This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (AngⅡ) and explored the possible mechanisms. Cell proliferation model of RASMCs was...This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (AngⅡ) and explored the possible mechanisms. Cell proliferation model of RASMCs was induced by treatmente with AngⅡ. Cells were randomly divided to 8 groups. Normally cultured VSMCs serves as blank control group; in AngⅡ model group, cells were treated with AngⅡ at 10–7 mol/L; in three astilbin groups, cells were treated with 10, 15, 30 mg/L of astilbin; in three AngⅡ+astilbin groups, cells were treated with AngⅡ (at 10–7 mol/L) and astilbin at 10, 15, 30 mg/L. Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined. The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR), and the expression of NF-κB in RASMCs was immunocytochemically observed. Our results showed that MTT metabo-lism in RASMCs in the basic and AngII stimulated situation was inhibited by astilbin, and the cells numbers of G0/G1 phase were increased and that of G2/S phase were decreased markedly. Not only highly expression of c-myc gene stimulated by AngⅡ could be inhibited by Astilbin significantly, but also the expression of NF-κB protein can be down regulated by Astilbin. We are led to conclude that astilbin astilbin can inhibit the AngⅡ-mediated proliferation of RASMCs by blocking the transition of RASMCs from G0/G1 phase to S phase and by down-regulating the expression of NF-κB, c-myc gene.展开更多
The allelic distribution of EcoRI and BamHI fragments of ras family genes between the human primary gastric cancer tissues and the corresponding adjacent normal tissues did not show any differences. Three genotypes of...The allelic distribution of EcoRI and BamHI fragments of ras family genes between the human primary gastric cancer tissues and the corresponding adjacent normal tissues did not show any differences. Three genotypes of BamHI restriction fragments length polymorphism of c-H-ras were revealed. No significant differences in the RFLPs were observed between normal individuals and gastric cancer patients. Four protooncogenes, c-H-ras, N-ras, c-myc and c-fos, were found to be transcriptionally active in the gastric cancer tissues in some cases examined. The comparison of the expression of these oncogenes between the malignant tissues and the corresponding normal tissues showed differential patterns. The expression of c-H-ras at cellular level was detected with in situ hybridization. The enhanced expression of c-H-ras in the gastric cancer cells was demonstrated, but the degree of the expession among the cancer cells was shown to be heterogeneous. In addition, the enhanced expression of c-H-ras was seen in the inflammatory cells.展开更多
Objective Despite advances in the understanding of the genotype - phenotype correlation in multiple endocrine neoplasia type 2A and 2B (MEN 2A, MEN 2B), and familial medullary thyroid carcinoma (FMTC), the frequency a...Objective Despite advances in the understanding of the genotype - phenotype correlation in multiple endocrine neoplasia type 2A and 2B (MEN 2A, MEN 2B), and familial medullary thyroid carcinoma (FMTC), the frequency and prognostic relevance of RET protoonco-gene mutations in sporadic medullary thyroid carcinomas (MTCs) remain controversial. Methods To study somatic mutations in the RET protooncogene in Japanese and Chinese sporadic MTCs and to comparatively analyze the correlation between RET mutation and tumor differentiation, we investigated somatic mutations in the RET protooncogene in 20 Japanese and 20 Chinese sporadic MTCs by the polymerase chain reaction - restriction fragment length polymorphism (PCR- RFLP) method. Results Of the 40 sporadic MTCs, 13 had a point mutation in codon 918 of exon 16, a frequency of 32.5%. There was no significant difference in the frequency between Japanese and Chinese sporadic MTCs, as 3096 of the Japanese and 35% of the Chinese sporadic MTCs contained this mutation.展开更多
