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PubMed2003

Factors affecting successful palliative surgery for malignant bowel obstruction due to peritoneal dissemination from colorectal cancer.

BACKGROUND: Nonresectable colorectal cancer often causes malignant intestinal obstruction due to peritoneal dissemination. However, no previous report has specifically investigated which patients, with peritoneal dissemination from colorectal cancer, would actually benefit from palliative surgery. This study defines the selection criteria for patients who are likely to benefit from palliative surgery. METHODS: Twenty-one patients underwent palliative surgery for malignant bowel obstruction due to peritoneal dissemination from colorectal cancer. In all cases, the advanced and nonresectable nature of the tumor was confirmed at laparotomy. Clinical factors such as age, gender, serum level of carcinoembryonic antigen, amount of ascites, location of the primary cancer, surgical procedure, and postoperative chemotherapy were analyzed for prognostic significance in symptom-free and overall survival using the Kaplan-Meier product limit method and the log-rank test. RESULTS: All the postoperative courses were uneventful. Obstruction recurred after a median symptom-free interval of 61 days in the group with less than 100 ml of ascites, whereas it recurred after 9 days in the group with more than 100 ml of ascites. Symptom-free survival rates in patients who manifested ascites were significantly lower than in those without ascites (P = 0.0321, log-rank method). The symptom-free and overall survival rates in patients who underwent postoperative chemotherapy were significantly higher (P = 0.0225 and 0.0003). CONCLUSIONS: Palliative surgery can be performed effectively for patients without ascites. For patients who do not meet this criterion, a non-surgical procedure may be preferable.

Adult↗

PubMed1990

Hypotheses for the etiology of colorectal cancer--an overview.

Colorectal cancer is the second most common cancer in the United States. Various dietary, colonic, and fecal components have been implicated as causative factors. Although numerous studies have been conducted to test them, so far no one factor has stood out as the most likely cause of colorectal cancer. This review presents the evidence for and against the major factors and concludes that bile acids are the most strongly implicated factors in the etiology of colorectal cancer.

Bile Acids and Salts↗

PubMed2001

The role of hPMS1 and hPMS2 in predisposing to colorectal cancer.

Hereditary nonpolyposis colorectal cancer (HNPCC) is attributable to a deficiency of mismatch repair. Inactivation of DNA mismatch repair underlies the genesis of microsatellite instability in colorectal cancer. Germline mutations in three DNA mismatch repair genes, hMSH2, hMLH1, and hMSH6, have been found to segregate in HNPCC and HNPCC-like families. The two DNA mismatch repair genes hPMS1 and hPMS2 have also been suggested to predispose to HNPCC. In this study, 84 HNPCC and HNPCC-like kindreds without known mutations in the other three known DNA mismatch repair genes were screened for germline mutations in the hPMS1 or hPMS2 gene. No clear-cut pathogenic mutations were identified. Conversion technology was used to detect a large hMSH2 deletion in two affected members of the kindred in which the hPMS1 mutation was originally reported, whereas the hPMS1 mutation was only present in one of these two individuals. Since the hPMS1 and hPMS2 genes were first reported, germline mutations in hPMS2 have been demonstrated primarily in patients with Turcot's syndrome. However, no mutation in any of the two genes has been found to segregate in HNPCC families. Until there is better evidence for an increased colorectal cancer risk associated with germline mutations in these genes, a conservative interpretation of the role of mutations in these genes is advised.

Adenosine Triphosphatases↗

PubMed1996

Prevention of gastrointestinal cancer--the potential role of NSAIDs in colorectal cancer.

