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NECROSIS AND APORTOSIS OF HUMAN PANCREATIC CANCER CELL LINES-FOR THE IMPROVEMENT OF ADJUVANT CHEMOTHERAPY FOR PANCREATIC CANCER

Research Project

Project/Area Number 06671289
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Digestive surgery
Research InstitutionKYUSHU UNIVERSITY

Principal Investigator

MIZUMOTO Kazuhiro  KYUSHU UNIVERSITY,ASSISTANT PROFESSOR, 医学部, 助手 (90253418)

Co-Investigator(Kenkyū-buntansha) TANAKA Masao  KYUSHU UNIVERSITY,PROFESSOR, 医学部, 教授 (30163570)
SHIMURA Hideo  KYUSHU UNIVERSITY,ASSOCIATE PROFESSOR, 医学部, 講師 (80178996)
Project Period (FY) 1994 – 1995
Project Status Completed (Fiscal Year 1995)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
KeywordsPancreatic cancer / Radiation / Apoptosis / Necrosis
Research Abstract

Apoptosis and necrosis of human pancreatic cancer cell lines were comparatively investigated after 50 Gy irradiation, etoposide and tert-butylhydroperoxide. Human pancreatic cancer cell lines, MIA paca2 and Panc-1, and a human gall bladder cancer cell line, GB-d1 were used in the experiment. Cell deaths were determined by trypan blue exclusion test with cell number counting separately both on the floating cells and on the attached cells. Over 60% of the cells from three cell lines were dead 5 days after 50 Gy irradiation and those were clearly protected by the addition of 1 uM cycloheximide, a protein synthesis inhibitor. Typical apoptotic nuclear fragmentations and apoptotic bodies were also observed on 3 different cell lines by Papanicolaou staining. Electrophoresis revealed DNA ladder pattern on Panc-1 and GB-d1, however, DNA from MIA paca2 showed smear pattern. Again, DNA smear pattern was shown on MIA paca2 after the addition of 10 uM etoposide. With the flowcytometry, complete G2-M arrest 24 hr after 50 Gy irradiation and the accumulation to G2-M after the treatment of etoposide were shown while any cell cycle delay or arrest was not observed on necrosis induced by the treatment of tert-butylhydroperoxide. The results indicated that cell deaths after high dose X-ray irradiation may be apoptosis which is completely different from conventional necrosis.

Report

(3 results)
  • 1995 Annual Research Report   Final Research Report Summary
  • 1994 Annual Research Report

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Published: 1994-04-01   Modified: 2016-04-21  

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