期刊文献+

口腔粘膜癌前病变和鳞癌组织细胞增殖和凋亡的原位观察 被引量:1

Cell apoptosis and proliferation in oral cancer and precancerous lesions
暂未订购
导出
摘要 目的 研究自口腔正常粘膜上皮向异常增生和鳞癌组织演变过程中细胞增殖和凋亡的变化 ,阐明口腔癌发病机制。方法 采用免疫组织化学S -P法和原位末端标记法检测 10例正常口腔粘膜上皮、48例异常增生上皮和 42例鳞癌组织中增殖细胞数和凋亡数。结果 异常增生上皮细胞增殖和凋亡数均明显高于正常组 (P <0 .0 5 ) ,但随着增生程度的加重 ,伴随着细胞增殖能力逐级增强 ,细胞凋亡数无明显提高 (P >0 .0 5 )。鳞癌组织中 ,随着组织学分级的增加 ,增殖数明显增多 ,凋亡数逐级减少。结论 癌前病变中 ,细胞凋亡速度增加跟不上增殖速度 ,导致向鳞癌转变。癌细胞增殖不断加强 ,凋亡不断下降 。 Objective To study the alteration of cell proliferation and cell apoptosis during the development of oral squamous cell carcinoma (SCC).Methods The number of cell proliferation (Ki67) and apoptosis (AI) was observed in 10 normal oral epithelial,48 epithelial dysplasia and 42 SCC by immunohistochemical and TUNEL evaluation.Results In dysplastic epithelia,the number of Ki67 and AI was more than that of normal epithelia,and with the dysplasis increasing,the Ki67 number increased significantly,while the AI had no significant elevation.In SCC,with the differentiation decreasing,the Ki67 number was increased,the AI was decreased.Conclusion The increasing rate of cell apoptosis can't keep up with the rate of cell proliferation,which induces the change towards oral SCC.The proliferation of cancer cell become more and more intensive,while the apoptosis are lastingly down-regulated.Both factors will result in the development of SCC.
出处 《现代口腔医学杂志》 CAS CSCD 2001年第5期326-328,I002,共4页 Journal of Modern Stomatology
基金 福建省教委资助 (99CA -173 )
关键词 口腔粘膜癌 癌前病变 鳞状细胞癌 细胞增殖 细胞凋亡 原位观察 Drecancerous lesion SCC Ki67 Apoptosis
  • 相关文献

参考文献8

  • 1[1]Wrone ST, Jsty R, Castle V, et al. Keratinocytes in psoriatic plaques contain single strand DAN breaks but are resistant to induction of apoptosis. J Invest Dermatol, 1996,106(5) :832 - 837.
  • 2[2]Matra RS, Phil S, Kimberly EF, et al. Apoptosis in keratinocytes is not dependent of induction of differentiation. Lab Invest, 1997, 76(1):99- 107.
  • 3[3]Birchall MA, Winterford CM, Gobe W, et al. Apoptosis and mitosis in oral and oropharyngeal epithelium: evodence for a topographical swicth in premalignant lesion. Cell Proliferation, 1996,29(3) :447 -456.
  • 4[4]Birchall MA, Schoch E, Hamon BV, et al. Apoptosis mitosis PCNA and bcl - 2 in normal, leukoplakic and malignant epithelia of the human oral cavity: prospective, in vivo study. Oral Oncology, 1997,33(3) :419 - 425.
  • 5[5]Jennifer K, Grace B, Richard CK, et al. Patterns of p53 and Ki67protein expression in epithelial dysplasia from thr floor of the mouth.Joumal of Pathology, 1997,183(2) :418 - 423.
  • 6[6]Christina I,Theodore DK, Lora H, et al. Both cell proliferation and apoptosis increase with lesion grade in cervical neoplasia but do not correlate with human papillomavirus type. Cancer Res, 1996,56(2):669 - 674.
  • 7[7]Veltri RR,Vukanovic J, Epstein J J, et al. Implication of cell kinetic changes during the progression of human prostatic cancer. Clin Cancer Res, 1995,1 ( 1 ) :473 - 480.
  • 8[8]Loro L, Vintermyr O, Johannessene A, et al. Suppression of fas receptor and negative correlation of fas ligand with differentiation and apoptosis in oral squarnous cell carcinoma. J Oral Pathol, 1999,28(1):82-87.

同被引文献9

引证文献1

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部