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PubMedDate not supplied

Postoperative infections in colorectal cancer patients.

BACKGROUND/AIMS: Colorectal surgery is associated with some of the highest rates of infective complications, and especially surgical site infections. It has recently been reported that postoperative infection in colorectal cancer surgery increases the risk of recurrence. The aim of this study was to analyze factors associated with the occurrence of postoperative infections in patients with colorectal cancer. METHODOLOGY: A total of 81 patients operated for colorectal cancer was included. Patients' characteristics and postoperative course were recorded and analyzed. RESULTS: Patients with tumors located in the rectum had significantly higher rate of postoperative infectious complications compared to patients with tumors located in the colon (p=0.002). In a logistic regression model, among all evaluated predictors, only preoperative hemoglobin concentration was found to be an independent significant predictor of postoperative infection (p=0.01). CONCLUSIONS: Preoperative anemia was found to be significant independent predictor of postoperative infection. Meticulous surgical technique with minimal blood loss is an important means of reduction of postoperative infections in colorectal surgery.

Adult↗

PubMed1997

Mutations predisposing to hereditary nonpolyposis colorectal cancer: database and results of a collaborative study. The International Collaborative Group on Hereditary Nonpolyposis Colorectal Cancer.

BACKGROUND & AIMS: Germline mutations in four DNA mismatch repair genes are known to cause susceptibility to hereditary nonpolyposis colorectal cancer (HNPCC). The rapidly increasing information about these mutations needs to be collected and appropriately stored to facilitate further studies on the biological and clinical significance of the findings. METHODS: The International Collaborative Group on HNPCC has established a database of DNA mismatch repair gene mutations and polymorphisms. In this report, 126 predisposing mutations were analyzed. RESULTS: A majority of the mutations affected either the Mut L homologue (MLH) 1 (n = 75) or the Mut S homologue (MSH) 2 (n = 48) and were quite evenly distributed, with some clustering in MSH2 exon 12 and MLH1 exon 16. Most MSH2 mutations consisted of frameshift (60%) or nonsense changes (23%), whereas MLH1 was mainly affected by frameshift (40%) or missense alterations (31%). Although most mutations were unique, a few common recurring mutations were identified. Of the families studied (n = 202), 82% met the Amsterdam criteria and 15% did not; the general mutation profile was similar in both groups. CONCLUSIONS: The construction of mutation profiles will facilitate the development of diagnostic strategies in HNPCC.

Adaptor Proteins, Signal Transducing↗

PubMed2002

The case for population-based screening for colorectal cancer.

Screening for colorectal cancer is commanding increasing attention. Other cancer screening programmes have been a part of public consciousness for some time, but, until recently, colorectal cancer screening has remained in the background. Fuelled by new research, market opportunities and increased recognition of individual risk, screening for colorectal cancer is becoming a recommended procedure, but controversy about how best to implement widespread screening remains.

Adenoma↗

PubMed1999

Deficient DNA repair capacity: a predisposing factor and high risk predictive marker in familial colorectal cancer.

Even though colorectal cancer tends to aggregate in families, there is paucity of information on the genetic determinism for familial colorectal cancer (FCRC) predisposition. Therefore, we investigated constitutional chromosome abnormalities and bleomycin induced chromosome sensitivity of 26 familial and 30 sporadic colorectal cancer (SCRC) patients, 60 unaffected family members (first/second degree relatives) and 30 normal healthy controls to determine whether these parameters could give any clues on genetic predisposing factors by which high risk members in CRC families could be identified. The test assay used bleomycin-induced chromatid breaks in short term microcultures of peripheral blood lymphocytes of the subjects. The CRC patients, the unaffected family members and the controls did not show any constitutional chromosomal abnormalities. However, with regard to bleomycin sensitivity, there was significant difference between the CRC patients, unaffected relatives and controls. The mean b/c values of 1.64+/-0.42 for the FCRC patients and 1.08+/-0.34 for the SCRC patients were significantly higher than the mean b/c values of 0.62+/-0.18 for the unaffected relatives and 0.52+/-0.12 for the controls (P<0.001). A noteworthy observation was that 6 unaffected members from 6 CRC families also showed bleomycin hypersensitivity, at the initiation of the study. Since they expressed mean b/c values greater than 1.0, which was as high a value as those of the patients, they were regularly followed up. Out of these 6 members, 2 developed CRC later. This clearly demonstrates that mutagen hypersensitivity among unaffected relatives in CRC families may be related to cancer predisposition. Hence, this cytogenetic assay could be utilised to identify the genetically high risk individuals in CRC families.

