Holland, A. Dickens, L. Marston, P. Wilson, R. Pitman, D. Strachan, F. Drobniewski, D. Banerjee","doi":"10.1136/mp.56.2.121","DOIUrl":"https://doi.org/10.1136/mp.56.2.121","url":null,"abstract":"Background: Tuberculosis notification rates for London have risen dramatically in recent years. Molecular typing of Mycobacterium tuberculosis has contributed to our understanding of the epidemiology of tuberculosis throughout the world. This study aimed to assess the degree of recent transmission of M tuberculosis in London and subpopulations of the community with high rates of recent transmission. Methods:M tuberculosis isolates from all persons from Greater London diagnosed with culture positive tuberculosis between 1 July 1995 and 31 December 1997 were genetically fingerprinted using IS6110 restriction fragment length polymorphism (RFLP) typing. A structured proforma was used during record review of cases of culture confirmed tuberculosis. Cluster analysis was performed and risk factors for clustering were examined in a univariate analysis followed by a logistic regression analysis with membership of a cluster as the outcome variable. Results: RFLP patterns were obtained for 2042 isolates with more than four copies of IS6110; 463 (22.7%) belonged to 169 molecular clusters, which ranged in size from two (65% of clusters) to 12 persons. The estimated rate of recent transmission was 14.4%. Young age (0–19 years) (odds ratio (OR) 2.65, 95% confidence interval (CI) 1.59 to 4.44), birth in the UK (OR 1.55, 95% CI 1.04 to 2.03), black Caribbean ethnic group (OR 2.19, 95% CI 1.15 to 4.16), alcohol dependence (OR 2.33, 95% CI 1.46 to 3.72), and streptomycin resistance (OR 1.82, 95% CI 1.15 to 2.88) were independently associated with an increased risk of clustering. Conclusions: Tuberculosis in London is largely caused by reactivation or importation of infection by recent immigrants. Newly acquired infection is also common among people with recognised risk factors. Preventative interventions and early diagnosis of immigrants from areas with a high incidence of tuberculosis, together with thorough contact tracing and monitoring of treatment outcome among all cases of tuberculosis (especially in groups at higher risk of recent infection), remains most important.","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 1","pages":"121 - 126"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64433514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L Huang, Y Y Cheng, L T C Chow, M H Zheng, S M Kumta
{"title":"Receptor activator of NF-kappaB ligand (RANKL) is expressed in chondroblastoma: possible involvement in osteoclastic giant cell recruitment.","authors":"L Huang, Y Y Cheng, L T C Chow, M H Zheng, S M Kumta","doi":"10.1136/mp.56.2.116","DOIUrl":"https://doi.org/10.1136/mp.56.2.116","url":null,"abstract":"<p><strong>Aims: </strong>Chondroblastoma is a rare, locally aggressive bone tumour that causes osteolytic destruction at the epiphyseal end of the affected bone. It is possible that tumour cells may stimulate osteoclastogenesis and osteolytic destruction through the production of receptor activator of NF-kappaB ligand (RANKL), which is a key molecule essential for regulating osteoclast formation and activity. Therefore, the expression of RANKL at both the mRNA and the protein level was investigated in chondroblastoma tumour tissue obtained from patients.</p><p><strong>Methods: </strong>The expression of RANKL gene transcripts was analysed by the reverse transcription-polymerase chain reaction (RT-PCR), and the cellular localisation of RANKL mRNA and protein was demonstrated by means of in situ hybridisation and immunohistochemistry.</p><p><strong>Results: </strong>RT-PCR analysis indicated that RANKL mRNA was present in all chondroblastoma specimens and normal cancellous bone samples, but not in normal articular cartilage and chondrosarcoma tissues. In contrast, gene transcripts of osteoprotegerin (OPG), the decoy receptor of RANKL, were detected in all types of tissues. The chondroid origin of neoplastic mononuclear cells in chondroblastoma was confirmed by positive S-100 immunohistochemical staining. Both RANKL mRNA and protein were exclusively expressed in these neoplastic mononuclear cells.</p><p><strong>Conclusions: </strong>These findings suggest that RANKL may be involved in the tumour cell induced recruitment of osteoclast-like cells and consequent osteolytic bone destruction in chondroblastoma.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 2","pages":"116-20"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.116","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22314694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D R Brigstock, R Goldschmeding, K-i Katsube, S C-T Lam, L F Lau, K Lyons, C Naus, B Perbal, B Riser, M Takigawa, H Yeger