In this article,we commented on the work done by Jiang et al,where they syn-thesized a kakkatin derivative,6-(hept-6-yn-1-yloxy)-3-(4-hydroxyphenyl)-7-me-thoxy-4H-chromen-4-one(HK),and investigated its antitumor activ...In this article,we commented on the work done by Jiang et al,where they syn-thesized a kakkatin derivative,6-(hept-6-yn-1-yloxy)-3-(4-hydroxyphenyl)-7-me-thoxy-4H-chromen-4-one(HK),and investigated its antitumor activities and me-chanism in gastric cancer MGC803 and hepatocellular carcinoma(HCC)SMMC-7721 cells.HK was evaluated for its antitumor activity as compared to kakkatin and cisplatin.This article focused on various risk factors of HCC,the mechanism of HCC progression and molecular targets of the kakkatin derivative,and limi-tations of available treatment options.HCC is a predominant form of primary liver cancer characterized by the accumulation of multiple gene modifications,overexpression of protooncogenes,altered immune microenvironment,and infilt-ration by immune cells.Puerariae flos(PF)has been used in traditional medicine in China,Korea,and Japan for lung clearing,spleen awakening,and relieving alcohol hangovers.PF exerts antitumor activity by inhibiting cancer cell prolif-eration,invasion,and migration.PF induces apoptosis in alcoholic HCC via the estrogen-receptor 1-extracellular signal-regulated kinases 1/2 signaling pathway.Kakkatin isolated from PF is known as a hepatoprotective bioflavonoid.The ka-kkatin derivative,HK,exhibited anticancer activity against HCC cell lines by in-hibiting cell proliferation and upregulating nuclear factor kappa B subunit 1 and phosphodiesterase 3B.However,further preclinical and clinical studies are required to establish its therapeutic potential against HCC.展开更多
BACKGROUND Ameloblastomas are common benign epithelial odontogenic neoplasms that present an aggressive and unpredictable behavior that may modify treatment strategies.Different signaling pathways that participate in ...BACKGROUND Ameloblastomas are common benign epithelial odontogenic neoplasms that present an aggressive and unpredictable behavior that may modify treatment strategies.Different signaling pathways that participate in the progression of these tumors have been identified.B-raf proto-oncogene serine/threonine kinase(BRAF)is a protein involved in the behavior of ameloblastomas,and it is related to many cell mechanisms.BRAF gene mutations have been identified in ameloblastomas,of which the BRAF V600E(valine substituted by glutamic acid at amino acid 600)mutation has been the most common and can be present concomitantly with other mutations that may be involved in its behavior.Targeted therapies have been used as an alternative in the case of resistance or contraindications to conventional treatments.AIM To document the presence of BRAF V600E and additional mutations,their behavior,and targeted therapies in these tumors.METHODS An electronic literature search was conducted according to PRISMA guidelines in PubMed/MEDLINE,Cochrane,EMBASE,and SpringerLink using the terms“ameloblastomas”,“BRAF V600E”,“additional mutations”,and“targeted therapies”.Ameloblastomas were classified according to WHO guidelines.Inclusion criteria were articles in English,published not more than 10 years ago,and studies with laboratory works related to BRAF V600E.Articles were evaluated by two independent reviewers and retrieved for full-text evaluation.The EBLIP Critical Appraisal Checklist was used to evaluate the quality of the eligible studies.Descriptive statistical analysis was performed.RESULTS Two independent reviewers,with a substantial concordance indicated by a kappa coefficient of k=0.76,evaluated a total of 19 articles that were included in this study.The analysis registered 521 conventional ameloblastomas(AM),81 unicystic ameloblastomas(UA),13 ameloblastic carcinomas(AC),three metastatic ameloblastomas(MA),and six peripheral ameloblastomas(PA),of which the histopathological type,anatomic location,laboratory tests,expression of BRAF mutation,and additional mutations were registered.The BRAF V600E mutation was found in 297 AM(57%),63 UA(77.7%),3 AC(23%),1 MA(50%),and 5 PA(83.3%).Follicular type predominated with a total of 116 cases(40%),followed by plexiform type with 63 cases(22.1%).Furthermore,both types presented additional mutations,in which alterations in JAK3 P132T,SMARCB1,PIK3CA,CTNNB1,SMO,and BRAF G606E genes were found.Four case reports were found with targeted therapy to BRAF V600E.CONCLUSION The identification of BRAF V600E and additional mutations as an aid in targeted therapies has been a breakthrough in alternative treatments of ameloblastomas where surgical treatments are contraindicated.展开更多