Gastrointestinal cancers are among the leading sites of cancer and leading causes of cancer-related deaths. Gastrointestinal cancers are often at an advanced stage at the time of diagnosis, and are highly resistant to non-surgical therapy. Thus early diagnosis and prevention are approaches that are under active investigation. Screening and surveillance are considered secondary prevention. Primary prevention is the use of dietary or environmental modification or chemopreventive agents. This written review will emphasize the potential role of acetylsalicylic acid and other non-steroidal anti-inflammatory drugs (NSAIDs) in the prevention of gastrointestinal cancer, and specifically colorectal cancer. Cell culture and animal studies have shown that NSAIDs possess anti-proliferative and anti-neoplastic effects. Recent epidemiologic surveys also suggest that individuals who regularly take NSAIDs, particularly acetylsalicylic acid, have about a 50% decrease in colorectal cancer incidence and mortality. However, in the only interventional trial of aspirin (and beta-carotene), a retrospective analysis had inadequate statistical power to demonstrate any protective effect against colorectal cancer. About a dozen small prospective intervention studies have been done in a total of about a hundred patients with familial adenomatous polyposis to test the efficacy of NSAIDs, particularly sulindac. All human trials have shown substantial partial and some complete regression of colorectal and perhaps also duodenal adenomatous polyps. But virtually all patients had regrowth of adenomatous polyps after sulindac was stopped. In addition, sulindac and other NSAIDs result in occasional adverse events such as gastrointestinal bleeding. Thus sulindac cannot be recommended for routine use outside of a study setting. One valid current approach to the prevention of gastrointestinal cancer, and colorectal cancer in particular, is the adoption of a healthy lifestyle and appropriate screening and surveillance. Screening and surveillance guidelines have been developed by several public agencies and their recommendations should be adopted. In addition, we should adopt a healthy lifestyle and diet, which consists of low fat ( < 30% to total calories), and high fiber (> 3 daily servings of fruits/vegetables), with the avoidance of red meats ( < 3 weekly servings) and alcohol ( < 2 drinks daily), and the absolute avoidance of tobacco smoking.

Adenomatous Polyposis Coli↗

PubMed2006

Molecular biology of colorectal cancer: new targets.

Colorectal cancer is an ideal model in which to study malignant progression from the molecular-genetic perspective because different stages of the same malignancy coexist within each patient. Approximately 75% of colorectal cancer cases are sporadic and the remaining are familial disease, yet genetic mutations that have been identified account for only 5% to 6% of inherited cases. The two major pathways by which mutational changes leading to colorectal cancer occur are chromosomal instability and microsatellite instability. This article discusses genes and signaling pathways involved in development of inherited disease, as well as the association of some of these pathways with sporadic cases. Furthermore, therapies targeting active pathways in colorectal carcinogenesis, including the vascular endothelial growth factor and epidermal growth factor receptor tyrosine kinase, have shown promising results in clinical trials are now included in standard recommended treatment.

Colorectal Neoplasms↗

PubMed1996

Cancer risk in families with hereditary nonpolyposis colorectal cancer diagnosed by mutation analysis.

BACKGROUND & AIMS: Hereditary nonpolyposis colorectal cancer is characterized by early-onset colorectal cancer and the occurrence of various other cancers. The recent isolation of four mismatch repair genes responsible for hereditary nonpolyposis colorectal cancer allows for the identification of carriers within affected families. The purpose of this study was to assess the age-specific cancer risk in a large series of gene carriers. METHODS: Thirty-four families were studied by mutation analysis. In 19 of these families, pathogenic mutations were found at hMSH2 or hMLH1. Of 382 relatives, 124 had a mutation in hMLH1 and 86 in hMSH2. RESULTS: The lifetime risk of colorectal cancer was the same in both groups of gene carriers (80%). The risk of endometrial cancer was greater in hMSH2 gene carriers compared with hMLH1 gene carriers (61% vs. 42%), but the difference was not statistically significant. A very high relative risk of cancer of the small bowel (relative risk of >100) was observed in carriers of either gene. Only the carriers of hMSH2 mutations had a significantly increased relative risk of cancer of the urinary tract (kidney and ureter) (relative risk of 75.3), stomach (relative risk of 19.3), and ovaries (relative risk of 8.0). CONCLUSIONS: This study provides estimates of cancer risk that may contribute to the appropriate management of gene carriers within families with hereditary nonpolyposis colorectal cancer.