{"title":"Proposal for a unified CCN nomenclature.","authors":"D R Brigstock, R Goldschmeding, K-i Katsube, S C-T Lam, L F Lau, K Lyons, C Naus, B Perbal, B Riser, M Takigawa, H Yeger","doi":"10.1136/mp.56.2.127","DOIUrl":"https://doi.org/10.1136/mp.56.2.127","url":null,"abstract":"<p><p>A proposal is put forth to unify the nomenclature of the CCN family of secreted, cysteine rich regulatory proteins. In the order of their description in the literature, CCN1 (CYR61), CCN2 (CTGF), CCN3 (NOV), CCN4 (WISP-1), CCN5 (WISP-2), and CCN6 (WISP-3) constitute a family of matricellular proteins that regulate cell adhesion, migration, proliferation, survival, and differentiation, at least in part through integrin mediated mechanisms. This proposal is endorsed by the International CCN Society and will serve to eliminate confusion from the multiple names that have been given to these molecules.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 2","pages":"127-8"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22314695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S L Preston, M R Alison, S J Forbes, N C Direkze, R Poulsom, N A Wright
{"title":"The new stem cell biology: something for everyone.","authors":"S L Preston, M R Alison, S J Forbes, N C Direkze, R Poulsom, N A Wright","doi":"10.1136/mp.56.2.86","DOIUrl":"https://doi.org/10.1136/mp.56.2.86","url":null,"abstract":"<p><p>The ability of multipotential adult stem cells to cross lineage boundaries (transdifferentiate) is currently causing heated debate in the scientific press. The proponents see adult stem cells as an attractive alternative to the use of embryonic stem cells in regenerative medicine (the treatment of diabetes, Parkinson's disease, etc). However, opponents have questioned the very existence of the process, claiming that cell fusion is responsible for the phenomenon. This review sets out to provide a critical evaluation of the current literature in the adult stem cell field.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 2","pages":"86-96"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.86","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22314691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T Kinjo, K Kamiyama, K Chinen, T Iwamasa, K Kurihara, T Hamada
{"title":"Squamous metaplasia induced by transfection of human papillomavirus DNA into cultured adenocarcinoma cells.","authors":"T Kinjo, K Kamiyama, K Chinen, T Iwamasa, K Kurihara, T Hamada","doi":"10.1136/mp.56.2.97","DOIUrl":"https://doi.org/10.1136/mp.56.2.97","url":null,"abstract":"<p><strong>Background/aim: </strong>It has been reported previously in cases of adenosquamous carcinoma of the lung in Okinawa, a subtropical island 2000 km south of mainland Japan, that the squamous cell carcinoma components were positive for human papillomavirus (HPV) by non-isotopic in situ hybridisation (NISH). The adenocarcinoma cells adjacent to the squamous cell carcinoma components were enlarged and also positive for HPV. This is thought to indicate that after adenocarcinoma cells are infected with HPV, they undergo morphological changes, and that \"squamous metaplasia\" follows. In this present study, the effects of HPV transfection into adenocarcinoma cells were examined. The relation between the region expressing the HPV gene and squamous metaplasia was also studied.</p><p><strong>Methods: </strong>Plasmid pBR322 containing HPV type 16 (HPV-16) was transfected into cultured colonic adenocarcinoma (DLD-1) and lung adenocarcinoma (PC-14) cells using the calcium phosphate method. Neomycin was used as a selection marker. The presence of HPV E1, E2, E4, E5, E6, E7, L1, and L2 mRNAs and also transglutaminase 1, involucrin, cyclin dependent kinases (CDKs), cyclins, caspases, apoptosis inducing factor, DNase gamma, Fas, and Fas ligand mRNAs in HPV transfected cells was investigated by means of reverse transcription polymerase chain reaction (RT-PCR). The G0-G1 cell population was analysed by flow cytometry. Morphological examination under light and electron microscopes was also carried out.</p><p><strong>Results: </strong>The virus transfected cells showed squamous metaplasia when they were injected into severe combined immunodeficient mice, expressing the high molecular weight keratin (Moll's number 1 keratin) and involucrin molecules immunohistochemically, and involucrin and transglutaminase I mRNAs by RT-PCR. The squamous metaplasia was most conspicuous in the HPV transfected DLD-1 cell when compared with HPV transfected PC-14 cells. Squamous metaplasia was most clearly demonstrated in one HPV transfected DLD-1 cell clone, which expressed not only E2 but also E6-E7 fusion gene mRNA. Viral L1 mRNA expression was absent in HPV transfected cell clones, and was not related to squamous metaplasia. The growth rate of HPV transfected cells was reduced. Transfection of the virus into the cultured adenocarcinoma cells increased the G0-G1 cell population greatly, as assessed by flow cytometer analysis. Furthermore, in the virus transfected cells, apoptosis was also observed by means of the terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling method.