Detecting early pancreatic cancer: Problems and prospects

被引:127
作者
Chari, Suresh T. [1 ]
机构
[1] Mayo Clin, Coll Med, Div Gastroenterol & Hepatol, Dept Internal Med, Rochester, MN 55905 USA
关键词
D O I
10.1053/j.seminoncol.2007.05.005
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Pancreatic cancer has a poor prognosis. Improving survival will require diagnosis of early pancreatic cancer, which can be defined based on resectability, size, or curability. Pancreatic cancer progresses from noninvasive precursor lesions to invasive cancer over a variable time period. Retrospective review of computed tomography (CT) scans performed prior to diagnosis suggests that pancreatic cancer resectability may be significantly improved if detected as few as 6 months before clinical diagnosis. Since pancreatic cancer is relatively uncommon, to allow cost-effective screening the populations will have to be enriched for the disease using two "sieves." The first sieve would identify a population of subjects at higher than average risk of pancreatic cancer and the second sieve could be a characteristic phenotype among the members of the high-risk group, an abnormality seen on noninvasive imaging or a serologic marker of early pancreatic cancer. So far two high-risk groups have been targets of screening for pancreatic cancer: hereditary pancreatic cancer kindreds and new-onset diabetes. There is no serologic marker of early pancreatic cancer. Confirmation of diagnosis usually requires invasive procedures such as endoscopic ultrasonography (EUS). Although much work still needs to be done, the developments in the field provide us with hope that screening for early pancreatic cancer could become a reality in the not-so-distant future. © 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:284 / 294
页数:11
相关论文
共 66 条
[1]   CANCER RISK IN PATIENTS WITH DIABETES-MELLITUS [J].
ADAMI, HO ;
MCLAUGHLIN, J ;
EKBOM, A ;
BERNE, C ;
SILVERMAN, D ;
HACKER, D ;
PERSSON, I .
CANCER CAUSES & CONTROL, 1991, 2 (05) :307-314
[2]   The dichotomy in the preinvasive neoplasia to invasive carcinoma sequence in the pancreas: Differential expression of MUC1 and MUC2 supports the existence of two separate pathways of carcinogenesis [J].
Adsay, NV ;
Merati, K ;
Andea, A ;
Sarkar, F ;
Hruban, RH ;
Wilentz, RE ;
Goggins, M ;
Iocobuzio-Donahue, C ;
Longnecker, DS ;
Klimstra, DS .
MODERN PATHOLOGY, 2002, 15 (10) :1087-1095
[3]   GLUCOSE-TOLERANCE AND INSULIN-SECRETION IN EXPERIMENTAL PANCREATIC-CANCER IN THE SYRIAN-HAMSTER [J].
AHREN, B ;
ANDRENSANDBERG, A .
RESEARCH IN EXPERIMENTAL MEDICINE, 1993, 193 (01) :21-26
[4]  
[Anonymous], EXP REV MOL MED, DOI DOI 10.1017/S146239940100309X
[5]  
Basso D, 1995, ANTICANCER RES, V15, P2585
[6]   SYSTEMIC CANCER AND THE FAMMM SYNDROME [J].
BERGMAN, W ;
WATSON, P ;
DEJONG, J ;
LYNCH, HT ;
FUSARO, RM .
BRITISH JOURNAL OF CANCER, 1990, 61 (06) :932-936
[7]   Progression of pancreatic intraductal neoplasias to infiltrating adenocarcinoma of the pancreas [J].
Brat, DJ ;
Lillemoe, KD ;
Yeo, CJ ;
Warfield, PB ;
Hruban, RH .
AMERICAN JOURNAL OF SURGICAL PATHOLOGY, 1998, 22 (02) :163-169
[8]  
Brentnall TA, 1999, ANN INTERN MED, V131, P247, DOI 10.7326/0003-4819-131-4-199908170-00003
[9]  
Brockie E, 1998, Ann Diagn Pathol, V2, P286, DOI 10.1016/S1092-9134(98)80020-8
[10]   Diabetes mellitus and pancreatic cancer mortality in a prospective cohort of United States adults [J].
Calle, EE ;
Murphy, TK ;
Rodriguez, C ;
Thun, MJ ;
Heath, CW .
CANCER CAUSES & CONTROL, 1998, 9 (04) :403-410