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PubMed1995

Radioimmunoguided Surgery system improves survival for patients with recurrent colorectal cancer.

BACKGROUND: Advanced colorectal cancer is fatal. No systemic therapies have resulted in increased patient survival. METHODS: One hundred thirty-one patients with recurrent colorectal cancer enrolled in two prospective nonrandomized studies using Radioimmunoguided Surgery (RIGS) system from May 1986 to April 1992 have been analyzed. Eighty-six patients were injected with the anti-tumor-associated glycoprotein (TAG) antibody B72.3, and 45 patients were injected with the second-generation anti-TAG monoclonal antibody CC49. Both monoclonal antibodies were radiolabeled with iodine 125. Both traditional and RIGS explorations were used to determine resectability. Follow-up was a minimum of 28 months. RESULTS: Forty-nine (37.4%) of the 131 patients underwent a curative resection. Twenty-seven of the patients (55%) are alive 2 to 8 years after operation. The cancers of the remaining 82 patients were unresectable, and only two patients (2%) are alive. In this unresectable group alternative intraoperative therapeutic methods (intraoperative radiation therapy, intraperitoneal hyperthermic perfusion, hepatic lines, and brachytherapy) were tried in 11 patients with two survivors. There were no survivors in 18 patients whose cancers were found to be traditionally resectable but unresectable with RIGS or in the 53 patients whose cancers were clearly unresectable by traditional exploration. Patients selected for curative resection had significantly increased survival (p < 0.0001). CONCLUSIONS: As an intraoperative tool RIGS significantly improves the selection of patients for curative resection.

Adenocarcinoma↗

PubMed2004

Clinical management of hereditary colorectal cancer syndromes.

PURPOSE OF REVIEW: Colorectal cancer is the second leading cause of cancer-related death in the United States. Although most colorectal cancers are sporadic, approximately 25% have a familial predisposition, and 5 to 7% are hereditary and occur in genetically distinct high-risk families. This review focuses on four hereditary colon cancer syndromes: familial adenomatosus polyposis, hereditary nonpolyposis colorectal cancer, juvenile polyposis syndrome, and Peutz-Jeghers syndrome. RECENT FINDINGS: The management of the inherited colorectal cancer syndromes has progressed substantially over the past years because of advancement of genetic understanding and testing options, which have led to the possibility of preclinical diagnosis and early surveillance and treatment. Genetic testing is based on identification of specific abnormalities and should be combined with counseling of affected families. SUMMARY: Recent advances have contributed to the understanding of the molecular basis of various types of colorectal cancer, and among these, the inherited colorectal cancer syndromes have attracted much attention. Expanding recognition of clinical characteristics, targeted surveillance strategies and new methods of treatment have led to improved clinical management of these syndromes.

Journal Article↗

PubMedDate not supplied

Colorectal cancer and peritoneal carcinomatosis.

Colorectal cancer ranks third in new cancer cases and in cancer deaths in men and women combined in the United States. Additionally, the probability of developing an invasive colorectal cancer over one's life-time is around 1 in 16. This amounts to approximately 133,000 new cancer cases and 55,000 cancer deaths yearly. Despite advances in adjuvant therapy for colorectal cancer, the peritoneal surface still remains a considerably high failure site for patients with recurrence of disease. Because of the favorable results of treating peritoneal metastases from ovarian cancer and pseudomyxoma peritonei with cytoreduction and intraperitoneal chemotherapy, this form of therapy has been investigated by several investigators in the management of patients with peritoneal metastases secondary to colorectal cancer. Preliminary studies seem to favor those patients with low-volume, low-grade peritoneal metastases, those with perforated cancers, and those patients in whom definitive cytoreduction is complete. Intraperitoneal chemotherapy with or without hyperthermia is a safe and logical way to administer dose-intensive therapy to the peritoneal cavity.

Antineoplastic Agents↗

PubMed2006

Promoter methylation precedes chromosomal alterations in colorectal cancer development.

