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N J Petrelli

Publications and source records attributed to N J Petrelli.

At least 37 records · Page 2Linked to original sources

The onset and extent of genomic instability in sporadic colorectal tumor progression.

Cancer cell genomes contain alterations beyond known etiologic events, but their total number has been unknown at even the order of magnitude level. By sampling colorectal premalignant polyp and carcinoma cell genomes through use of the technique inter-(simple sequence repeat) PCR, we have found genomic alterations to be considerably more abundant than expected, with the mean number of genomic events per carcinoma cell totaling approximately 11,000. Colonic polyps early in the tumor progression pathway showed similar numbers of events. These results indicate that, as with certain hereditary cancer syndromes, genomic destabilization is an early step in sporadic tumor development. Together these results support the model of genomic instability being a cause rather than an effect of malignancy, facilitating vastly accelerated somatic cell evolution, with the observed orderly steps of the colon cancer progression pathway reflecting the consequences of natural selection.

Adenomatous Polyps↗

Validation of a new classification system for curatively resected colorectal adenocarcinoma.

BACKGROUND: The parameters within which colorectal adenocarcinoma is currently staged are often insufficient for decisions regarding therapy after potentially curative surgery. Consequently, oncologists make frequent use of additional prognostic indicators when assessing individual prognosis and selecting patients for adjuvant systemic treatment. Follow-up programs are generally uniform for all patients, regardless of disease stage and prognosis. As a result, patients with a favorable prognosis are needlessly subjected to stressful, costly follow-up too early and too frequently. This study was conducted to validate a new classification system that is a superior predictor of individual prognosis following curative surgery and may serve as a guide for personalized, cost-effective postoperative management and follow-up. METHODS: A total of 231 American colorectal carcinoma patients who underwent curative resection were retrospectively staged according to a new classification (containing 4 stage-groups) for curatively resected colorectal adenocarcinoma. This classification is based on statistical analysis of the impact on prognosis of numerous characteristics of 363 consecutive Israeli colorectal carcinoma patients who underwent curative resection. All the patients in both cohorts had had surgery at least 5 years previously. The new classification is based on three histologic variables (venous invasion, depth of primary tumor penetration, and regional lymph node status) and a scoring system that correlates higher numeric score with worse prognosis. In both cohorts, the new classification was compared with the Dukes, Astler-Coller, and TNM staging systems for patient distribution and survival (both disease free and cancer-related survival). RESULTS: In both cohorts, the 4 stage-groups of the new classification differed significantly in both the rate of and the time to first recurrence and cancer-related death, with progression from Group 4 to Group 1. Groups of high risk lymph node negative patients were defined, and lymph node positive patients were subdivided according to prognosis. It is suggested that, by using this new classification as a guide, selection for adjuvant systemic treatment may be refined, and postoperative follow-up may be personalized and therefore more cost-effective. CONCLUSIONS: The new classification for curatively resected colorectal adenocarcinoma, based on an analysis of the Israeli cohort and validated in the American cohort, is superior to the Dukes, Astler-Coller, and TNM staging systems as a predictor of individual prognosis, most probably because it incorporates the microscopic forerunner of distant, hematogenous spread (i.e., venous invasion) with the locoregional parameters of extent of disease (i.e., T and N values). It is suggested that the new classification may serve as a guide for more refined selection of patients for adjuvant systemic treatment and for individualized and more cost-effective postoperative follow-up. The new classification is simple and easy to use, requires no sophisticated equipment or tests, and can be applied in any health care system worldwide.

Adenocarcinoma↗

Accuracy of biopsy and cytology for the preoperative diagnosis of colorectal adenocarcinoma.

BACKGROUND AND OBJECTIVES: Endoscopic biopsy for the diagnosis of colorectal adenocarcinoma is not accurate in every case. Brush cytology can increase the sensitivity for the diagnosis of gastroesophageal lesions when combined with biopsy, but very little information is available for these techniques in the diagnosis of colorectal adenocarcinoma. METHODS: A retrospective medical records review of 110 patients was performed. All patients underwent a colorectal resection for primary adenocarcinoma after a diagnostic endoscopy. Biopsy and brush cytology was evaluated for their respective sensitivity. Seventy-three patients had both biopsy and cytology. RESULTS: The sensitivity of biopsy was 83.6% (92/110); for cytology, 78.1% (57/73; P = 0.44). From the 73 patients who had both diagnostic techniques, 68.5% (50/73) had both positive biopsy and cytology, 12.3% (9/73) only a positive biopsy, and 9.6% (7/73) only a positive cytology. The two techniques combined were not significantly superior to biopsy alone (90.4%, 66/73, vs. 80.8%, 59/73, respectively; P = 0.16), but tended to be superior to cytology alone (P = 0.07). CONCLUSIONS: Cytology and biopsy have a comparable sensitivity. The combination of the two techniques compares favorably, but does not significantly increase the sensitivity of biopsy alone. Both techniques should be used whenever there are any uncertainties concerning the diagnosis of colorectal adenocarcinoma.