Adult↗

PubMed1997

Altered mRNA expression of specific molecular species of fucosyl- and sialyl-transferases in human colorectal cancer tissues.

Human colorectal cancers express various cancer-associated carbohydrate determinants such as Lewis Y or sialyl Lewis A, suggesting a considerable alteration in glycosyltransferase activities occurring upon malignant transformation. We investigated the mRNA amounts of fucosyltransferase (Fuc-T) and sialyltransferase (ST) isoenzymes, including Fuc-T III, IV, V, VI and VII and ST-3N, ST-30 and ST-4, in human colorectal cancer tissues by Northern blotting and RT-PCR. Regarding fucosyltransferases, mRNA of Fuc-T III and VI was not significantly altered, and only Fuc-T IV mRNA showed a moderate increase in cancer tissues when compared with adjacent non-malignant colonic epithelia taken from the same patient (273 +/- 96%; p < 0.001). The moderate increase of Fuc-T IV message may be related to an enhanced expression of Lewis Y in colon cancer tissues. In the ST isoenzymes, mRNA for ST-3N remained unchanged, whereas that for ST-4 decreased significantly in cancer tissues, to 32 +/- 29%, (p < 0.005). The most remarkable finding was that the message of ST-30 was prominently increased in cancer tissues compared with non-malignant colorectal mucosa. When further investigated by quantitative RT-PCR assays on a larger series of patients with colorectal cancers, the average increase in mRNA for ST-30 was 459 +/- 200% compared with that in adjacent non-malignant epithelium (significant at p < 0.0001). The increase of ST-30 message was more prominent in the cancer tissues strongly expressing sialyl Lewis A than in the cancer tissues expressing sialyl Lewis A only weakly or moderately (significant at p < 0.05). The marked increase in the message of ST-30 is suggested to be related to an enhanced expression of sialylated carbohydrate determinants in colon cancer tissues including sialyl Lewis A, since the enzyme exhibited a significant activity against the type 1 chain carbohydrate substrate and produced the precursors for sialyl Lewis A synthesis, when its cDNA was expressed in Cos-7 cells.

Adenocarcinoma↗

PubMed1999

Advances in cross-sectional imaging of colorectal cancer.

Imaging of colorectal cancer is primarily accomplished with computed tomography (CT) and magnetic resonance imaging (MRI). These two modalities have been used for more than a decade in imaging both primary and metastatic colorectal cancer. Recent advances in the CT and MRI technologies are redefining the precise role of these imaging modalities in the work-up and evaluation of patients with colorectal cancer.

Colonoscopy↗

PubMed1979

[Colorectal cancer].

Incidence of colorectal cancer is increasing during the last years. 5% of the population get affected. From these a group of patients with a higher carcinoma risk must be separated: that with adenomas, familial polyposis and ulcerative colitis. Nourishment seems to be one of the main factors for the development of cancer. Although all important principles of radical surgery are realized, this 5-year survival rate for colorectal cancer is less than 40%. Prophylaxis, early diagnosis and the effect of irradiation and drug therapy must improve the relatively poor prognosis of colorectal cancer, which has reached in Germany the highest mortality and even -- with the exception of skin cancer -- the highest morbidity of all malignant neoplastic diseases.

Colonic Neoplasms↗

PubMed2000

Risk of gastric cancer in hereditary nonpolyposis colorectal cancer in Korea.