BACKGROUND: Colorectal cancers are characterized by genetic and epigenetic alterations. This study aimed to explore the timing of promoter methylation and relationship with mutations and chromosomal alterations in colorectal carcinogenesis. METHODS: In a series of 47 nonprogressed adenomas, 41 progressed adenomas (malignant polyps), 38 colorectal carcinomas and 18 paired normal tissues, we evaluated promoter methylation status of hMLH1, O6MGMT, APC, p14ARF, p16INK4A, RASSF1A, GATA-4, GATA-5, and CHFR using methylation-specific PCR. Mutation status of TP53, APC and KRAS were studied by p53 immunohistochemistry and sequencing of the APC and KRAS mutation cluster regions. Chromosomal alterations were evaluated by comparative genomic hybridization. RESULTS: Our data demonstrate that nonprogressed adenomas, progressed adenomas and carcinomas show similar frequencies of promoter methylation for the majority of the genes. Normal tissues showed significantly lower frequencies of promoter methylation of APC, p16INK4A, GATA-4, and GATA-5 (P-values: 0.02, 0.02, 1.1x10(-5) and 0.008 respectively). P53 immunopositivity and chromosomal abnormalities occur predominantly in carcinomas (P values: 1.1x10(-5) and 4.1x10(-10)). CONCLUSIONS: Since promoter methylation was already present in nonprogressed adenomas without chromosomal alterations, we conclude that promoter methylation can be regarded as an early event preceding TP53 mutation and chromosomal abnormalities in colorectal cancer development.

Adenoma↗

PubMed1997

Molecular genetic analysis of a patient with hereditary nonpolyposis colorectal cancer syndrome.

Hereditary nonpolyposis colorectal cancer types I and II constitute approximately 5% to 10% of the cases of colorectal cancer annually. Recognition of its clinical features and identification of affected families are imperative for appropriate medical and surgical management. Furthermore, molecular analysis can be performed in such families because the DNA mismatch repair genes have been identified as being mutated, thereby leading to microsatellite instability. We describe a 33-year-old woman with ovarian, uterine, and colorectal cancer, whose family, on close examination, had features consistent with hereditary nonpolyposis colorectal cancer. The patient had evidence of microsatellite instability in her colon cancer.

Adult↗

PubMed2006

IGF1 gene polymorphism and risk for hereditary nonpolyposis colorectal cancer.

Hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant disorder caused by germline mutations in DNA mismatch repair (MMR) genes. Insulin-like growth factor-I (IGF-I) is involved in colorectal carcinogenesis, and elevated plasma IGF-I levels are associated with sporadic colorectal cancer (CRC) risk. We investigated the relationship between IGF1 promoter cytosine-adenine (CA) dinucleotide-repeat polymorphism length and CRC risk in 121 MMR gene mutation carriers using Cox regression and Kaplan-Meier analysis. All statistical tests were two-sided. Time to onset for CRC increased for each decrease in CA-repeat number (median = 19 repeats, range = 12-22 repeats; hazard ratio [HR] = 1.17, 95% confidence interval [CI] = 1.05 to 1.31; P = .006). Patients carrying a CA(< or = 17) repeat allele had a statistically significantly higher CRC risk (HR = 2.36; 95% CI = 1.28 to 4.36; P = .006) than all others and were younger at onset (44 years versus 56.5 years; P = .023). These findings indicate a statistically significant association between shorter IGF1 CA-repeat lengths and increased risk for CRC in HNPCC. This is the first report, to our knowledge, to show that IGF1 variant genotypes modify risk of a hereditary form of cancer.

Adenine↗

PubMed1997

Colorectal cancer. Screening strategies.

Colorectal cancer is both curable and preventable; however, systemic screening has not yet been instituted in the United States. There are a number of diagnostic tests, imaging procedures, and endoscopic examinations available to detect colorectal cancer and polyps in their early stages. This article reviews these various screening options and concludes that the barium enema is the most cost-effective method.

Colorectal Neoplasms↗

PubMedDate not supplied

[Emergency surgery for colorectal cancer: our experience].