Adenocarcinoma↗

Clinical implications of multiple colorectal carcinomas in hereditary nonpolyposis colorectal carcinoma.

PURPOSE: An increased incidence of multiple (synchronous and metachronous) colorectal carcinomas has been reported in hereditary nonpolyposis colorectal cancer. This review was undertaken to determine the clinical implications of multiple colorectal carcinomas in hereditary nonpolyposis colorectal cancer. METHODS: A retrospective review of the records of patients in the hereditary nonpolyposis colorectal cancer registry at Roswell Park Cancer Institute who had either synchronous or metachronous colorectal carcinomas was conducted. RESULTS: Twenty-five of 93 patients with documented pathology were found to have multiple colorectal carcinomas. The mean age at diagnosis of the index colorectal carcinoma was 46.7 (range, 28-65) years. There were 7 (7.5 percent) patients with synchronous colorectal carcinomas and 20 (21.5 percent) patients with metachronous colorectal carcinomas. Two of the seven (28.6 percent) patients with synchronous colorectal carcinomas developed a metachronous colorectal carcinoma. In the patients with metachronous colorectal carcinomas, 29 metachronous events were noted: colon (23) and rectum (6). The mean and median time interval for metachronous colorectal carcinomas were 10.9 and 11.8 (range, 1.5-43.8) years, respectively. The mean times to first, second, and third events were 11.7 (range, 1.5-43.5), 7.9 (range, 2.7-18.7), and 12.3 (range, 11.8-12.7) years, respectively. The majority of patients with metachronous colorectal carcinomas did not have stage progression at the diagnosis of the metachronous colorectal carcinomas: 13 patients had lower or same stage at first event, 4 had lower or same stage at second event, and 2 patients had lower stage at third event. Three of 20 patients with metachronous colorectal carcinomas died of their disease. CONCLUSION: Multiple colorectal cancers are common in hereditary nonpolyposis colorectal cancer. Even though stage progression may not be evident at diagnosis of metachronous colorectal cancer, some of these patients will nevertheless die of their disease.

Colorectal Neoplasms↗

New approach to the substaging of node-positive colorectal adenocarcinoma.

BACKGROUND: Future developments in adjuvant modalities may require substaging of node-positive colorectal adenocarcinoma that is accurately indicative of individual prognoses, upon which therapeutic decisions (e.g., choice of agents and intensity of treatment) may be based. This study compares substaging of node-positive colorectal cancer by venous invasion with substaging by three currently used methods, with respect to the ability of each method to define patient subsets that differ significantly in both disease-free and cancer-related survival rates. METHODS: A total of 171 patients with node-positive colorectal cancer, who had undergone potentially curative resection at least 5 years earlier, were retrospectively substaged by the tumor, node, metastasis (TNM) N1/N2, Astler-Coller C1/C2, Gastrointestinal Tumor Study Group (GITSG) C1/C2, and venous invasion (positive/negative) methods. Disease-free and cancer-related survival curves were calculated (by the Kaplan-Meier method) and compared for statistical significance (using the log-rank test). RESULTS: The separation of disease-free and cancer-related survival curves using the four methods of substaging node-positive colorectal cancer was as follows: TNM, P = .16 (not significant) and P = .12 (not significant); Astler-Coller, P < .01 and P = .006; GITSG, P = .067 (not significant) and P = .03; venous invasion, P = .016 and P = .007, respectively. CONCLUSIONS: Numerical substaging of node-positive colorectal cancer (TNM and GITSG methods) is an inferior predictor of prognosis, compared with substaging by the T value (Astler-Coller) or venous invasion methods. We think that the latter method is the method of choice, because it separates patients who have only lymphatic metastasis from patients who display microscopic hematogenous spread as well. This separation obviously has biological/oncological significance, and it may have practical therapeutic implications in the future.