After endometrial cancer, gastric cancer is the second most common extracolonic cancer in cases of hereditary nonpolyposis colorectal cancer (HNPCC), where the relative risk in HNPCC familial members is known to be 4-fold. However, it is not yet clear whether HNPCC families from Korea, an endemic area for gastric cancer, have the same relative risk or whether the incidence of gastric cancer is high enough to justify familial screening. To clarify these questions, we investigated 1011 individuals from 66 Korean HNPCC families (28 families fulfilled the Amsterdam criteria and 38 did not). The overall and age-specific relative risk of gastric cancer in HNPCC families when compared with the background population was calculated. Twenty-five patients with gastric cancer were identified from among 22 HNPCC families. The calculated risk of gastric cancer in patients with HNPCC and their first-degree relatives was 2.1-fold greater than in the general population (95% confidence interval; range, 1.4-3.2). However, the relative risk of gastric cancer in the younger generations was much greater (11.3-fold in the 30s and 5.5-fold in the 40s). Additionally, the relative risk was greater in mutation carrier families than noncarrier families (3.2-fold versus 1.6-fold). This study demonstrates that the risk of gastric cancer in members of HNPCC families in a gastric cancer endemic population, particularly in younger subjects and mutation carrier families, is high enough to justify careful screening.

Adult↗

PubMed1986

[Prognostic significance of immunoreactivity of regional lymph nodes in colorectal cancer--an analysis of 2,502 cases. National Cooperative Group on Pathology and Prognosis of Colorectal Cancer].

This paper presents an analysis of the relation between immunoreactivity of the regional lymph node and survival rate. 2,502 cases of colorectal cancer collected from 13 areas in China were studied. The immunomorphology of the regional lymph node in this study was shown by sinus histiocytosis (SH), paracortical hyperplasia (PH) and germinal hyperplasia (GH). Each of these reactions was divided into 4 grades (-, +, ++, +++). The results show: A significant correlation exists between the extent of immunoreaction and prognosis. The 5 year survival rates of patients with SH (++, +++), PH (++, +++), GH (++, +++) are 59.0%, 58.1% and 62.1% respectively, much higher than those in the negative groups (P less than 0.001). The effect of these three immunoreactive features on prognosis is diverse. The 5 year survival rate of cases with simple GH (++, +++) is 62.9%, statistically higher than those of cases with simple PH (++, +++) or SH (++, +++). It seems that the B-cell may play a very important role in the host defence mechanism. It was found that SH (++, +++), PH (++, +++) and GH (++, +++) occurred more frequently in Dukes' A stage than those in Dukes' C stage. The same phenomenon is also identified in comparing the well-differentiated with the poorly-differentiated cases.

Adenocarcinoma, Mucinous↗

PubMed2006

Chemotherapeutic implications in microsatellite unstable colorectal cancer.

Chemotherapy for colorectal cancer is currently offered to patients based on the stage of their cancer, and there is evidence to show an overall survival benefit with 5-fluorouracil-based (5-FU) therapy for patients with lymph node metastasis who receive it. The pathogenesis of colorectal cancer involves genomic instability, with about 15% of tumors demonstrating a form of genomic instability called high-frequency microsatellite instability (MSI-H) and due to loss of DNA mismatch repair function, and the remainder of colorectal tumors lacking MSI-H with retained DNA mismatch repair function and called microsatellite stable (MSS), with a large proportion of these tumors demonstrating another form of genomic instability called chromosomal instability. There is now evidence to show that the form of genomic instability that is present in a patient's colorectal cancer may predict a survival benefit from 5-FU. In particular, patients whose colorectal tumors have MSI-H do not gain a survival benefit with 5-FU as compared to patients with MSS tumors. In vitro evidence supports these findings, as MSI-H colon cancer cell lines are more resistant to 5-FU compared to MSS cell lines. More specifically, components of the DNA mismatch repair system have been shown to recognize and bind to 5-FU that becomes incorporated into DNA and which could be a trigger to induce cell death. The binding and subsequent cell death events would be absent in colorectal tumors with MSI-H, which have lost intact DNA mismatch repair function. These findings suggest that: (a) tumor cytotoxicity of 5-FU is mediated by DNA mechanisms in addition to well-known RNA mechanisms, and (b) patients whose tumors demonstrate MSI-H may not benefit from 5-FU therapy. Future studies should include a better understanding of the cellular mechanisms of the DNA recognition of 5-FU, multi-centered prospective trials investigating the survival benefit of 5-FU based on genomic instability, and the investigation of alternative chemotherapeutic regimens for patients with MSI-H tumors to improve survival.

Antineoplastic Agents↗

PubMed2006

Characterization of tumour-infiltrating lymphocytes and apoptosis in colitis-associated neoplasia: comparison with sporadic colorectal cancer.