IM To study the number of AgNOR and rasp21 expression in different gastric mucosal lesions with Helicobacter pylori (Hp) infection to evaluate their biological behaviour and possible mechanism of Hp. METHODS Hp (usi...IM To study the number of AgNOR and rasp21 expression in different gastric mucosal lesions with Helicobacter pylori (Hp) infection to evaluate their biological behaviour and possible mechanism of Hp. METHODS Hp (using CLO test combined with WathinStarry staining), AgNOR (silver colloid technique) and rasp21 (monoclonal antibody and immunohistochemical staining—ABC method) were detected in 278 patients with endoscopically and pathologically confirmed gastric mucosal lesions, including chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), intestinal metaplasia (IM), dysplasia (Dys), and gastric cancer (GC). Among them, 146 cases were Hp positive, and 132 cases Hp negative. RESULTS The mean number of AgNOR in Hp positive group was significantly higher than that in Hp negative group in the gastric mucosal lesions except for CSG (P<005 or P<001). The positive rate of rasp21 expression in Hp positive group was also significantly higher than that in Hp negative group in gastric mucosal lesions except for CSG and CAG (P<005).CONCLUSION Hp+ gastric mucosal lesions have more biological behaviour of tumors. Hp may act as a promoter to activate ras gene and to stimulate cell over proliferation.展开更多
The human promyelocytic cell line HL-60 overexpresses the c-myc protooncogene. Plasmid pDACx carrying antisense human c-myc DNA and neo gene was introduced into HL-60 cells with lipofectin reagent. Upon DNA entering t...The human promyelocytic cell line HL-60 overexpresses the c-myc protooncogene. Plasmid pDACx carrying antisense human c-myc DNA and neo gene was introduced into HL-60 cells with lipofectin reagent. Upon DNA entering the tar-geted celis and expression of antisense transcripts to c-myc, C-MYC protein level, cell proliferation and colony-forming potentiality were all definitely inhibited.展开更多
Cancer after transplantation is the third cause of death and one of the more relevant comorbidities. Aim of this review is to verify the role of different pathogenetic mechanisms in cancer development in transplant pa...Cancer after transplantation is the third cause of death and one of the more relevant comorbidities. Aim of this review is to verify the role of different pathogenetic mechanisms in cancer development in transplant patients and in general population as well. In particular has been outlined the different role exerted by two different families of drug as calcineurin inhibitor and mammalian target of rapamycin(m TOR) inhibitor. The role of m TOR pathways in cell homeostasis is complex but enough clear. As a consequence the m TOR pathway deregulation is involved in the genesis of several cancers. Hence the relevant role of m TOR inhibitors. The authors review the complex mechanism of action of m TOR inhibitors, not only for what concerns the immune system but also other cells as endothelial, smooth muscle and epithelial cells. The mechanism of action is still now not completely defined and understood. It implies the inhibition of m TOR pathway at different levels, but mainly at level of the phosphorylation of several intracellular kinases that contribute to activate m TOR complex. Many prospective and retrospective studies in transplant patients document the antineoplastic role of m TOR inhibition. More recently m TOR inhibitors proven to be effective in the treatment of some cancers also in general population. Kidney cancers, neuroendocrine tumors and liver cancers seem to be the most sensitive to these drugs. Best results are obtained with a combination treatment, targeting the m TOR pathway at different levels.展开更多
Sprague-Dawley rats were implanted with silastic capsules containing β-estradiol. After 60 days, their pituitary weights, serum prolactin contentsand transcription level of c-myc proto-oncogene were found increasedsi...Sprague-Dawley rats were implanted with silastic capsules containing β-estradiol. After 60 days, their pituitary weights, serum prolactin contentsand transcription level of c-myc proto-oncogene were found increasedsignificantly. It was also found that the anterior pituitary cells proliferatedsignificantly, but their differentiation was suppressed.展开更多
To investigate the expression sequence and distribution characteristics of the p rotooncogenes c fos, c myc and endogenous basic fibroblast growth factor (bFGF ) genes in burned tissues, and to explore the possible ...To investigate the expression sequence and distribution characteristics of the p rotooncogenes c fos, c myc and endogenous basic fibroblast growth factor (bFGF ) genes in burned tissues, and to explore the possible effects of changes in the se genes' functions on wound healing Methods Partial thickness burns of 30% TBSA were established on backs of Wistar rats In situ hybridization and histological methods were used to detect expression of c fos, c myc and bFGF genes in normal and burned tissue at 3 h, 6 h, 1 d, 3 d , 7 d and 14 d postburn Results Although expression