Colorectal cancers have an extremely negative prognosis in the elderly, with a high percentage of clinical presentations requiring emergency surgery and high perioperative mortality rates. The clinical manifestations of this type of cancer set in a cutely in 20% of cases due to the sudden onset of one of the basic complications. The authors report on their experience with 79 patients undergoing emergency surgery for colorectal cancer. The choice of operation was made on the basis of the patient's general condition, as estimated by his or her ASA score, and the presence of associated diseases.

Aged↗

PubMed1986

Contribution from descriptive studies to the etiological knowledge of colorectal cancer.

Incidence of colorectal cancer increasing exponentially with age is confirmed but sex-age differences in incidence throughout the large bowel are shown. Observations of incidence within countries indicate that colorectal cancer is a disease of affluent societies. Furthermore, it is hypothesized that a high dietary fat intake leads to an increase in faecal components associated with colon cancer risk.

Adult↗

PubMed2005

Relationship between thymidylate synthase (TS) genotype and TS expression: a tissue microarray analysis of colorectal cancers.

Response of colorectal cancers to 5-fluorouracil appears to be influenced by differences in thymidylate synthase (TS) expression. To explore the relationship between TS 5' genotype and expression, we analyzed paired tumor and normal tissue from 87 colorectal cancers by tissue microarray. A trend to an association between TS genotype and expression was observed, but the correlation was weak. Although the 2R homozygote was preferentially associated with TS expression (p<0.03), no relationship was observed for the 3R homozygote (p=1.0). The relationship between 5' TS genotype and TS expression is not simple. For clinical trials incorporating TS status, detection of TS expression in tumors by immunohistochemistry must still remain the benchmark over genotype.

5' Untranslated Regions↗

PubMed1999

Colorectal cancer in adolescents.

Colorectal cancer, one of the most common malignancies among adults, is rare in adolescence. This low incidence coupled with non-specific symptoms and aggressive natural history leads to a poorer prognosis than in reported adult series. This article describes two cases of colorectal cancer in adolescents and reviews the literature regarding this rare condition. Earlier diagnosis and a greater understanding of the natural history may lead to improved treatment with concomitant improvements in survival.

Adenocarcinoma↗

PubMed2005

Large genomic aberrations in MSH2 and MLH1 genes are frequent in Chinese colorectal cancer.

Hereditary nonpolyposis colorectal cancer is caused by inactivating mutations in the genes of the DNA mismatch repair (MMR) system. Studies have shown that large-fragment aberrations in MMR genes are responsible for a considerable proportion of hereditary colorectal cancer (CRC), but it has been rarely reported in Chinese patients. Here we used multiplex ligation-dependent probe amplification to analyze the genomic rearrangements of 45 Chinese hereditary CRC families, 20 young-age CRC patients (onset of CRC at younger than 50 years and no family history), and 13 patients with sporadic CRC diagnosed at age 50 years or older. Overall, we found 9 (13.8%) large genomic deletions or duplications: 7 out of 45 CRC patients with family history and 2 out of 20 young CRC patients. In all alterations, five genomic deletions were uncovered in the MSH2 gene, as well as one deletion and three duplications in the MLH1 gene. Furthermore, two of the duplications unveiled in this study may have more than a four-copy increase of the exon showing duplication in MLH1. The results indicate that genomic aberrations, large-fragment deletions and duplications, in both MSH2 and MLH1 genes play a role in the pathogenesis of Chinese CRC patients with a family history, as reported in western populations. Moreover, the genomic aberrations in these genes might also be a frequent cause of CRC at a young age in China.

Adaptor Proteins, Signal Transducing↗

PubMed1996

Establishment of a hereditary nonpolyposis colorectal cancer registry.