Adolescent↗

PubMed1998

Influence of cardiopulmonary bypass surgery on cancer-specific survival rate of patients with colorectal cancer.

PURPOSE: There is evidence of a relationship between inflammation and cancer growth and spread. Cardiopulmonary bypass surgery is known to induce a systemic inflammatory response. The aim of this study was to determine whether cardiopulmonary bypass surgery influences the cancer-specific survival rate in patients with colorectal cancer. METHODS: The Fremantle Hospital database on patients with colorectal cancer (477 patients) was linked to the Western Australian Hospital Morbidity Database System. Patients who had colorectal cancer after having undergone cardiopulmonary bypass surgery (n = 7) were identified. The cancer-specific survival rate for these patients was compared with that for a group of controls derived from the hospital database. Controls were matched for age, gender, tumor location, tumor stage, operative procedure, and adjuvant therapy (n = 26). RESULTS: The cancer-specific survival rate of the seven patients with colorectal cancer who had undergone cardiopulmonary bypass surgery was significantly lower than that for control patients (5-year survival rate, 34 vs. 71 percent, respectively; P < 0.05; hazard ratio, 2.9; 95 percent confidence interval, 1.5-4.4). Of the two patients in the study group who survived for 18 months, one had liver metastases and the other had local recurrence of a rectal cancer. CONCLUSION: In patients with colorectal cancer, having undergone cardiopulmonary bypass surgery was associated with a reduced cancer-specific survival rate. Additional studies are required to validate this association and explore the possibility of a causal relationship.

Aged↗

PubMed2000

Adjuvant chemotherapy with 5-fluorouracil, L-folinic acid and levamisole for patients with colorectal cancer: non-randomised comparison of weekly versus four-weekly schedules--less pain, same gain. QUASAR Colorectal Cancer Study Group.

BACKGROUND: QUASAR is a large trial of adjuvant chemotherapy for colorectal cancer in which clinicians could choose to deliver a standard adjuvant cytotoxic chemotherapy regimen, 5-fluorouracil (5-FU) and L-folinic acid (L-FA), in either a once-weekly or a four-weekly schedule. We report results of a non-randomised comparison between these schedules with respect to survival, recurrence and differential toxicity. PATIENTS AND METHODS: In a factorial (2 x 2) trial design, QUASAR compared high-dose (175 mg) versus low-dose (25 mg) L-FA and levamisole versus placebo. The dose of 5-FU was fixed at 370 mg/m2 and although the recommended schedule was i.v. bolus delivery, daily for 5 days repeated four-weekly for 6 months, a significant proportion of randomising clinicians were constrained to deliver once-weekly 5-FU-L-FA for 30 weeks. RESULTS: Four thousand nine hundred twenty-seven patients were entered into QUASAR between May 1994 and October 1997, eighteen hundred twenty-nine of whom have recurred and sixteen hundred eighty-nine died. Similar numbers 2370 vs. 2559 were treated with the once-weekly and four-weekly schedules and the demographic features of the 2 groups were well balanced: stage C, 73.3% once-weekly vs. 71.0% four-weekly; colon, 68.0% vs. 68.3%; high-dose FA, 50.1% vs. 49.9%; levamisole, 49.3% vs. 49.3%; females, 40.2% vs. 41.7%; median age (years) 62 vs. 61. The risk of recurrence and survival were similar regardless of schedule: three-year survival was 70.6% once-weekly vs. 71.0% four-weekly; three-year recurrence risk was 35.6% once-weekly vs. 35.5% four-weekly; But, the once-weekly regimen was much less toxic: number of patients for whom toxicity was reported (once-weekly: four-weekly), stomatitis, 37 vs. 337; diarrhoea, 260 vs. 440; neutropenia, 20 vs. 153. CONCLUSIONS: The once-weekly regimen is much less toxic than and, apparently, about as effective as the four-weekly schedule. This suggests that the toxicity of 5-FU-L-FA adjuvant chemotherapy could be reduced substantially by weekly scheduling without compromising efficacy. Alternatively, efficacy might be enhanced with equal toxicity by more dose-intense weekly FU-L-FA regimens. However, this conclusion from a non-randomised comparison needs confirmation in prospective randomised studies.