Adenocarcinoma↗

Disseminated peritoneal adenomucinosis: a critical review.

BACKGROUND: The term pseudomyxoma peritonei has been used in reference to any condition, benign or malignant, in which the peritoneal cavity becomes filled with a gelatinous substance. The term is nonspecific and does not denote therapeutic or prognostic significance. Controversy centers around which patients benefit from and should be treated by aggressive surgical debulking. METHODS: A review of the current literature pertaining to the classification, treatment, and prognosis of patients with pseudomyxoma peritonei was undertaken. RESULTS: Disseminated peritoneal adenomucinosis refers to a subset of patients with pseudomyxoma peritonei who derive the greatest long-term benefit from multimodality therapy including aggressive surgical debulking. These patients have a benign form of the disease in which the peritoneal implants are derived from the extrusion of epithelial cells from an adenoma of the appendix. The pathophysiology of mucin deposition is defined by the redistribution phenomenon. The adenomatous cells are distributed according to the fluid flow and gravitational forces within the peritoneal cavity. The small bowel is relatively spared until late in the disease (visceral sparing), and therefore aggressive surgical debulking should be attempted at the first laparotomy by an experienced surgeon. Preoperative computed tomographic imaging can establish the diagnosis and aid in defining which groups of patients are resectable for cure. CONCLUSIONS: Attempts at curative treatment should include aggressive debulking and intraperitoneal chemotherapy. Those patients with a high-grade malignant process should be treated symptomatically, because aggressive therapy is associated with high morbidity rates and no long-term improvement in survival.

Humans↗

Delayed cervical esophagogastric anastomosis.

Although uncommon, ischemia of the gastric fundus can lead to catastrophic anastomotic complications after transhiatal esophagectomy. "Delaying" the anastomosis may prevent complications in occasional patients with particularly compromised gastric fundal perfusion.

Anastomosis, Surgical↗

Genome-wide allelotyping indicates increased loss of heterozygosity on 9p and 14q in early age of onset colorectal cancer.

Colorectal cancer remains a significant public health challenge, despite our increased understanding of the genetic mechanisms involved in the initiation and progression of this disorder. It has become clear that multiple mechanisms lead to the tumorigenic phenotype, with familial predisposition syndromes accounting for less than 15% of all colorectal cancers. A genome-wide scan for loss of heterozygosity (LOH) was carried out with 150 highly polymorphic markers in an effort to identify additional loci involved in colorectal tumorigenesis in DNA samples from 42 colorectal cancer patients. The results confirm earlier observations that tumor DNAs from patients with hereditary nonpolyposis colon cancer (HNPCC) either maintain heterozygosity or exhibit altered or additional alleles. DNAs from patients with early onset colorectal carcinomas (diagnosed prior to age 50) revealed a higher overall degree of LOH than DNAs from patients with sporadic colorectal cancers diagnosed later in life (after age 50). While regions on 1p, 10q and 14q are suggestive, statistical analysis of LOH at these regions failed to reach significance. However, LOH at 9p did reveal a statistically significant increase in the early onset patient group, compared to the greater than age 50 group. LOH on 9p may involve inactivation of p16/CDKN2 through aberrant DNA methylation on the remaining chromosome, resulting in a situation analogous to a homozygous deletion of p16 and providing a selective growth advantage to these cells. This marker may prove to be a useful prognostic indicator for patient stratification in the design of therapy for early onset colorectal cancer patients.

Age of Onset↗

Recommended colorectal cancer surveillance guidelines by the American Society of Clinical Oncology.

OBJECTIVE: To determine the most effective, evidence-based, postoperative surveillance strategy for the detection of recurrent colon and rectal cancer. Tests are to be recommended only if they have an impact on the outcomes listed below. POTENTIAL INTERVENTION: All tests described in the literature for postoperative monitoring were considered. In addition, the data were critically evaluated to determine the optimal frequency of monitoring. OUTCOMES: Outcomes of interest included overall and disease-free survival, quality of life, toxicity reduction, and cost-effectiveness. The American Society of Clinical Oncology (ASCO) Colorectal Cancer Surveillance Expert Panel was guided by the principle of cost minimization, ie, when two strategies were believed to be equally effective, the least expensive test was recommended. EVIDENCE: A complete MEDLINE search was performed of the past 20 years of the medical literature. Keywords included colorectal cancer, follow-up, and carcinoembryonic antigen, as well as the names of the specific tests. The search was broadened by articles from the tumor marker ASCO panel literature search, as well as from bibliographies of selected articles. VALUES: Levels of evidence and guideline grades were rated by a standard process. More weight was given to studies that tested a hypothesis directly relating testing to one of the primary outcomes in a randomized design. BENEFITS/HARMS/COSTS: The possible consequences of false-positive and false-negative tests were considered in evaluating a preference for one of two tests that provide similar information. Cost alone was not a determining factor. RECOMMENDATIONS: The expert panel's recommended postoperative monitoring schema is discussed in this article. VALIDATION: Five outside reviewers, the ASCO Health Services Research Committee, and the ASCO Board of Directors examined this document. SPONSOR: American Society of Clinical Oncology.