INTRODUCTION: Hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant condition characterized by early age of onset colorectal cancer, right-sided predominance, excess of synchronous and metachronous colonic neoplasms, and extracolonic cancers. The purpose of this study is to report clinical characteristics of HNPCC families in our registry. METHODS: This is a retrospective review of medical records of patients with a significant history of colorectal cancer and interviews with their families. RESULTS: Three hundred one people with cancer in 40 HNPCC families were identified. In 284 of 301 (94 percent) people, 363 cancers were identified. Colorectal cancer only was identified in 182 people (64 percent) and, in conjunction with extracolonic tumors, in another 31 people (11 percent). Extracolonic cancer alone was noted in 71 people (25 percent). Median age at diagnosis of colorectal cancer was 48 (range, 17-92) years. In patients with documented pathology, right-sided tumors predominated (55 percent), synchronous and metachronous tumors were noted in 53 percent, and synchronous of metachronous adenomas were documented in 51 percent of people. Generational anticipation was also noted. CONCLUSION: This study demonstrates and confirms characteristics that have been described in HNPCC. Namely, early age of onset of colorectal cancer, right-sided predominance, multiple synchronous and metachronous neoplasms, increased extracolonic cancers, and generational anticipation.

Adolescent↗

PubMed2001

Trocar site recurrence in laparoscopic surgery for colorectal cancer.

BACKGROUND: Laparoscopic colorectal surgery has been associated with less postoperative pain, an early return of bowel function, a shorter period of hospitalization and disability, and better cosmetic results. However, the application of laparoscopic techniques to the curative resection of colorectal cancer is still controversial, owing to reports of cancer recurrence at the port site wounds. The accumulation of numerous such reports in a relatively short period raised concern that there might be an extraordinary high rate of port site metastases after laparoscopic colorectal surgery. This concern has led to intense clinical and basic research aimed at determining the incidence and causes of wound recurrence and developing preventative measures to address this problem. Despite these efforts, it is still not clear whether port site metastasis is really an inherent drawback to laparoscopic cancer surgery. METHODS: In this review of the literature on port site metastasis, we gathered data from clinical series of laparoscopic surgery for colorectal cancer. We eliminated series of <50 patients, since they may be flawed by the learning curve required for this technically demanding procedure. RESULTS: The rate of port site recurrences in the 1737 patients who participated in these series was 1%. Although the methods and criteria for patient selection in these studies varied, this figure appears to be comparable to the incidence reported for other malignancies and for laparotomies performed to treat colorectal cancer. CONCLUSION: This review suggests that wound recurrence may actually be the result of an unfortunate learning curve, rather than an inherent concern. However, we must await the final results of large randomized studies before drawing any definitive conclusions.

Adenocarcinoma↗

PubMed1999

Frequent microsatellite instability and mismatch repair gene mutations in young Chinese patients with colorectal cancer.

BACKGROUND: The incidence of colorectal cancer in persons under 46 years of age is substantially higher in Hong Kong than in Scotland and many other countries. Consequently, we examined whether there is a hereditary predisposition for colorectal cancer in this Southern Chinese population. METHODS: We investigated the incidence of microsatellite instability (MSI) at 10 DNA sites in 117 colorectal cancer specimens from Chinese patients of various ages. Those tumors with new alleles at 40% or more of the sites investigated were identified as highly unstable MSI (MSI-H). In young patients, we also searched for germline mutations in three mismatch repair genes (hMSH2, hMLH1, and hMSH6). RESULTS: The incidence of MSI-H varied statistically significantly with age, being observed in more than 60% of those younger than age 31 years at diagnosis and in fewer than 15% of those age 46 years or older. In 15 patients (<46 years old) whose colorectal cancers showed MSI-H, eight possessed germline mutations in either hMSH2 or hMLH1. When mutations in hMSH6 were included, more than 80% of Chinese colorectal cancer patients younger than 31 years had germline mutations in mismatch repair genes. We found a novel germline missense mutation in hMSH6 in a 29-year-old man whose tumor showed no MSI. Two patients had a 4-base-pair insertion in exon 10 causing a truncated protein; this insertion is a common polymorphism with a population allele frequency in Chinese of 5.6%. CONCLUSIONS: Our results indicate that germline mutations in mismatch repair genes contribute substantially to the pathogenesis and high incidence of colorectal cancer in young Hong Kong Chinese. However, because young Chinese and Caucasians show similar proportions of colorectal cancers with MSI-H, despite the higher incidence in the former, additional factors may underlie the high susceptibility of young Chinese to colorectal cancer.