Antineoplastic Combined Chemotherapy Protocols↗

PubMedDate not supplied

Second primary extracolonic cancers in Japanese hereditary nonpolyposis colorectal cancer.

We examined the occurrence of second primary extracolonic cancers in 1,170 patients with nonpolyposis colorectal cancer who underwent a resection between 1972 and 1994. Such cancers occurred more often in cases with hereditary nonpolyposis colorectal cancer (HNPCC) than in those without (11.1% vs. 3.6%, P=0.0286). Five HNPCC cases developed 6 cancers in the stomach, endometrium, ovary, and ureter. The mean interval between the first and second operation was 66 months (range: 18-153). These findings thus indicate the importance of targetted surveillance for any second primary cancers in the upper gastrointestinal, female genital, or upper urologic tract, especially in HNPCC patients.

Adult↗

PubMed2005

The results of the expression array studies correlate and enhance the known genetic basis of gastric and colorectal cancer.

Gastric and colorectal cancers belong to the most frequent cancer types in the world today. This fact emphasizes the importance of identification of useful diagnostic and prognostic markers, in the earliest stage of the disease. The examination of gene expression profile in gastric and colorectal cancer may develop the bases of early diagnosis and of individual therapeutic strategies. In the microarray examinations done so far for these types of cancers, the expression of hundreds and thousands of genes were studied, however, both the sample collection and the results showed wide variations. The diversity of expression array methods and data analysis makes the comparison of microarray results difficult. Beside the exposition of the practical aspects of the chip technology, our aims are the systematization of data that are currently available in the international scientific literature and the description of the results in a comprehensive way. Microarray results show that the gene expression pattern, detected in gastric and colon cancers, highly depends on the histological type and heterogeneity of the sample, array type, and softwares, used for data analysis. Recent experiments point out not just the changes of the alterations of tumor suppression, apoptosis, cell-cycle regulation, and signal transduction, but tumor cell metabolism and cell-microenvironment interactions also. Results show connection to and make more complete the already known molecular background of gastric and colorectal cancers. Based on the accumulation of recent and further data, such kind of multifunctional diagnostic microarrays that can be suited for completing the conventional histological diagnostics and subtypization will certainly become available in the near future.

Colorectal Neoplasms↗

PubMed1999

Transanal endoscopic microsurgery for T1 rectal cancer in patients with synchronous colorectal cancer.

We treated T1 rectal cancer in three patients with synchronous colorectal cancer by transanal endoscopic microsurgery (TEM) before performing a radical operation for the second lesion. On pathological examination, all rectal specimens resected by TEM showed cancer invasion within the submucosal layer, while the margins of the specimen were completely free of cancerous tissue. Few complications were encountered with either the TEM for the rectal lesions or the succeeding radical operation for the second lesions. When patients present with synchronous colorectal cancer, including T1 rectal cancer, local excision of the rectal lesion via TEM can help to improve the patient's quality of life without affecting the curability of the disease.

Aged↗

PubMed1988

Cigarette smoking and the risk of colorectal cancer in women.