The development of colorectal cancer is a major complication for patients with chronic idiopathic colitis. Colitis-associated tumours tend to occur at a younger age and be more aggressive than sporadic colorectal cancers. While we have previously associated the presence of tumour-infiltrating lymphocytes (TILs) and increased apoptosis in sporadic colorectal cancer with high-level microsatellite instability and improved prognosis, little is known of the relationship between these variables in colitis-associated colorectal cancer. The aim of this study was to correlate TILs and tumour cell apoptosis in colitis-associated neoplasms stratified according to microsatellite instability. Twenty tumour and 11 dysplastic samples resected from 21 patients with long-standing colitis were analysed for microsatellite instability at 10 microsatellite markers. TIL distribution (CD3, CD8) and function (granzyme B) were quantified by immunohistochemistry. Neoplastic cell apoptosis was assessed using the M30 CytoDEATH antibody. These findings were compared with 40 microsatellite stable (MSS) sporadic colorectal cancers previously evaluated for TILs and neoplastic apoptosis. Low-level microsatellite instability was found in 1/20 colitis-associated tumours. All other colitis-associated lesions were designated MSS. CD3(+) and CD8(+) TIL counts were significantly higher in colitis-associated lesions compared with MSS sporadic colorectal cancer (p < 0.0001, p = 0.001 respectively). Despite their higher TIL density, colitis-associated tumours were more likely to present late (Dukes' stage C or D) (p = 0.02). Functionally, colitis-associated TILs demonstrated significantly less granzyme B expression compared to sporadic cancers (p = 0.002). The level of tumour cell apoptosis was similar between the two groups (sporadic, 1.53%; colitis cancers, 1.45%). In conclusion, MSS colitis-associated tumours have a higher prevalence of CD3(+)/CD8(+) TILs but no associated increase in tumour cell killing by apoptosis. Unlike cytotoxic T cells in sporadic colorectal cancer, TILs do not appear to enhance the prognosis of colitis-associated colorectal cancer. This may be related to an impairment of granzyme B expression within these lesions.

Aged↗

PubMed2001

Predictors of proximal vs. distal colorectal cancers.

BACKGROUND: Because proximal colorectal cancers have a tendency to present at a more advanced stage and thus have a poorer prognosis, it is important to understand the factors associated with the development of proximal colorectal cancer. We hypothesized that older age, female gender, and the presence of comorbid illness would be associated with proximal cancers. METHODS: Incident cases of colorectal cancer (n = 9,550) occurring in 1994 were identified from Florida's population-based statewide cancer registry. We categorized colorectal cancers as either proximal (cecum, ascending colon, and transverse colon) or distal (descending colon, sigmoid colon, rectosigmoid, and rectum). Multiple logistic regression analysis was used to determine the multivariable relationship between clinical characteristics and the odds of a proximal-occurring lesion. RESULTS: Four characteristics emerged as independent predictors of a proximal lesion. Each year of increasing age was associated with a 2.2 percent increase in the odds of a proximal lesion, whereas female gender was associated with a 38 percent increase in the odds of a proximal lesion. The presence of a comorbid condition was associated with a 28 percent greater odds of a proximal lesion, and, finally, black, non-Hispanic race was associated with a 24 percent greater odds of a proximal lesion. CONCLUSIONS: We found that increasing age, female gender, black, non-Hispanic race, and the presence of comorbid illnesses were factors associated with a greater likelihood of developing colorectal cancer in a proximal location. Further studies will be required to confirm these findings and to establish the mechanism by which comorbidity influences the site of colorectal cancer development.

Age Factors↗

PubMed2001

Gene therapy for colorectal cancer: therapeutic potential.

Colorectal cancer is a leading cause of cancer mortality in Western countries. Gene therapy has been proposed as a potential novel treatment modality for colorectal cancer, but it is still in an early stage of development. The preclinical data have been promising and numerous clinical trials are underway. This brief review aims to summarise the current status of clinical trials of different gene therapy strategies, including immune stimulation, mutant gene correction, prodrug activation and oncolytic virus therapy, for patients with colorectal cancer. Data from phase I trials have proven the safety of the reagents but have not yet demonstrated significant therapeutic benefit. In order to achieve this and extend the scope of the treatment, continuing efforts should be made to improve the antitumour potency, efficiency of gene delivery and accuracy of gene targeting.