Adenocarcinoma↗

PubMed1997

Overview of the epidemiology of colorectal cancer.

INTRODUCTION: The epidemiology of colorectal cancer has generated more interest recently, because recent developments in genetics, molecular biology, and genetic epidemiology have increased our understanding of the role of genes in the etiology of colorectal cancer. Interactions between genetic susceptibility and environmental factors in the etiology of cancer may be easier to define. EPIDEMIOLOGY: Colorectal cancer is common in the Western world and is rare in developing countries. A sharp increase is seen in Eastern Europe and Japan. ETIOLOGY: Molecular genetics has shown that accumulation of genetic changes is important in the development of colorectal cancer. Mutations in at least four to five genes are required for the formation of a malignant tumor. Environmental mutagenic factors may determine which susceptible individuals grow carcinomas. Environmental risk factors for colorectal cancer are found in a western diet, rich in fat, meat, and animal protein and low in fiber, fruit, and vegetables. The complex interrelations between food components make it difficult to define the precise role of specific food factors. PREVENTION: Conclusive evidence of the effectiveness of primary prevention of colorectal cancer via dietary measures or nonsteroidal anti-inflammatory drugs is lacking. Secondary prevention by interrupting the adenoma carcinoma sequence is an actual possibility, its effectiveness, however, needs to be determined. Molecular genetics holds a promise for identifying populations at high risk for colorectal cancer, therefore, targeting the screening to make it more cost-effective.

Age Distribution↗

PubMed2002

Microsatellite instability and immunohistochemical analysis of MLH1 and MSH2 in normal endometrium, endometrial hyperplasia and endometrial cancer from a hereditary nonpolyposis colorectal cancer patient.

Hereditary nonpolyposis colorectal cancer (HNPCC)-related endometrial cancer is associated with mutations in DNA mismatch repair genes. However, chronological changes of these genes in the endometrium have not been studied in women from HNPCC families. Tissue samples of normal endometrium, endometrial hyperplasia without atypia and endometrial cancer were collected at different times from a 41-year-old Japanese woman with a family history of HNPCC. Combined microsatellite instability (MSI) and immunohistochemical analysis of MLH1 and MSH2 predicted the presence of a mutation in MSH2 when she had endometrial hyperplasia without atypia 7 months before the diagnosis of endometrial cancer. Endometrial hyperplasia without atypia may indicate an early development of endometrial cancer in women from HNPCC families.

Adaptor Proteins, Signal Transducing↗

PubMed1998

A comparison of flow cytometry and immunohistochemistry in human colorectal cancers.

In human colorectal cancer it has been reported that some tumours lack the HLA-ABC antigens. This has been interpreted as reflecting tumour escape from the immune system. Earlier data have been obtained by immunohistochemistry. In this study, we compared the expression of HLA-ABC, HLA-DR, CD80 (B7-1) and CD54 (ICAM-1) in 20 tumours using both a conventional immunohistochemistry two-layer technique and multiparameter flow cytometry, gating on an epithelial cell marker. Colorectal cancer tissue used in flow cytometry was dissociated with collagenase, deoxyribonuclease and hyaluronidase. The intensity of expression of HLA-ABC, HLA-DR and CD80 was unaffected by the enzymes, but CD54 was decreased by 30%. The reproducibility of flow cytometry was good. Microscopy of sections revealed that about 5% of each tumour sample consisted of normal epithelium, but even after correction for this, flow cytometry was superior to immunohistochemistry in 33 out of 80 cases, and showed that tumours described as HLA-ABC negative by immunohistochemistry were in fact weakly positive for HLA-ABC. We conclude that flow cytometry and immunohistochemistry are complementary, and that flow cytometry is superior to immunohistochemistry for detecting antigens/epitopes present in low amounts.

Aged↗