</p><p><strong>Conclusion: </strong>HPV transfection into adenocarcinoma cells induced clear squamous metaplasia. One of the HPV transfected cell clones that expressed E2 and E6-E7 fusion gene mRNA showed the squamous metaplasia particularly clearly, and apoptosis was also demonstrated.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 2","pages":"97-108"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.97","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22314692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"CCN posters","authors":"D. Ball","doi":"10.1136/mp.56.2.76","DOIUrl":"https://doi.org/10.1136/mp.56.2.76","url":null,"abstract":"The primary translational product of human connective tissue growth factor (CTGF) is predicted to comprise 349 residues, which, after cleavage of the signal peptide, is expected to produce a protein of 323 residues with a Mr of 38 000. Lower mass forms of CTGF comprising modules 3 and 4 or module 4 alone appear to exhibit some of the activities of the full-length CTGF protein, suggesting that functional domains are present in the C-terminal region of CTGF. To facilitate studies of the lowest mass form of CTGF identified to date, we have used an E coli expression system to produce a 10 kDa CTGF protein that comprises essentially module 4 and corresponds to residues 247–349 of human CTGF. The cDNA encoding 10 kDa CTGF (commencing at Glu247) was cloned into the pMAL-c2 vector (New England Biolabs) and the construct was transformed into E coli strain BL21. Escherichia coli carrying the cDNA for the maltose-binding protein–CTGF fusion protein were induced with isopropylthiogalactoside (IPTG) for one hour and then mechanically lysed using a French press. The cell extract was passed through an amylose resin and the bound fusion was eluted with 10 mM maltose. This protein was digested with factor Xa and the cleavage products further purified by heparin-affinity chromatography and reverse-phase high performance liquid chromatography. Recombinant 10 kDa CTGF demonstrated comparable immunoreactive and heparin-binding properties to native CTGF and promoted adhesion of several cell types including fibroblasts, endothelial cells, and epithelial cells. For each cell type tested, CTGFmediated cell adhesion was heparin dependent and was ablated by prior treatment of the CTGF with reducing agents. In conclusion, recombinant 10 kDa CTGF produced in E coli appears to mimic the biological activity and heparin-binding properties of native CTGF. The intrachain disulfide bridges within 10 kDa CTGF appear to be essential for promoting cell adhesion. This system is a viable source of truncated CTGF with which to perform structure– function studies.","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 1","pages":"76 - 79"},"PeriodicalIF":0.0,"publicationDate":"2003-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.2.76","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64433593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"p73 gene mutations in gastric adenocarcinomas.","authors":"E Pilozzi, C Talerico, A Platt, C Fidler, L Ruco","doi":"10.1136/mp.56.1.60","DOIUrl":"https://doi.org/10.1136/mp.56.1.60","url":null,"abstract":"<p><strong>Background/aims: </strong>The p73 gene encodes a protein that shares structural and functional homology with the p53 gene product. The highest degree of homology is in the DNA binding domain, which is the region of p53 that is most frequently mutated in cancer. In contrast to p53 there is little evidence that p73 acts as a classic tumour suppressor gene. Because of the similarities between the p53 and p73 genes and the high frequency of mutation of p53, this study was designed to investigate the p73 gene in patients with gastric adenocarcinoma.</p><p><strong>Methods: </strong>The mutational status of the p73 gene was investigated in a series of 13 cases of gastric adenocarcinoma from the antro-pyloric region and the gastro-oesophageal junction, using the polymerase chain reaction, single strand conformational polymorphism, and direct DNA sequencing.</p><p><strong>Results: </strong>A glutamine to arginine mutation was detected in exon 5 of the p73 gene in a case of adenocarcinoma at the gastro-oesophageal junction.</p><p><strong>Conclusion: </strong>Although limited to a small series of cases, these results suggest that p73 may have a potential pathogenetic role in this tumour.</p>","PeriodicalId":79512,"journal":{"name":"Molecular pathology : MP","volume":"56 1","pages":"60-2"},"PeriodicalIF":0.0,"publicationDate":"2003-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/mp.56.1.60","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22221839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}