Pancreatic cancer

被引:1916
作者
Li, DH [1 ]
Xie, KP [1 ]
Wolff, R [1 ]
Abbruzzese, JL [1 ]
机构
[1] Univ Texas, MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA
关键词
D O I
10.1016/S0140-6736(04)15841-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Pancreatic cancer remains a major unsolved health problem, with conventional cancer treatments having little impact on disease course. Almost all patients who have pancreatic cancer develop metastases and die. The main risk factors are smoking, age, and some genetic disorders, although the primary causes are poorly understood. Advances in molecular biology have, however, greatly improved understanding of the pathogenesis of pancreatic cancer. Many patients have mutations of the K-ras oncogene, and various tumour-suppressor genes are also inactivated. Growth factors also play an important part. However, disease prognosis is extremely poor. Around 15-20% of patients have resectable disease, but only around 20% of these survive to 5 years. For locally advanced, unresectable, and metastatic disease, treatment is palliative, although fluorouracil chemoradiation for locally advanced and gemcitabine chemotherapy for metastatic disease can provide palliative benefits. Despite pancreatic cancer's resistance to currently available treatments, new methods are being investigated. Preoperative chemoradiation is being advocated, with seemingly sound reasoning, and a wider role for gemcitabine is being explored. However, new therapeutic strategies based on the molecular biology of pancreatic cancer seem to hold the greatest promise.
引用
收藏
页码:1049 / 1057
页数:9
相关论文
共 111 条
[1]  
Abbruzzese J.L., 2001, P AN M AM SOC CLIN, V20, P518
[2]   Continuing controversy over adjuvant therapy of pancreatic cancer [J].
Abrams, RA ;
Lillemoe, KD ;
Piantadosi, S .
LANCET, 2001, 358 (9293) :1565-1566
[3]   Occupational exposure to organic solvents and K-ras mutations in exocrine pancreatic cancer [J].
Alguacil, J ;
Porta, M ;
Malats, N ;
Kauppinen, T ;
Kogevinas, M ;
Benavides, FG ;
Partanen, T ;
Carrato, A .
CARCINOGENESIS, 2002, 23 (01) :101-106
[4]   MOST HUMAN CARCINOMAS OF THE EXOCRINE PANCREAS CONTAIN MUTANT C-K-RAS GENES [J].
ALMOGUERA, C ;
SHIBATA, D ;
FORRESTER, K ;
MARTIN, J ;
ARNHEIM, N ;
PERUCHO, M .
CELL, 1988, 53 (04) :549-554
[5]  
[Anonymous], 1996, Cancer epidemiology and prevention
[6]   Genetic polymorphism of N-acetyltransferases, glutathione S-transferase M1 and NAD(P)H:quinone oxidoreductase in relation to malignant and benign pancreatic disease risk [J].
Bartsch, H ;
Malaveille, C ;
Lowenfels, AB ;
Maisonneuve, P ;
Hautefeuille, A ;
Boyle, P .
EUROPEAN JOURNAL OF CANCER PREVENTION, 1998, 7 (03) :215-223
[7]  
Berger DH, 1999, CANCER, V85, P326, DOI 10.1002/(SICI)1097-0142(19990115)85:2<326::AID-CNCR9>3.0.CO
[8]  
2-O
[9]   Phase III study of gemcitabine in combination with fluorouracil versus gemcitabine alone in patients with advanced pancreatic carcinoma: Eastern Cooperative Oncology Group Trial E2297 [J].
Berlin, JD ;
Catalano, P ;
Thomas, JP ;
Kugler, JW ;
Haller, DG ;
Benson, AB .
JOURNAL OF CLINICAL ONCOLOGY, 2002, 20 (15) :3270-3275
[10]   Phase I trial of twice-weekly gemcitabine and concurrent radiation in patients with advanced pancreatic cancer [J].
Blackstock, AW ;
Bernard, SA ;
Richards, F ;
Eagle, KS ;
Case, LD ;
Poole, ME ;
Savage, PD ;
Tepper, JE .
JOURNAL OF CLINICAL ONCOLOGY, 1999, 17 (07) :2208-2212