O’Connell JB, Maggard MA, Ko CYColon cancer survival rates with the new American Joint Committee on Cancer sixth edition staging. J Natl Cancer Inst 96: 1420-1425

Department of Surgery, David Geffen School of Medicine at University of California, Los Angeles, 10833 Le Conte Ave., Rm. 72-215 CHS, Los Angeles, CA 90095, USA. .
Journal of the National Cancer Institute (Impact Factor: 12.58). 10/2004; 96(19):1420-5. DOI: 10.1093/jnci/djh275
Source: PubMed


The recently revised American Joint Committee on Cancer (AJCC) sixth edition cancer staging system increased the stratification within colon cancer stages II and III defined by the AJCC fifth edition system. Using nationally representative Surveillance, Epidemiology, and End Results (SEER) data, we compared survival rates associated with colon cancer stages defined according to both AJCC systems.
Using SEER data (from January 1, 1991, through December 31, 2000), we identified 119,363 patients with colon adenocarcinoma and included all patients in two analyses by stages defined by AJCC fifth and sixth edition systems. Tumors were stratified by SEER's "extent of disease" and "number of positive [lymph] nodes" coding schemes. Kaplan-Meier analyses were used to compare overall and stage-specific 5-year survival. All statistical tests were two-sided.
Overall 5-year survival was 65.2%. According to stages defined by the AJCC fifth edition system, 5-year stage-specific survivals were 93.2% for stage I, 82.5% for stage II, 59.5% for stage III, and 8.1% for stage IV. According to stages defined by the AJCC sixth edition system, 5-year stage-specific survivals were 93.2% for stage I, 84.7% for stage IIa, 72.2% for stage IIb, 83.4% for stage IIIa, 64.1% for stage IIIb, 44.3% for stage IIIc, and 8.1% for stage IV. Under the sixth edition system, 5-year survival was statistically significantly better for patients with stage IIIa colon cancer (83.4%) than for patients with stage IIb disease (72.2%) (P<.001).
The AJCC sixth edition system for colon cancer stratifies survival more distinctly than the fifth edition system by providing more substages. The association of stage IIIa colon cancer with statistically significantly better survival than stage IIb in the new system may reflect current clinical practice, in which stage III patients receive chemotherapy but stage II patients generally do not.