Adenoviridae↗

PubMed1995

Relation of family history of cancer and environmental factors to the risk of colorectal cancer: a case-control study.

The relation of a family history of cancer and environmental factors to colorectal cancer was investigated in a case-control study conducted from 1992 to 1994 at 10 medical institutions in Japan using a self-administered questionnaire, and 363 cases of colorectal cancer were compared with 363 controls matched for sex and age. A family history of colorectal cancer was positively associated with colon cancer (odds ratio (OR) = 2.0, 95% confidence interval (CI) 1.03-3.87) and rectal cancer (OR = 2.1 CI 0.94-4.48), but a family history of other cancers did not increase the risk. The proportion of patients with a family history of colorectal cancer within first-degree relatives was 12.4%--appreciably higher than figures previously reported in Japan. On the other hand, the incidence of hereditary non-polyposis colorectal cancer was 1.4%, and lower than previous estimates. Among dietary factors, a western-style diet significantly increased the risk of both colon and and rectal cancer (OR = 2.3 CI 1.30-3.88 and OR = 2.1 CI 1.26-3.63, respectively). Consumption of rice was protective against both colon and rectal cancer (OR = 0.5 CI 0.31-0.82 and OR = 0.3 CI 18-0.65, respectively). Animal meat, oily food, fish, vegetables and fruit were shown to affect the risk, but no statistically significant correlation was found. Among other factors, constipation increased the risk of colon cancer (OR = 2.0 CI 1.02-3.76) and consumption of coffee raised the risk of rectal cancer (OR = 1.7 CI 1.07-2.82). Our findings suggest that a family history of colorectal cancer is an important risk factor for this disease, and does not contradict the hypothesis that the risk of colorectal cancer in Japan may be influenced by westernization of lifestyle. However, we were unable to find conclusive evidence that familial clustering of this disease is strongly affected by environmental factors or genetic diseases such as hereditary non-polyposis colorectal cancer.

Adenocarcinoma↗

PubMed1991

Cancer incidence among parents of patients with colorectal cancer.

To investigate the genetic factor in the development of colorectal cancer, a cohort study was undertaken of parents of patients with this disease. All 1,524 patients, who were diagnosed with colorectal cancer in Denmark in 1982-84 and were below the age of 60 years, were selected from the National Cancer Register. The parents of these patients were identified from the public population registers. The index persons had a total of 1,478 eligible mothers, of whom 96% were successfully traced, and a total of 1,414 eligible fathers, of whom 96% were traced. These parents were sought in the Cancer Register for cancer cases diagnosed in the period January 1, 1943 to December 31, 1986. The incidence rates for the Danish population were used to estimate the expected numbers of colorectal cancer cases among the parents. Both the mothers and the fathers exhibited an increased risk of colorectal cancer. The standardized incidence ratios were 1.62 (95% CI 1.31-2.01) and 1.87 (95% CI 1.54-2.27), respectively. In a previous study we found that spouses of patients with colorectal cancer in Denmark did not have an increased risk of this disease. The increased risk found in the present study among the parents of patients therefore indicates that a possible genetic factor is present in the aetiology of colorectal cancer, and that it is of importance in the general population.

Aged↗

PubMed2004

Comparative study of proteome between primary cancer and hepatic metastatic tumor in colorectal cancer.

