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C M Fenoglio-Preiser

Publications and source records attributed to C M Fenoglio-Preiser.

At least 37 records · Page 2Linked to original sources
PubMed1996

The pattern of cell proliferation in neoplastic and nonneoplastic lesions of ulcerative colitis.

BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory disease of the colon characterized by repeated episodes of inflammation and epithelial regeneration. Patients with long-standing UC have an increased risk for the development of dysplasia and subsequent colon carcinoma. Because dysplasia likely results from deregulatec cell proliferation, the authors examined Ki-67 immunoreactivity in tissues from UC patients to examine patterns of proliferation in neoplastic and nonneoplastic lesions. METHODS: One hundred and eighty-seven specimens were obtained from 41 patients with UC and each lesion evaluated according to the International Classification for Dysplasia in Inflammatory Bowel Disease. All sections were stained with a monoclonal antibody directed against the proliferation marker Ki-67, and evaluated by three observers. RESULTS: Statistically significant differences in the pattern of Ki-67 immunoreactivity were observed between nonneoplastic and neoplastic lesions. In regenerative mucosa, Ki-67 immunoreactivity localized to the bases of the crypts, and the proliferative zone appeared expanded. In dysplasia, Ki-67 staining was prominent in cells in the superficial mucosa, as well as in cells at the crypt bases. In some dysplasias and all invasive carcinomas, Ki-67 staining was diffusely distributed throughout the crypts, suggesting complete deregulation of normal cell proliferation. CONCLUSIONS: Cell proliferation is markedly increased in patients with UC, and appears abnormally regulated in neoplastic lesions. Furthermore, Ki-67 staining helps delineate areas of dysplasia in cases in which the distinction from regenerative mucosa is unclear. The increased cell proliferation that occurs in patients with UC may predispose the mucosa to mutational events, thereby increasing cancer risk in these patients.

Adult↗
PubMed1996

Detection of human papillomavirus in esophageal squamous cell carcinoma.

BACKGROUND: Human papillomavirus (HPV) DNA has been identified in esophageal carcinomas. However, the incidence of HPV varies significantly in different geographic locations. In the current study, neoplasms from two separate geographic regions were analyzed for the presence of HPV DNA: METHODS: One hundred and ten esophageal squamous cell carcinomas, 83 from Beijing, China and 27 from Cincinnati, Ohio, were examined for the presence of HPV DNA: In situ hybridization and polymerase chain reaction (PCR) using both consensus primers for the HPV L1 gene and type specific primers for the E6 gene of HPV types 6, 16, and 18 were performed. RESULTS: In situ hybridization failed to demonstrate any HPV type (6, 11, 16, 18, 31, 33, or 35) in any tumor specimen. Likewise, PCR using consensus primers for the HPV L1 gene was negative in all samples. Three of the Chinese specimens (4.29%) were positive for HPV using E6 type specific primers. One tumor contained HPV type 6 DNA, whereas the other 2 contained HPV type 16 DNA. One Cincinnati tumor (4.35%) was positive for HPV 16 by type specific primer. None of the specimens contained HPV 18 DNA. CONCLUSIONS: The incidence of HPV DNA in esophageal carcinoma specimens from Beijing, China and Cincinnati, Ohio is similar. The incidence of HPV in tumors from Beijing is significantly lower than that reported for those from other regions of China where the incidence of esophageal cancer is higher. Thus, although HPV may play a role in esophageal carcinogenesis, this role may be more pronounced in those regions of the world with a high incidence of the disease, and may be less important in areas with moderate or low risks for esophageal cancer.

Adult↗
PubMed1996

Hematologic malignancies developing in Syrian golden hamsters during induction of pancreatic carcinoma.

We report 30 hematologic malignancies arising in 25 of 236 Syrian golden hamsters (SGH) that received combinations of N-nitrobis(2-oxopropyl)amine (BOP) and Streptozotocin (STZ). Lesions developed with morphological similarity to human small lymphocytic (n = 7), diffuse mixed (n = 2), diffuse large cell lymphoma (n = 13), follicular lymphoma (n = 2), anaplastic large cell lymphoma (n = 3), hairy cell leukemia (n = 2), malignant histiocytosis (n = 1) and discordant lymphomas (n = 5). The types and distribution of these lesions are different from epizootic lymphomas in SGH. We also report a higher percentage (12 versus 4.6%) and the earlier appearance (< or = 40 versus 80-112 weeks) compared with aging-associated spontaneous SGH lymphoma. The features of these hematologic malignancies have not been previously reported in epizootic or aging-associated spontaneous lymphomas and therefore suggest a new class of hematologic lesions in SGH. Benign and atypical hyperplasia correlated with STZ administration (r = 0.97, P = 0.03). The malignant lesions correlated with areas of lymphoid hyperplasia (r = 0.78, P= 0.004). Only one of the 21 untreated SGH spontaneously developed a low grade lymphoma. The unusual types, distribution and occurrence of these lesions may suggest a role for these carcinogens in their induction.

Aging↗
PubMed1996

Plasma membrane phosphotyrosine, Her2-NEU, and epidermal growth factor receptor in human breast cancer. A comparative study.