Colorectal Neoplasms↗

Prognostic factors affecting survival in patients with colorectal carcinomatosis.

This study evaluates prognostic factors that may influence survival in patients who present with carcinomatosis from colorectal cancer. Patients may present with carcinomatosis as the pattern of metastases at the initial diagnosis of colorectal cancer. Little is known about the natural history of carcinomatosis and the prognostic factors affecting outcome. All patients treated at Roswell Park Cancer Institute from 1988 to 1994 who presented with carcinomatosis at the initial diagnosis of colorectal cancer were identified. A retrospective review of the medical records for patient and tumor demographics was performed. Estimated survival distributions were calculated by the method of Kaplan and Meier. Tests of significance with respect to survival distribution were based on the log-rank test. Cox proportional hazards model was used for the multivariate analysis. There were 31 males and 38 females. The median age was 61 years (range, 26-80). The primary cancers were in the sigmoid with 24 patients (35%), cecum with 14 patients (20%), and transverse colon with 11 patients (16%). The remainder were distributed throughout the colon and rectum. The most common presentation was large bowel obstruction in 29 patients (42%). T3 and T4 cancers were present in 39 (57%) and 13 patients (19%), respectively. Lymph nodes were positive in 39 patients (57%), and mucin-producing tumors were also present in 39 patients (57%). Twelve patients (17%) had one site of disease, 17 patients (25%) had two sites of disease, and 37 (54%) patients had three or more sites of disease. Ascites was present in 29 patients (42%). Residual disease was present at the completion of surgery in 45 patients, absent in 13 patients, and status unknown in 11. The presence of residual disease (p = 0.0001), presence of ascites (p = 0.02), stage greater than T3 (p = 0.02), and increasing number of carcinomatosis sites (p = 0.006) were found to have a negative impact on survival on univariate analysis. On multivariate analysis, only the presence of residual disease at the completion of surgery was found to be an independent predictor of survival (p = 0.04). Overall median survival was 14 months with a 26% estimated 2-year survival. The presence of gross residual disease at the completion of surgery was shown to be the only independent factor negatively affecting survival. This has potential implications for the operative management of patients presenting with colorectal carcinomatosis.

Adenocarcinoma↗

Utility of routine postoperative laboratory studies in patients undergoing potentially curative resection for adenocarcinoma of the colon and rectum.

In an effort to lower healthcare costs, this study was undertaken to evaluate the utility of routine postoperative (PO) laboratory studies and determine whether abnormalities alter patient (PT) care. This was a retrospective review of 105 PTs undergoing elective curative resection for colorectal cancer. A serum electrolyte and liver panel and a hematologic panel were drawn in all PTs. OF 8749 total laboratory values obtained, 5894 (67%) were normal. Two of these (0.03%) elicited a therapeutic intervention. Of the 2004 values that were low (23%), 103 (5.1%) elicited a therapeutic response. Of the 851 that were high (10%), 21 (2.5%) elicited a therapeutic response. Of 2089 preoperative laboratory values, 252 (12%) were abnormal, but in only 15 incidences in 9 PTs was any action taken. Three PTs required potassium supplementation and 6 PTs were transfused packed red blood cells before surgery. In the PO period 2603 laboratory values of 6660 obtained (39%) were abnormal. Of these, 735 (28%) were high and 1868 (72%) were low. Twenty of 735 (27%) high values triggered a therapeutic response that most commonly required administration of insulin for elevated serum glucose in 17 of 197 occasions in five diabetic PTs. On three occasions potassium was removed from intravenous fluids. Five of 275 (1.8%) low calcium values were treated in five patients. Potassium was replaced in 17 of 32 occasions in 14 patients where it was low. In this group of PTs, PO serum potassium, hemoglobin levels, and serum glucose in diabetics were the only values important in making therapeutic decisions. If laboratory studies can be streamlined into only those necessary, substantial savings in health care will be seen without sacrificing quality medical care.