of c fos and c myc genes and bFGF gene could be found in n ormal skin, the expression of all three were markedly induced by burn wounds and the expression models in sequence and distribution were quite different Expre ssion of c fos gene increased and peaked at 6 h Signals were mainly localiz ed in both nuclei of dermal fibroblasts and monocytes The expression of bFGF gene increased at 6 h and peaked at 1 d postburn, and was distributed in the cyt oplasm of fibroblasts C myc gene peaked 3 d postburn and was also distributed in the cytoplasm of fibroblasts Conclusions These results indicated that thermal injury could induce the expression of c fo s, c myc and bFGF at gene level, showing phasic control and regional distributi on The phasic expression of these genes suggests that there is an interaction between protooncogenes and bFGF, which may play an important role in wound heali ng The different expressions of c fos and c myc play an inducing role in reg ulating bFGF, and in turn affect wound healing展开更多
基金supported by agrant from the National Natural Science Foundation of China(No.30500656)
文摘This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (AngⅡ) and explored the possible mechanisms. Cell proliferation model of RASMCs was induced by treatmente with AngⅡ. Cells were randomly divided to 8 groups. Normally cultured VSMCs serves as blank control group; in AngⅡ model group, cells were treated with AngⅡ at 10–7 mol/L; in three astilbin groups, cells were treated with 10, 15, 30 mg/L of astilbin; in three AngⅡ+astilbin groups, cells were treated with AngⅡ (at 10–7 mol/L) and astilbin at 10, 15, 30 mg/L. Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined. The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR), and the expression of NF-κB in RASMCs was immunocytochemically observed. Our results showed that MTT metabo-lism in RASMCs in the basic and AngII stimulated situation was inhibited by astilbin, and the cells numbers of G0/G1 phase were increased and that of G2/S phase were decreased markedly. Not only highly expression of c-myc gene stimulated by AngⅡ could be inhibited by Astilbin significantly, but also the expression of NF-κB protein can be down regulated by Astilbin. We are led to conclude that astilbin astilbin can inhibit the AngⅡ-mediated proliferation of RASMCs by blocking the transition of RASMCs from G0/G1 phase to S phase and by down-regulating the expression of NF-κB, c-myc gene.
文摘The allelic distribution of EcoRI and BamHI fragments of ras family genes between the human primary gastric cancer tissues and the corresponding adjacent normal tissues did not show any differences. Three genotypes of BamHI restriction fragments length polymorphism of c-H-ras were revealed. No significant differences in the RFLPs were observed between normal individuals and gastric cancer patients. Four protooncogenes, c-H-ras, N-ras, c-myc and c-fos, were found to be transcriptionally active in the gastric cancer tissues in some cases examined. The comparison of the expression of these oncogenes between the malignant tissues and the corresponding normal tissues showed differential patterns. The expression of c-H-ras at cellular level was detected with in situ hybridization. The enhanced expression of c-H-ras in the gastric cancer cells was demonstrated, but the degree of the expession among the cancer cells was shown to be heterogeneous. In addition, the enhanced expression of c-H-ras was seen in the inflammatory cells.
文摘Objective Despite advances in the understanding of the genotype - phenotype correlation in multiple endocrine neoplasia type 2A and 2B (MEN 2A, MEN 2B), and familial medullary thyroid carcinoma (FMTC), the frequency and prognostic relevance of RET protoonco-gene mutations in sporadic medullary thyroid carcinomas (MTCs) remain controversial. Methods To study somatic mutations in the RET protooncogene in Japanese and Chinese sporadic MTCs and to comparatively analyze the correlation between RET mutation and tumor differentiation, we investigated somatic mutations in the RET protooncogene in 20 Japanese and 20 Chinese sporadic MTCs by the polymerase chain reaction - restriction fragment length polymorphism (PCR- RFLP) method. Results Of the 40 sporadic MTCs, 13 had a point mutation in codon 918 of exon 16, a frequency of 32.5%. There was no significant difference in the frequency between Japanese and Chinese sporadic MTCs, as 3096 of the Japanese and 35% of the Chinese sporadic MTCs contained this mutation.
基金Supported by the Indian Council of Scientific and Industrial Research,No.MLP0204(CSIR-IHBT no.5712).