Colorectal cancer incidence rates for smokers, nonsmokers living with smokers (i.e., passive smokers), and nonsmokers in smoke-free households were compared in a 12-year prospective study of 25,369 women who participated in a private census conducted in Washington County, MD, in 1963. Women who smoked had a decreased relative risk of colorectal cancer compared with the risk for nonsmokers (age-adjusted relative risk, 0.76; 95% confidence interval, 0.52-1.10). The risk for passive smokers was similar to that for smokers. The relative risks were significantly reduced for older women; relative risks were 0.42 for smokers and 0.66 for passive smokers over age 65. The data suggest that older women who smoke have a lower risk of colorectal cancer than nonsmokers. The effect may be mediated by an antiestrogenic effect of smoking.

Adult↗

PubMed1997

Trimetrexate: review and current clinical experience in advanced colorectal cancer.

Unresectable metastatic colorectal cancer remains a significant cause of morbidity and mortality in both the United States and Europe. To date, no chemotherapeutic regimen for this disease has demonstrated a definitive survival advantage compared with 5-fluorouracil (5-FU) plus leucovorin (LV). However, recent trials have raised the possibility that the combination of trimetrexate (TMTX) plus 5-FU/LV may improve response rates and survival in patients with metastatic colorectal cancer. Trimetrexate is a nonclassical antifolate that has demonstrated antitumor activity against a number of malignancies, including those resistant to the classical antifolate methotrexate. While the single-agent activity of TMTX remains modest in metastatic colorectal cancer, the combination of TMTX/5-FU/LV has shown significant activity in several phase II trials. Reported studies include a phase II trial in chemotherapy failures that demonstrated a 20% response rate, and two multicenter phase II trials in previously untreated patients that demonstrated 50% and 38% overall response rates, respectively. Diarrhea was the dose-limiting toxicity in all trials, although a regimen of scheduled loperamide was quite effective in mitigating this complication. These studies are being followed up with two confirmatory phase II studies in chemorefractory patients and two randomized phase III trials comparing TMTX/5-FU/LV with standard 5-FU/LV.

Antimetabolites, Antineoplastic↗

PubMed2006

[S-1 as a single agent for colorectal cancer].

Chemotherapy for colorectal cancer is now improving rapidly due to new drugs like oxaliplatin and molecular targeting drugs. The key drug, however, is still 5-fluorouracil (5-FU). S-1 is an oral 5-FU anti-tumor drug that combines three pharmacological agents: tegafur, 5-chloro-2,4-dihydroxypyridine, which inhibits dihydropyrimidine dehydrogenase activity, and potassium oxonate, which reduces gastrointestinal toxicity. The results of the phase II study suggested that S-1 as a single agent was active against metastatic colorectal cancer: CR rate was 36-40% and MST was about one-year. Toxicity was all tolerable. Clinical trials of S-1 with oxaliplatin or CPT-11 combination chemotherapy are ongoing in Japan. S-1 with molecular targeting drugs will also be studied. Therefore, S-1 is expected to play an important part in chemotherapy for colorectal cancer.

Administration, Oral↗

PubMed1987

[In families of ovarian cancer patients, breast cancer in females and colorectal cancers in males are overrepresented].

A detailed tumour-related family history was obtained from 30 women with histologically verified epithelial ovarian carcinomas. 46% of the anamnestic tumour diagnoses were also verified by obtaining copies of histology reports. Breast cancer was overrepresented among the female relatives and colorectal cancer among the male relatives. This study demonstrates that persons at high cancer risk as well as tumour-prone families of interest for aetiological cancer research can be identified by the simple method of obtaining a family history.

Adult↗

PubMed2007

Surveillance for endometrial cancer in hereditary nonpolyposis colorectal cancer syndrome.

