Follow-up after Colorectal Cancer Surgery

Ohlsson, Björn; Pålsson, Birger

doi:10.1080/02841860310019016

Cited by 49 publications

(27 citation statements)

References 73 publications

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“…Only studies where randomisation occurred at the time of initial surgery were included, and survival was calculated at 5 years after initial treatment, hence circumventing potential lead and lag biases. The reported absolute overall survival benefit of 10% is similar to that estimated independently by others (Ohisson and Paisson, 2003), while the figure of 2% of lives saved through salvage alone is close to the 2.4% estimated using a recurrence -salvage -outcome model (Kievit, 2002). This apparent discrepancy emphasises the importance of determining the effectiveness of colorectal cancer followup based on all-cause mortality, as judging effectiveness simply based on the number of asymptomatic recurrences detected and salvaged underestimates the true potential impact of intensive followup.…”

Section: Discussionsupporting

confidence: 89%

Mechanisms of improved survival from intensive followup in colorectal cancer: a hypothesis

et al. 2005

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A meta-analysis of six randomised trials demonstrated that intensive followup in colorectal cancer was associated with an absolute reduction in all-cause 5-year mortality of 10% (95% confidence interval (CI): 4 -16) -however, only two percent (95% CI: 0 -5) was attributable to cure from salvage re-operations. We postulate that other factors, such as increased psychological well-being and/or altered lifestyle, and/or improved treatment of coincidental disease may contribute to the remaining lives saved, and form important future research questions. Approximately two-thirds of patients presenting with colorectal cancer undergo resection with curative intent, and most subsequently enter protocols for long-term followup (Kievit, 2002). The rationale for surveillance is three-fold: psychological support, facilitation of audit, and an opportunity for the early detection and treatment of recurrent disease, with potential improvement in survival. Recently, the authors (Renehan et al, 2002b) reported a meta-analysis of five randomised trials and demonstrated a significant improvement in all-cause 5-year mortality in patients followed intensively. A Cochrane review (Jeffery et al, 2002) independently found similar results, and, subsequently, a sixth randomised trial reported additional results supporting these conclusions (Secco et al, 2002). These data offer the first direct evidence that intensive followup improves survival, but fall short of evaluating the mechanisms underlying the observed survival benefit. This study updates and extends our previous metaanalysis to explore the survival mechanisms associated with intensive followup. MATERIALS AND METHODSThe search strategy, inclusion and exclusion criteria, data extraction, and study quality assessment have been published elsewhere (Renehan et al, 2002b(Renehan et al, , 2004, with further details at www.christie.man.ac.uk/profinfo/departments/surgery/default. htm. The key features were:Updated search strategy (to December 2003) using Cochrane methodology.Inclusion criteria were: randomised controlled trial; patients with colorectal cancer treated surgically with curative intent; randomisation at or shortly after surgery, and availability of 5-year survival data. Data were extracted independently by two investigators (AGR, MPS). Important components of methodological quality, namely adequacy of concealment of patients' allocation to treatment groups, double-blinding, and withdrawals, were assessed. Statistical analysisMeta-analyses were performed at two levels. First, comparisons of events (e.g. all-cause deaths) for intensive vs conventional followup were performed and pooled estimates expressed as risk ratios (RR) and 95% confidence intervals (95% CIs). Second, estimates of the proportion of overall lives gained, and lives gained through to salvage re-operation, were calculated using absolute risk differences (and 95% CIs) (Deeks and Altman, 2001). The difference between these estimates was taken as an estimate of the gain in lives attributable to nonsalvage-related ...

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Section: Discussionsupporting

confidence: 89%

Mechanisms of improved survival from intensive followup in colorectal cancer: a hypothesis

et al. 2005

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“…Even after successful resection of the primary tumor, about one-third of the patients develop metastases in the liver and lungs (1,2). Metastatic colorectal cancer is associated with a poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

No functional and transductional significance of specific neuropilin 1 siRNA inhibition in colon carcinoma cell lines lacking VEGF receptor 2

Quante

Raskopf²,

Stahl³

et al. 2009

Oncol Rep

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Abstract. Neuropilins are membrane proteins that mediate effects on tumor cells directly and indirectly by affecting angiogenesis. Recent findings indicate that neuropilin 1 (NRP1) and the associated tyrosine kinase vascular endothelial growth factor receptor 2 (VEGFR2) play a regulatory role in developmental angiogenesis as well as in tumor angiogenesis. NRP1 and VEGFR2 might play a role in colon carcinogenesis and development of metastases. The significance of NRP1 expression in colon cancer seems to be controversial. Therefore, we aimed to distinguish between different expression patterns of signalling cascades in human colon carcinoma cell lines in order to analyze the role of NRP1 in tumorigenesis. We analyzed the biological significance of NRP1 in respect to VEGFR, EGFR, neuropilin and their ligands by RT-PCR and Western blot with functional knock-out of NRP1 in different colon adenocarcinoma cell lines. There was no expression of VEGFR2 in tumor cell lines. There were cells that expressed: i) only NRP1 (HT-29, LS174T), ii) NRP2 (Colo320) or iii) both (SW480, LoVo). Cells without NRP1 expression strongly expressed EGFR but only when NRP2 was co-expressed. Inhibition of NRP1 expression by RNA interference did not alter growth characteristics in soft agar experiments. Furthermore, there were no differences in intracellular signalling pathways (ERK1/2 or AKT) in NRP1 inhibited cells. In ex vivo transfer experiments animals with tumors from siRNA-NRP1 transfected cells showed no significant inhibition of tumor growth compared to siRNA control. In conclusion, our results question the role of NRP1 function in VEGFR2 negative colon adenocarcinoma cells. NRP1 seems to have no detectable effect on proliferation or migration nor does it induce any changes in intracellular signalling pathways without the expression of VEGFR2. According to our data, further studies are needed to analyze the therapeutic relevance of NRP1 inhibition in vivo.

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“…Most patients have potentially resectable disease at diagnosis: about 50% to 55% have stage II or stage III disease and about 15% to 19% have stage IV disease [2,3]. Of those with stage II or III disease, approximately one third develop recurrent disease after undergoing potentially curative therapy [4]. Whether patients present initially with metastatic disease or develop a recurrence, many will have involvement of a single site or organ, and the liver is by far the most common site of metastatic disease.…”

Section: Introductionmentioning

confidence: 99%

Use of neoadjuvant and postoperative chemotherapy with surgical resection of colorectal cancer hepatic metastases

Alberts

2008

Curr colorectal cancer rep

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Follow-up after Colorectal Cancer Surgery

Cited by 49 publications

References 73 publications

Mechanisms of improved survival from intensive followup in colorectal cancer: a hypothesis

Mechanisms of improved survival from intensive followup in colorectal cancer: a hypothesis

No functional and transductional significance of specific neuropilin 1 siRNA inhibition in colon carcinoma cell lines lacking VEGF receptor 2

Use of neoadjuvant and postoperative chemotherapy with surgical resection of colorectal cancer hepatic metastases

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