Acute Kidney Injury↗

The effect of keratinocyte growth factor-2 on esophagogastric anastomotic wound healing in rats.

BACKGROUND AND OBJECTIVES: Esophagogastric anastomotic leaks complicate 5-20% of esophagectomies for esophageal cancer, and they are responsible for approximately one-third of perioperative deaths. Growth factors enhance healing in several wound healing models. Keratinocyte growth factor-2 (KGF-2) is a newly identified growth factor that accelerates skin incisional healing. An animal experiment was done to test the hypothesis that KGF-2 would enhance esophagogastric anastomotic wound healing. METHODS: Forty rats had single layer esophagogastric anastomoses constructed using interrupted 7-0 polypropylene sutures. In the experimental group (20 rats) 1 mg of KGF-2 was administered by intraperitoneal injection on the day of surgery, and for three consecutive days thereafter. Placebo (buffer solution only) was given to the control rats (20 rats). Rats were sacrificed on the fourth postoperative day and their anastomoses were excised, mounted in a tensiometer, and distracted at 10 mm/min to measure breaking strength. After that, anastomotic tissue was subjected to hydroxyproline analysis (an indicator of wound collagen). Skin and fascial wounds were also tested in a tensiometer. RESULTS: There were two anastomotic leaks in the KGF-2 treated rats and none in the control rats (p = 0.26, not significant). Esophagogastric anastomotic breaking strength was 1.00 +/- 0.61 N in the KGF-2 treated rats and 1.58 +/- 0.62 N in the control rats (p = 0.017). Esophagogastric anastomotic tissue hydroxyproline concentration was 95.9 +/- 19.9 nmol/mg in the KGF-2 treated rats and 114.1 +/- 38.0 nmol/mg in the control rats (p = 0.10, not significant). Skin and fascia breaking strengths were also lower in the KGF-2 rats, but the difference was not significantly different (KGF-2 skin -0.97 +/- 0.48 N, Control skin -1.46 +/- 0.89 N, p = 0.064; KGF-2 fascia -3.60 +/- 2.06 N, Control fascia -4.67 +/- 1.88 N, p = 0.14). CONCLUSIONS: Keratinocyte growth factor-2 did not enhance esophagogastric anastomotic wound healing in this model. However, the dosage and route of administration of KGF-2 may have been sub-optimal for promotion of anastomotic healing. Further studies with this new growth factor are needed.

Anastomosis, Surgical↗

Intraoperative determinants of unresectability for patients with colorectal hepatic metastases.

BACKGROUND: Intrahepatic and extrahepatic factors are utilized by the surgeon in the decision-making process for the performance of hepatic resection for patients with colorectal metastases. Accurate preoperative and intraoperative staging are mandatory to avoid unnecessary surgery. In this report the intraoperative determinants of hepatic unresectability were evaluated. METHODS: This was a retrospective review of medical records from January 1985 to March 1996 of 62 patients with colorectal hepatic metastases who at the time of exploratory laparotomy were deemed to have unresectable disease based on intrahepatic or extrahepatic factors. The stage of the primary tumor, disease free interval, preoperative carcinoembryonic antigen, computed tomography portography, intraoperative ultrasound, and assessment of intrahepatic and extrahepatic tumor extension were evaluated. RESULTS: Intraoperative determination of the extent of required hepatic resection, including trisegmentectomy (9 patients; 15%) and total hepatectomy (10 patients; 16%), accounted for the majority of unresectable patients. Patients with > 4 metastases (8 patients; 13%) and satellitosis (6 patients; 10%) accounted for 23% of unresectable patients. Four patients had extensive nonmalignant hepatic parenchymal disease precluding resection. Thorough abdominal exploration revealed extrahepatic disease in 13 of 62 patients (21%). Routine periportal/celiac lymph node biopsies revealed metastases in an additional 12 patients (19%), 7 of whom (11%) had only periportal/celiac lymph node metastases. CONCLUSIONS: A meticulous abdominal exploration prior to hepatic resection for patients with colorectal metastases is essential to identify those patients with extrahepatic disease. Periportal and celiac lymph nodes commonly are involved by tumor. Therefore, routine periportal/celiac lymph node biopsies should be performed in the absence of other extrahepatic disease.