AIM: To identify the differential proteins associated with colorectal cancer genesis and hepatic metastasis. METHODS: Hydrophobic protein samples were extracted from normal colorectal mucosa, primary cancer lesion and hepatic metastatic foci of colorectal cancer. With two-dimensional electrophoresis and image analysis, differentially expressed protein spots were detected, and the proteins were identified by matrix assisted laser desorption/ionization-time of flight-mass spectrometry and peptide mass fingerprint analysis. RESULTS: Significant alterations of the proteins in number and expression levels were discovered in primary cancer and hepatic metastatic foci, the expression of a number of proteins was lost in 25-40 ku, but protein spots was increased in 14-21 ku, compared with normal mucosa. Nine differentially expressed protein spots were identified. Three proteins expressed in normal mucosa, but lost in primary cancer and hepatic metastasis, were recognized as calmodulin, ribonuclease 6 precursor and mannosidase-alpha. Proapolipoprotein was expressed progressively from normal mucosa to primary cancer and hepatic metastasis. The differentially expressed protein of beta-globin was found in normal mucosa and hepatic metastatic tumor, but lost in primary cancer lesion. Cdc 42, a GTP-binding protein, was identified in hepatic metastasis. The protein spots of C4 from primary cancer, M7 and M9 from hepatic metastasis had less homology with the proteins in database. CONCLUSION: Variations of hydrophobic protein expression in colorectal cancer initiation and hepatic metastasis are significant and can be observed with two-dimensional electrophoresis. The expression of calmodulin, ribonuclease 6 precursor and mannosidase-alpha is lost but the expression of proapolipoprotein is enhanced which is associated with colorectal cancer genesis and hepatic metastasis. Cdc 42 and beta-globin are expressed abnormally in hepatic metastasis. Protein C4, M7 and M9 may be associated with colorectal cancer genesis and hepatic metastasis.

Adult↗

PubMed1998

Family history of cancer and risk of colorectal cancer in Italy.

Subjects with a family history of colorectal cancer (CRC) are at increased risk of CRC, but quantification of the risk in different populations, the possible differences in risk according to localization of the cancer and the association of family history of other cancers with CRC risk are still open issues. We have therefore analysed data from a multicentric case-control study conducted in six Italian areas between 1992 and 1996 of 1225 incident cases of colon cancer, 728 cases of rectal cancer and 4154 controls admitted for acute conditions to the same network of hospitals as the cases. Unconditional logistic regression models including terms for gender, age, study centre, years of education and number of siblings were used to estimate the odds ratios (ORs) of CRC according to various aspects of history of CRC and other cancers in first-degree relatives. The OR for family history of CRC was 3.2 (95% confidence interval, CI, 2.5-4.1) for colon cancer and 2.2 (95% CI 1.6-3.1) for rectal cancer. Colon cancer was significantly associated with a family history of stomach (OR 1.4), bone (OR 2.1) and kidney (OR 2.3) cancers, while rectal cancer was significantly associated with a family history of lymphomas (OR 2.8). There was a 30% higher risk of colon and rectal cancer in subjects with a family history of any cancer, excluding intestine. The ORs for family history of CRC were 5.2 for colon and 6.3 for rectum when the proband's age was below 45 years. The ORs were similar when the affected relative was a parent or a sibling and in different strata of age of relative(s). For subjects with two or more first-degree relatives with CRC, the risk was 6.9 for the right colon, 5.8 for the transverse and descending colon, 3.8 for the sigma, 3.2 for the rectosigmoid junction and 1.9 for the rectum. This study confirms that a family history of CRC in first-degree relatives increases the risk of both colon and rectal cancer, the association being stronger at younger ages and for right colon.

Adult↗

PubMed1991

[Cooperative study of surgical adjuvant chemotherapy for colorectal cancer (third report): five-year results. Cooperative Study Group of Surgical Adjuvant Chemotherapy for Colorectal Cancer in Japan].

A randomized controlled study was carried out by the envelope method with 491 institutions in participation across the country in order to find an optimal surgical adjuvant chemotherapy for curatively resected colorectal cancer. The schedules for drug administration were different in four districts: ACNU + Futraful (FT) group and FT alone group in the Hokkaido-Shikoku district; the same schedule groups plus untreated group in the Chubu-Kinki district; MMC+FT group, FT alone group in the Tohoku-Kanto district; and ADM+FT group and FT alone group in the Chugoku-Kyushu district. The numbers of patients admitted to this study were 2,450 cases with colon cancer and 2,456 cases met the evaluation criteria of this study. The 5-year survival rate on the whole did not differ from combination therapy to single drug therapy in either colon cancer or rectal cancer, but in Dukes C rectal cancer the five-year survival rate tended to be higher with the combination therapies. In n2 (+) or a2(s) rectal cancer in particular, combination therapies with MMC and FT and with ADM and FT achieved significantly higher five-year survival rate, and the rate of local recurrence was significantly lower with ADM+FT.

Antineoplastic Combined Chemotherapy Protocols↗