文摘In this article,we commented on the work done by Jiang et al,where they syn-thesized a kakkatin derivative,6-(hept-6-yn-1-yloxy)-3-(4-hydroxyphenyl)-7-me-thoxy-4H-chromen-4-one(HK),and investigated its antitumor activities and me-chanism in gastric cancer MGC803 and hepatocellular carcinoma(HCC)SMMC-7721 cells.HK was evaluated for its antitumor activity as compared to kakkatin and cisplatin.This article focused on various risk factors of HCC,the mechanism of HCC progression and molecular targets of the kakkatin derivative,and limi-tations of available treatment options.HCC is a predominant form of primary liver cancer characterized by the accumulation of multiple gene modifications,overexpression of protooncogenes,altered immune microenvironment,and infilt-ration by immune cells.Puerariae flos(PF)has been used in traditional medicine in China,Korea,and Japan for lung clearing,spleen awakening,and relieving alcohol hangovers.PF exerts antitumor activity by inhibiting cancer cell prolif-eration,invasion,and migration.PF induces apoptosis in alcoholic HCC via the estrogen-receptor 1-extracellular signal-regulated kinases 1/2 signaling pathway.Kakkatin isolated from PF is known as a hepatoprotective bioflavonoid.The ka-kkatin derivative,HK,exhibited anticancer activity against HCC cell lines by in-hibiting cell proliferation and upregulating nuclear factor kappa B subunit 1 and phosphodiesterase 3B.However,further preclinical and clinical studies are required to establish its therapeutic potential against HCC.
文摘BACKGROUND Ameloblastomas are common benign epithelial odontogenic neoplasms that present an aggressive and unpredictable behavior that may modify treatment strategies.Different signaling pathways that participate in the progression of these tumors have been identified.B-raf proto-oncogene serine/threonine kinase(BRAF)is a protein involved in the behavior of ameloblastomas,and it is related to many cell mechanisms.BRAF gene mutations have been identified in ameloblastomas,of which the BRAF V600E(valine substituted by glutamic acid at amino acid 600)mutation has been the most common and can be present concomitantly with other mutations that may be involved in its behavior.Targeted therapies have been used as an alternative in the case of resistance or contraindications to conventional treatments.AIM To document the presence of BRAF V600E and additional mutations,their behavior,and targeted therapies in these tumors.METHODS An electronic literature search was conducted according to PRISMA guidelines in PubMed/MEDLINE,Cochrane,EMBASE,and SpringerLink using the terms“ameloblastomas”,“BRAF V600E”,“additional mutations”,and“targeted therapies”.Ameloblastomas were classified according to WHO guidelines.Inclusion criteria were articles in English,published not more than 10 years ago,and studies with laboratory works related to BRAF V600E.Articles were evaluated by two independent reviewers and retrieved for full-text evaluation.The EBLIP Critical Appraisal Checklist was used to evaluate the quality of the eligible studies.Descriptive statistical analysis was performed.RESULTS Two independent reviewers,with a substantial concordance indicated by a kappa coefficient of k=0.76,evaluated a total of 19 articles that were included in this study.The analysis registered 521 conventional ameloblastomas(AM),81 unicystic ameloblastomas(UA),13 ameloblastic carcinomas(AC),three metastatic ameloblastomas(MA),and six peripheral ameloblastomas(PA),of which the histopathological type,anatomic location,laboratory tests,expression of BRAF mutation,and additional mutations were registered.The BRAF V600E mutation was found in 297 AM(57%),63 UA(77.7%),3 AC(23%),1 MA(50%),and 5 PA(83.3%).Follicular type predominated with a total of 116 cases(40%),followed by plexiform type with 63 cases(22.1%).Furthermore,both types presented additional mutations,in which alterations in JAK3 P132T,SMARCB1,PIK3CA,CTNNB1,SMO,and BRAF G606E genes were found.Four case reports were found with targeted therapy to BRAF V600E.CONCLUSION The identification of BRAF V600E and additional mutations as an aid in targeted therapies has been a breakthrough in alternative treatments of ameloblastomas where surgical treatments are contraindicated.