13 Reads
  • Source
    • "Colorectal cancer (CRC) is the third most commonly diagnosed cancer in males and second in females, with over 1 million new cancer cases and 0.5 million deaths estimated to have occurred each year [1]. The stage where CRC is detected determines patients outcome, with 5-year survival rates of more than 90% for stage I disease and less than 10% for stage IV [2]. High CRC death rates can be significantly reduced by improved treatment and early detection. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Glucose transporter1 (Glut1) plays important roles in treatment of colorectal cancer (CRC) involving early-stage diagnosis, subtype, TNM stage, and therapeutic schedule. Currently, in situ marking and tracking of the tumor biomarkers via clinical imaging remains great challenges in early stage CRC diagnosis. In this study, we have developed a unique cell-targeted, paramagnetic-fluorescent double-signal molecular nanoprobe for CRC in vivo magnetic resonance imaging (MRI) diagnosis and subsequent biopsy. The unique molecular nanoprobe is composed of a fluorescent quantum dot (QD) core; a coating layer of paramagnetic DTPA-Gd coupled BSA ((Gd)DTPA∙BSA), and a surface targeting moiety of anti-Glut1 polyclonal antibody. The engineered (Gd)DTPA∙BSA@QDs-PcAb is 35 nm in diameter and colloidally stable under both basic and acidic conditions. It exhibits strong fluorescent intensities and high relaxivity (r1 and r2: 16.561 and 27.702s(-1) per mM of Gd(3+)). Distribution and expression of Glut1 of CRC cells are investigated by in vitro cellular confocal fluorescent imaging and MR scanning upon treating with the (Gd)DTPA∙BSA@QDs-PcAb nanoprobes. In vivo MRI shows real-time imaging of CRC tumor on nude mice after intravenously injection of the (Gd)DTPA∙BSA@QDs-PcAb nanoprobes. Ex vivo biopsy is subsequently conducted for expression of Glut1 on tumor tissues. These nanoprobes are found biocompatible in vitro and in vivo. (Gd)DTPA∙BSA@QDs-PcAb targeted nanoprobe is shown to be a promising agent for CRC cancer in vivo MRI diagnosis and ex vivo biopsy analysis. The "imaging-biopsy" is a viable strategy for tumor reconfirmation with improved diagnostic accuracy and biopsy in personalized treatment. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Biomaterials 04/2015; 48. DOI:10.1016/j.biomaterials.2015.01.011 · 8.56 Impact Factor
  • Source
    • "Therefore, in patients with stage II CRC (pT3–pT4, N0, M0), supplemental risk estimation is crucial, because some patients may experience outcome inferior to stage III patients. Identification of these patients is important, as they might benefit from adjuvant therapy.4 Ideal histopathological prognostic markers are readily assessable on routine examination, ie, hematoxylin and eosin-stained slides. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Tumor staging according to the American Joint Committee on Cancer/Union for International Cancer Control tumor, node, metastasis (TNM) system is currently regarded as the standard for staging of patients with colorectal cancer. This system provides the strongest prognostic information for patients with early stage disease and those with advanced disease. For patients with intermediate levels of disease, it is less able to predict disease outcome. Therefore, additional prognostic markers are needed to improve the management of affected patients. Ideal markers are readily assessable on hematoxylin and eosin-stained tumor slides, and in this way are easily applicable worldwide. This review summarizes the histological features of colorectal cancer that can be used for prognostic stratification. Specifically, we refer to the different histological variants of colorectal cancer that have been identified, each of these variants carrying distinct prognostic significance. Established markers of adverse outcomes are lymphatic and venous invasion, as well as perineural invasion, but underreporting still occurs in the routine setting. Tumor budding and tumor necrosis are recent advances that may help to identify patients at high risk for recurrence. The prognostic significance of the antitumor inflammatory response has been known for quite a long time, but a lack of standardization prevented its application in routine pathology. However, scales to assess intra- and peritumoral inflammation have recently emerged, and can be expected to strengthen the prognostic significance of the pathology report.
    Cancer Management and Research 07/2014; 6(1):291-300. DOI:10.2147/CMAR.S38827
  • Source
    • "Early diagnosis results in a highly favorable prognosis, such that stage 1 and stage 2 disease have an 80–90% five year survival. By contrast stage 3 and stage 4 metastatic disease are associated with five year survival of 60% and 8%, respectively [1]. Genetic aberrations arising in early stage disease include APC mutations, while KRAS, BRAF, p53, and PIK3CA mutations are found in later stages of tumor development [2]–[4]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Aberrant kinase activation resulting from mutation, amplification, or translocation can drive growth and survival in a subset of human cancer. FGFR2 is amplified in breast and gastric cancer, and we report here the first characterization of FGFR2 gene amplification in colorectal cancer in the NCI-H716 colorectal cancer cell line. FGFR2 is highly expressed and activated in NCI-H716 cells, and FGFR selective small molecule inhibitors or FGFR2 shRNA strongly inhibited cell viability in vitro, indicating "addiction" of NCI-H716 cells to FGFR2. NCI-H716 growth in a xenograft model was also inhibited by an FGFR small molecule inhibitor. FGFR2 was required for activation of multiple downstream signaling proteins including AKT, ERK, S6RP and NFKB. Inhibition of downstream kinases such as AKT or ERK alone had modest effects on proliferation, whereas combined inhibition of AKT and ERK signaling resulted in a loss of viability similar to FGFR2 inhibition. We identified elevated FGFR2 expression in a small subset of primary colorectal cancer, however FGFR2 amplification was not observed. Although FGFR2 amplification is not common in primary colon cancer or lymph node and liver metastases, other subsets of colorectal cancer such as ascites, from which the NCI-H716 cell line was derived, have yet to be tested. These results suggest that emerging FGFR inhibitor therapeutics may have efficacy in a subset of colon cancer driven by FGFR2 amplification.
    PLoS ONE 06/2014; 9(6):e98515. DOI:10.1371/journal.pone.0098515 · 3.23 Impact Factor
Show more