The estimated lifetime risk for endometrial carcinoma (EC) in hereditary nonpolyposis colorectal cancer syndrome (HNPCC) is 32-60%, thus supporting surveillance. The survival rate of EC patients is, however, favourable questioning the need for surveillance. Yet, the effectiveness of gynecological surveillance remains to be shown. The 2 previously published studies were based on transvaginal ultrasound (TVUS) alone. Intrauterine biopsy has not been tested in surveillance for EC in HNPCC families. The effect of gynecological surveillance was evaluated among 175 Finnish mutation carriers. During 759 person years at risk, there were 503 surveillance visits including TVUS and intrauterine biopsy of endometrium at 94% and 74% of the visits, respectively. EC occurred in 14 cases, 11 of which were diagnosed by surveillance, 8 by intrauterine biopsies. TVUS indicated only 4 EC patients but missed 6 other cases. Intrauterine sampling detected 14 additional cases of potentially premalignant hyperplasia. The stage distribution and survival tended to be more favorable in the 14 EC cases of the surveilled group (no deaths) than in the group of 83 symptomatic mutation carriers of whom 6 died of EC, but with no statistical significance. Four cases of ovarian cancer occurred but none was detected by surveillance in TVUS examinations. In conclusion, EC surveillance in HNPCC seems more effective with endometrial biopsies than with TVUS alone. A definite improvement in survival remains to be shown. The detection of early cancer stages and premalignant lesions offers the opportunity to avoid extensive adjuvant treatment.

Adult↗

PubMed2001

CYCLIN D1 as a genetic modifier in hereditary nonpolyposis colorectal cancer.

Hereditary nonpolyposis colorectal cancer is associated with inherited defects in DNA mismatch repair. Clinical variation even in cases with identical predisposing mutations suggests the existence of other factors contributing to the phenotype. We addressed the modifying role of the common A/G polymorphism in exon 4 and the alternatively spliced transcripts a and b of the CCND1 gene encoding cyclin D1 in a series of 146 affected carriers of 10 MLH1 and 3 MSH2 mutations. No correlation was observed between a particular allele (A versus G) and age at onset. However, the presence of the variant transcript b in blood/normal mucosa, by multiplex reverse transcription-PCR, was associated with a significantly lower age at onset of colon cancer as compared with individuals with transcript a only (35 versus 46 years; P = 0.02). Whereas our data do not support a modifying role of A versus G allele of CCND1, the results do suggest that the relative abundance of a and b transcripts may modify the age at onset of colon cancer in hereditary nonpolyposis colorectal cancer.

Adaptor Proteins, Signal Transducing↗

PubMed1994

Double modulation of 5-fluorouracil in advanced colorectal cancer with low-dose interferon-alpha 2b and folinic acid. The "GISCAD" experience. Italian Group for the Study of Digestive Tract Cancer.

In advanced colorectal cancer the addition of folinic acid (FA) has been shown to lead to increased activity, at least in terms of response rate, in comparison with 5-fluorouracil (5FU) alone. Similarly, interferon-alpha (IFN) is able to potentiate 5FU, although high doses cause heavy toxicity. Given the different mechanisms of action of the two agents, the double modulation of 5FU deserves clinical evaluation. In a multicenter study (involving both primary care and referral institutions) 63 patients with advanced colorectal cancer, previously untreated with chemotherapy, received, in an outpatient setting, FA (200 mg/m2 i.v. bolus) + 5FU (400 mg/m2 i.v. in 15 min) for 5 consecutive days every 4 weeks + IFN 3 x 10(6) U on alternate days, starting 1 week before chemotherapy. During the 5 days of 5FU + FA, IFN was administered daily. The antitumour activity, the impact on response duration and survival and toxicity of the combination were evaluated according to WHO criteria. Of the 63 enrolled patients, 56 were evaluable: there were 2 complete responses (3%) and 13 partial responses (21%), giving an objective response rate of 24% (95% confidence interval 13-35%); no change was observed in 17 cases and progressive disease in 24. Median duration of response was 9 months and median survival (all patients) 13 months. Toxicity was acceptable, even though 4 patients presented reversible grade 4 side-effects (2 mucositis and 2 diarrhoea). With this schedule and these doses, addition of IFN did not lead to any increase in the activity of 5FU + FA. In colorectal cancer, further clinical studies with these drugs should be based on a deeper experimental knowledge of their mechanisms of interaction.

Adult↗