文摘IM To study the number of AgNOR and rasp21 expression in different gastric mucosal lesions with Helicobacter pylori (Hp) infection to evaluate their biological behaviour and possible mechanism of Hp. METHODS Hp (using CLO test combined with WathinStarry staining), AgNOR (silver colloid technique) and rasp21 (monoclonal antibody and immunohistochemical staining—ABC method) were detected in 278 patients with endoscopically and pathologically confirmed gastric mucosal lesions, including chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), intestinal metaplasia (IM), dysplasia (Dys), and gastric cancer (GC). Among them, 146 cases were Hp positive, and 132 cases Hp negative. RESULTS The mean number of AgNOR in Hp positive group was significantly higher than that in Hp negative group in the gastric mucosal lesions except for CSG (P<005 or P<001). The positive rate of rasp21 expression in Hp positive group was also significantly higher than that in Hp negative group in gastric mucosal lesions except for CSG and CAG (P<005).CONCLUSION Hp+ gastric mucosal lesions have more biological behaviour of tumors. Hp may act as a promoter to activate ras gene and to stimulate cell over proliferation.
文摘The human promyelocytic cell line HL-60 overexpresses the c-myc protooncogene. Plasmid pDACx carrying antisense human c-myc DNA and neo gene was introduced into HL-60 cells with lipofectin reagent. Upon DNA entering the tar-geted celis and expression of antisense transcripts to c-myc, C-MYC protein level, cell proliferation and colony-forming potentiality were all definitely inhibited.
文摘Cancer after transplantation is the third cause of death and one of the more relevant comorbidities. Aim of this review is to verify the role of different pathogenetic mechanisms in cancer development in transplant patients and in general population as well. In particular has been outlined the different role exerted by two different families of drug as calcineurin inhibitor and mammalian target of rapamycin(m TOR) inhibitor. The role of m TOR pathways in cell homeostasis is complex but enough clear. As a consequence the m TOR pathway deregulation is involved in the genesis of several cancers. Hence the relevant role of m TOR inhibitors. The authors review the complex mechanism of action of m TOR inhibitors, not only for what concerns the immune system but also other cells as endothelial, smooth muscle and epithelial cells. The mechanism of action is still now not completely defined and understood. It implies the inhibition of m TOR pathway at different levels, but mainly at level of the phosphorylation of several intracellular kinases that contribute to activate m TOR complex. Many prospective and retrospective studies in transplant patients document the antineoplastic role of m TOR inhibition. More recently m TOR inhibitors proven to be effective in the treatment of some cancers also in general population. Kidney cancers, neuroendocrine tumors and liver cancers seem to be the most sensitive to these drugs. Best results are obtained with a combination treatment, targeting the m TOR pathway at different levels.
文摘Sprague-Dawley rats were implanted with silastic capsules containing β-estradiol. After 60 days, their pituitary weights, serum prolactin contentsand transcription level of c-myc proto-oncogene were found increasedsignificantly. It was also found that the anterior pituitary cells proliferatedsignificantly, but their differentiation was suppressed.
基金ThisworkwassupportedinpartbytheNationalOutstandingYoungResearcher (No 3952 50 2 4 )NationalNatureandScienceFoundation(No 30 1 90 9766)andNational"973"Program (No G1 9990 542 0 4 )
文摘To investigate the expression sequence and distribution characteristics of the p rotooncogenes c fos, c myc and endogenous basic fibroblast growth factor (bFGF ) genes in burned tissues, and to explore the possible effects of changes in the se genes' functions on wound healing Methods Partial thickness burns of 30% TBSA were established on backs of Wistar rats In situ hybridization and histological methods were used to detect expression of c fos, c myc and bFGF genes in normal and burned tissue at 3 h, 6 h, 1 d, 3 d , 7 d and 14 d postburn Results Although expression of c fos and c myc genes and bFGF gene could be found in n ormal skin, the expression of all three were markedly induced by burn wounds and the expression models in sequence and distribution were quite different Expre ssion of c fos gene increased and peaked at 6 h Signals were mainly localiz ed in both nuclei of dermal fibroblasts and monocytes The expression of bFGF gene increased at 6 h and peaked at 1 d postburn, and was distributed in the cyt oplasm of fibroblasts C myc gene peaked 3 d postburn and was also distributed in the cytoplasm of fibroblasts Conclusions These results indicated that thermal injury could induce the expression of c fo s, c myc and bFGF at gene level, showing phasic control and regional distributi on The phasic expression of these genes suggests that there is an interaction between protooncogenes and bFGF, which may play an important role in wound heali ng The different expressions of c fos and c myc play an inducing role in reg ulating bFGF, and in turn affect wound healing
