Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.

ÃëÀå¾Ï¿¡¼­ Inducible Nitric Oxide SynthaseÀÇ ¿ªÇÒ The roles of inducible nitric oxide synthase expression in pancreatic cancer

´ëÇѳ»°úÇÐȸÁö 2001³â 61±Ç 6È£ p.597 ~ 605
¼Ò¼Ó »ó¼¼Á¤º¸
ÀÌ¿ë¿í/Yong Wook Lee À̱ÔÅÃ/¾Èº´ÈÆ/¹Úµ¿ÀÏ/ÀÌÁ¾±Õ/¹é½Â¿î/ÀÌÁ¾Ã¶/ÃÖ±Ô¿Ï/±è¿Ï¼·/±èÀº°æ/°ø±¸/Kyu Taek Lee/Byeong Hoon Ahn/Dong Il Park/Jong Kyun Lee/Seung Woon Paik/Jong Chul Rhee/Kyoo Wan Choi/Wan Seop Kim/Eun Kyung Kim/Gu Kong

Abstract

¸ñÀû: ÃéÀå¾Ï¿¡¼­ iNOS ¹ßÇöÀº ´Ù¸¥ °íÇü¾Ï¿¡¼­ ó·³ ¹ß¾Ï°úÁ¤°ú Á¾¾çÀÇ ÁøÇà¿¡¼­ Áß¿äÇÑ ¿ªÇÒÀ» ÇÒ °ÍÀ¸·Î »ý°¢µÇ°í ÀÖ´Ù. ÀÌ¿¡ iNOS ¹ßÇöÀÌ ÃéÀå¾Ï¿¡¼­ ¹ß¾Ï°úÁ¤À̳ª ¾ÏÀÇ ÁøÇà¿¡ ±â¿©ÇÏ´Â ¹Ù¸¦ ¾Ë¾Æº¸°íÀÚ º» ¿¬±¸¸¦ ½ÃÇàÇÏ¿´´Ù. ´ë»ó¹×¹æ¹ý
ÃéÀå¾ÏÀ¸·Î
¼ö¼ú ¹ÞÀº 72¿¹¸¦ ´ë»óÀ¸·Î ÃéÀå¾Ï Á¶Á÷¿¡ ´ëÇÏ¿© iNOS ¸é¿ªÁ¶Á÷È­ÇÐ ¿°»öÀ» ÇÏ¿´°í °¢ Á¶Á÷¿¡¼­ ¼¼Æ÷°í»ç Á¤µµ¿Í ¼¼Æ÷Áõ½Ä Á¤µµ ±×¸®°í Ç÷°üÇü¼º Á¤µµ¸¦ °¢°¢ TUNEL ¿°»ö°ú Ki-67°ú CD34¿¡ ´ëÇÑ Ç×ü¸¦ ÀÌ¿ëÇÑ ¸é¿ªÁ¶Á÷È­ÇÐ ¿°»öÀ» ÅëÇÏ¿© °üÂûÇÏ¿´´Ù. ¶ÇÇÑ
ÀÓ»óº´¸®ÇÐÀû
Ư¡°ú iNOS ¹ßÇö°úÀÇ °ü°è¸¦ ¾Ë¾Æº¸±â À§ÇÏ¿© ȯÀÚÀÇ ³ªÀÌ, ÃéÀå¾ÏÀÇ Å©±â, À§Ä¡, º´±â, ÀüÀÌÀ¯¹«, ºÐÈ­µµ ¹× ¿¹ÈÄ¿ÍÀÇ »ó°ü°ü°è¸¦ ºÐ¼®ÇÏ¿´´Ù. °á°ú: (1) ÃéÀå¾ÏÀÇ »óÇǼ¼Æ÷¿Í °£Áú¼¼Æ÷¿¡¼­ iNOS ¹ßÇöÀÌ °üÂûµÇ¾úÀ¸¸ç (2) iNOS ¹ßÇöÀÌ µÈ Á¶Á÷¿¡¼­
¼¼Æ÷°í»ç
Áö¼ö°¡ ÀǹÌÀÖ°Ô ³ô¾ÒÀ¸¸ç iNOS ¹ßÇö °­µµ°¡ Áõ°¡Çϸ鼭 ¼¼Æ÷°í»ç Áö¼öµµ Áõ°¡ÇÏ´Â °æÇâÀ» º¸¿´°í (3) ¼¼Æ÷Áõ½Ä Áö¼ö³ª ¹Ì¼¼Ç÷°ü ¹Ðµµ´Â iNOS ¹ßÇö¿¡ µû¶ó Â÷À̸¦ º¸ÀÌÁö ¾Ê¾Ò´Ù. (4) ÃéÀå¾ÏÀÇ ¿©·¯ ÀÓ»óº´¸®ÇÐÀû ¼Ò°ßÀº iNOS ¹ßÇö À¯¹«¿¡ µû¶ó Â÷À̸¦ º¸ÀÌÁö
¾Ê¾Ò´Ù.
°á·Ð: ÃéÀå¾Ï¿¡¼­ÀÇ iNOS ¹ßÇöÀº ¼¼Æ÷°í»ç¿Í °ü·ÃÀÌ ÀÖÀ¸¸ç ¼¼Æ÷ÀÇ Áõ½Ä¾ïÁ¦´Â µ¿¹ÝµÇÁö ¾Ê¾Æ »ýü³»¿¡¼­ ¼¼Æ÷Áõ½ÄÀº ¼¼Æ÷°í»ç¿Ü ´Ù¸¥ ¿©·¯ÀÎÀڵ鿡 ÀÇÇÏ¿© Á¶Àý¹Þ°í ÀÖ´Â °ÍÀ¸·Î »ý°¢ÀÌ µÇ¸ç ÀÓ»óÀûÀ¸·Îµµ »ýÁ¸À²À̳ª ÀüÀÌ µî°úÀÇ °ü·ÃÀ» ãÀ» ¼ö ¾ø¾ú´Ù.
µû¶ó¼­
ÃéÀå¾ÏÀÇ Ä¡·á·Î iNOS Á¶ÀýÀº ÇâÈÄ Áö¼ÓÀûÀÎ ¿¬±¸°¡ ÇÊ¿äÇÒ °ÍÀ¸·Î »ý°¢µÈ´Ù.

