【Abstract】Objective To find out if apoptosis is induced after intra-radiotherapy and its effects on pericarcinomal tissue.
Methods From 1994 to 1998, 44 patients with unresectable liver cancer received 32P-GMS intra-radiotherapy. After 2 to 6 months the tumors in 3 cases could be resected and we used this cases as the treatment group. We use 4 patients with resectional HCC of same age, diseased region, differentiated but without anyother therapy as the control group. The TUNEL staining was used to stain the resected tissue, and the apoptosis index was counted.
Results The apoptosis index of carcinoma was 29%～34%, average (31±16)% in the treatment group and that of the control group was 4%～6%, average (5±12.2)%. The apoptosis index of pericarcinomal tissue was 27%～37%, average (35±11)% in the treatment group and that of the control group was 0.3%～5%, average (4.1±3.3)%.
Conclusion 32P-GMS intra-radiotherapy can enhance the apoptosis of HCC and its adjacent tissue.
Citation：
LI Zhihui,YAN Lnan,LI Li,GUAN Yongsong.. Apoptosis after Phosphorus-32 Glass Microspheres Intra-Radiotherapy in Hepatocellular Carcinoma. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2004, 11(6): 515-517. doi:
Copy
Copyright ? the editorial department of CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY of West China Medical Publisher. All rights reserved
| 1. |
傅清揚，趙慧揚. 臨床同位素手冊 [M]. 第1版. 鄭州： 河南人民出版社， 1981∶18～22.
|
| 2. |
嚴律南，李立，陳曉理，等. 32磷玻璃微球肝動脈栓塞治療晚期肝癌的初步研究 [J]. 中華外科雜志， 1996； 34（9）∶526.
|
| 3. |
Seong J, Kim SH, Suh CO. Enhancement of tumor radioresponse by combined chemotherapy in murine hepatocarcinoma [Ｊ]. J Gastroenterol Hepatol， 2001; 16(8)∶883.
|
| 4. |
Chmura SJ, Nodzenski E, Beckett MA, et al. Loss of ceramide production confers resistanced to radiationinduce apoptosis [Ｊ]. Cancer Res, 1997; 57(7)∶1270.
|
| 5. |
Rehemtulla A, Hamilton CA, Chinnaiyan AM, et al. Ultraviolet radiationinduced aopotosis is mediated by activation of CD95(Fas/APO1) [Ｊ]. J Biol Chem, 1997; 272(41)∶25783.
|
| 6. |
Fuchs EJ, Mckenna KA, Bedi A. p53dependent DNA damageinduced apotosis requires Fas/APO1independent activation of CPP32 beta [Ｊ]. Cancer Res, 1997; 57(13)∶2550.
|
| 7. |
吳瑋，孔憲濤，李莉，等. 亞致死量γ射線照射后小鼠脾臟CD95陰性淋巴細胞變化規律的研究 [Ｊ]. 中華放射醫學與防護雜志， 1997； 17（5）∶305.
|
- 1. 傅清揚，趙慧揚. 臨床同位素手冊 [M]. 第1版. 鄭州： 河南人民出版社， 1981∶18～22.
- 2. 嚴律南，李立，陳曉理，等. 32磷玻璃微球肝動脈栓塞治療晚期肝癌的初步研究 [J]. 中華外科雜志， 1996； 34（9）∶526.
- 3. Seong J, Kim SH, Suh CO. Enhancement of tumor radioresponse by combined chemotherapy in murine hepatocarcinoma [Ｊ]. J Gastroenterol Hepatol， 2001; 16(8)∶883.
- 4. Chmura SJ, Nodzenski E, Beckett MA, et al. Loss of ceramide production confers resistanced to radiationinduce apoptosis [Ｊ]. Cancer Res, 1997; 57(7)∶1270.
- 5. Rehemtulla A, Hamilton CA, Chinnaiyan AM, et al. Ultraviolet radiationinduced aopotosis is mediated by activation of CD95(Fas/APO1) [Ｊ]. J Biol Chem, 1997; 272(41)∶25783.
- 6. Fuchs EJ, Mckenna KA, Bedi A. p53dependent DNA damageinduced apotosis requires Fas/APO1independent activation of CPP32 beta [Ｊ]. Cancer Res, 1997; 57(13)∶2550.
- 7. 吳瑋，孔憲濤，李莉，等. 亞致死量γ射線照射后小鼠脾臟CD95陰性淋巴細胞變化規律的研究 [Ｊ]. 中華放射醫學與防護雜志， 1997； 17（5）∶305.