Aged↗

Long-term survival in patients with ovarian metastases from colorectal carcinoma.

BACKGROUND: Ovarian metastases (OM) are a relatively uncommon consequence of primary colorectal carcinoma (CRC). The authors present a retrospective review of the impact of elective and therapeutic oophorectomy on the natural history of CRC. METHODS: Patients with primary CRC from January 1964 through March 1996 were reviewed. Survival from the time of OM diagnosis was estimated by the Kaplan-Meier method; differences between groups were based on the log-rank test. RESULTS: A total of 155 patients were studied. Synchronous OM occurred in 90 patients (58.1%); metachronous OM occurred in 65 patients (41.9%). Estimated 5-year survival for patients with synchronous OM was 9%, versus 20% for metachronous OM (P < .0001). Resection of metastatic disease was associated with an improved 5-year survival for synchronous OM (15% vs. 0%, P=.0001) and metachronous OM (24% vs. 0%, P < .0001) if patients were disease-free postoperatively. Other clinical characteristics, including age, menopausal status, stage, and location of primary tumor, had no significant impact on survival. CONCLUSIONS: Ovarian metastases from colorectal carcinoma are associated with a poor outcome. Although there is no survival advantage associated with resection of occult microscopic disease, long-term survival is possible if patients are rendered surgically disease-free.

Adenocarcinoma↗

Clinicopathologic effects of cryotherapy on hepatic vessels and bile ducts in a porcine model.

BACKGROUND: The proximity of a hepatic tumor to major vessels and bile ducts limits the use of cryotherapy because of the potential damage to these structures. However, the effects of cryotherapy on major hepatic vessels and bile ducts are not well understood. METHODS: Nine pigs underwent laparotomy and intraoperative ultrasound to identify hepatic vessels larger than 5.0 mm. Cryotherapy consisting of two freeze-thaw cycles was performed, incorporating the identified vessel. In four pigs the Pringle maneuver was performed to determine the effects of partial vascular occlusion on the hepatic parenchyma and structures undergoing cryotherapy. The animals were sacrificed 30 days postoperatively, and the livers were processed for histologic examination. RESULTS: Eight of the nine livers had vessels larger than 5.0 mm incorporated into the iceball, with all vessels having evidence of infarction but remaining patent. All the livers had major bile ducts incorporated in the iceball, with eight having evidence of infarction. The Pringle maneuver had no real effect on the degree of vessel and bile duct infarction. There was no incidence of hepatic bleeding, liver fracture, bile leak, or hemobilia. CONCLUSIONS: Cryotherapy results in the infarction of major hepatic vessels and bile ducts but can be safely performed in the porcine model. Proximity of tumors to major vascular and biliary structures may not be a contraindication to the use of cryotherapy. Further studies are necessary to determine whether cryotherapy can be used in humans.

Animals↗

Absence of frequent involvement of modifier of Min(APC) in sporadic colorectal cancer.

BACKGROUND: Mutations in the multiple intestinal neoplasia (Min) gene, the mouse homologue of the APC gene, result in the development of intestinal tumors. The degree of tumor expression is suppressed by the modifier of Min (MOM). Alterations in the MOM gene result in markedly increased tumor expression in the mouse. The human homologue of the MOM gene has been mapped to a locus on chromosome 1p35-36, but the role of the MOM gene in the development of human sporadic colorectal cancers has not been defined. METHODS: The microsatellite marker D1S199 has been previously mapped to the region of the MOM gene and was used as a primer for PCR amplification. The PCR products were subjected to denaturing electrophoresis and analyzed for loss of heterozygosity (LOH) and the mismatch repair phenomenon (RER) of each tumor compared to its mucosal control. RESULTS: 48 consecutive sporadic colorectal cancers and normal adjacent mucosa were analyzed. LOH was noted in 2 of 48 tumors and the RER phenomenon was noted in 6 of 48 tumors. Thus, 8 of 48 tumors (16.7%) showed alterations in the region of the locus of the MOM gene. There was no association between alterations in this region and TNM stage, disease-free survival, overall survival, or p53 mutation. CONCLUSIONS: Although mutation of the APC gene is an integral component of sporadic colorectal carcinogenesis, alteration in the region including the MOM gene does not appear to play a significant role in the development or clinicopathologic behavior of human sporadic colorectal tumors.

Alleles↗