Background: The finding of frequent inducible nitric oxide synthase (iNOS) expression in human cancer indicates that nitric oxide has a pathological role in tumor progression. Increased expression of iNOS in human pancreatic cancer cells
was
also
recently reported. but the clinicopathological and biological significance of the iNOS expression remains unclear. The aim of our study was to look for possible roles and clinical significance of iNOS expression in pancreatic cancer.
Methods: 72
pancreatic adenocarcinoma tissue specimens were obtained from surgical resection. We investigated the immunohistochemical expression of iNOS in respect to variable clinicopathological characteristics, proliferation activity (assayed by Ki-67
expression), apoptosis (by TUNEL stain), and microvessel density (by CD34 expression; angiogenesis). Results: Immunohistochemical positivity for iNOS in pancreatic epithelial cells was observed in 48/72 (66.7%). Apoptotic index (AI) of
positive
iNOS expressions were significantly higher than for negative expression (p£¼0.001) and increasing intensity of COX-2 expression showed a trend with increasing AI (p£¼0.001). No significant association was found between iNOS expression and
proliferation
index or microvessel density in pancreatic cancer. The expression of iNOS protein did not correlated with age, bilirubin, CA 19-9, location, size, AJCC stage, differentiation, distant metastasis or patient survival. Conclusion: The
expression of
iNOS enzyme in pancreatic cancer contributes to apoptosis of tumor cells. However, we could not find any correlation between iNOS expression and cell proliferation, angiognesis of clinical characteristics. Further in vivo investigations are
necessary to
determine the putative role of the iNOS expression for tumor progression in human pancreatic cancer.

Nitric Oxide Synthase; Inducible Adenocarcinoma; Adenocarcinoma; Pancreatic; Apoptosis; Proliferation; Angiogenesis;

Å°¿öµå

¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸

 

µîÀçÀú³Î Á¤º¸

KCI
KoreaMed
KAMS