Experimental therapeutic regimens for breast cancer include strategies to block the activity of specific oncogenes. Because oncogenesis is a multistep process, specific oncogenes may drive tumor production at one stage yet not function in another. Since the effectiveness of therapy targeted against oncogenes depends on their function in the tumor, correlation of oncogene function to specific stages of tumor development has therapeutic implications. Among the oncogenes known to be important in breast cancer production are two cell surface growth factor receptors, epidermal growth factor receptor (EGFR) and Her2-NEU (NEU). These proteins are receptor tyrosine kinases that autophosphorylate specific tyrosine residues on activation. The oncogenic potential of these receptors depends on this autophosphorylation. We examined 86 primary formalin-fixed, paraffin-embedded breast tumors for overexpression of EGFR and NEU and correlated our findings with the presence of cell surface phosphotyrosine as an indicator of tyrosine kinase activity at the plasma membrane. Our data indicate that only 34% of tumors that overexpress EGFR or NEU show plasma membrane phosphotyrosine, indicating that in the majority of these tumors, the overexpressed oncogene may not be active at this stage.

Breast Neoplasms↗
PubMed1996

Pathologic and phenotypic features of gastric cancer.

This article covers the basic pathologic features of gastric cancer. Gastric cancer is not a single entity but consists of several major tumor types. The risk factors for their development and their pathological features are discussed. The two major forms of gastric cancer, intestinal and diffuse, are described, as are the settings in which they arise. A number of prognostic factors exist for gastric cancer, including traditional pathologic variables such as histological staging grade and tumor type. Some more recent potential markers involve determinants of biologic behavior. The more frequently encountered types are covered, as well as their clinical implications. Finally, a scheme for standardized handling of gastric resection specimens is presented.

Biomarkers, Tumor↗
PubMed1996

Immunohistochemical analysis of Bcl-2 family proteins in adenocarcinomas of the stomach.

The apoptosis-regulating proteins Bcl-2, Bax, Bcl-X, Bak, and Mcl-1 were examined by immunohistochemical methods in 48 archival specimens of adenocarcinoma of the stomach, and the results were correlated with tumor histology (intestinal versus diffuse pattern) and clinical stage (early- versus late-stage disease, ie, stages I and II versus stage III). Tumor cells containing immunostaining for the anti-apoptotic proteins Bcl-2, Bcl-X, and Mcl-1 were present in 26 (54%), 41 (85%), and 36 (75%) of the 48 cases evaluated, respectively, whereas immunopositivity for the pro-apoptotic proteins Bax and Bak was found in 44 (92%) and 42 (88%) specimens Comparisons of these immunostaining results with tumor histology revealed statistically significant differences for Bax (P = 0.03), Bcl-X (P = 0.003), and Mcl-1 (P = 0.005), which were all more frequently immunopositive for tumors with an intestinal than a diffuse histological pattern (chi 2 analysis). In addition, the percentage of immunopositive tumor cells was significantly higher for Bcl-X (62 +/- 6% versus 45 +/- 6%, mean +/- SE, P = 0.01) and for Mcl-1 (48 +/- 6% versus 30 +/- 6%; P = 0.04) in tumors with intestinal versus diffuse histology (unpaired t-test). In contrast, the percentage of Bcl-2-immunopositive tumor cells was higher in tumors with diffuse histology compared with intestinal (32 +/- 5% versus 12 +/- 5%; P = 0.01), whereas the percentages of Bax- and Bak-immunopositive tumor cells were not significantly different between these two histological types. In 34 specimens, residual normal gastric epithelial cells (foveolar cells) were present for direct comparisons of immunointensity with tumor cells. The immunointensity for the Bcl-2, Bcl-X, and Mcl-1 proteins was stronger in tumor cells compared with normal foveolar cells in 7 (21%), 15 (44%), and 8 (2.1%) of 34 cases, respectively, whereas the immunointensity of the proapoptotic proteins Bax and Bak was reduced compared with normal cells in 8 (24%) and 24 (71%) cases. Immunointensity, however, did not correlate with histology. clinical stage was not significantly associated with the presence or absence of immunopositive tumor cells, the percentage of immunopositive cells, or immunointensity. Taken together, these results establish for the first time that several Bcl-2 family proteins are expressed in gastric adenocarcinomas and suggest that the repertoire of these proteins may differ depending on the histological type. The findings therefore support the notion that the intestinal and diffuse types of gastric cancer arise at least in part through different mechanisms.

Adenocarcinoma↗
PubMed1995

Determinants of black/white differences in colon cancer survival.

BACKGROUND: Blacks have lower survival rates for colon cancer than whites, possibly related to more advanced stages of disease at diagnosis and to socioeconomic differences between blacks and whites. While the black/white difference in colon cancer survival is well documented, the few studies that have investigated this difference have been limited by the modest number and type of explanatory factors that were considered. PURPOSE: We analyzed data from the National Cancer Institute Black/White Cancer Survival Study to determine 1) what characteristics might contribute to the racial difference in colon cancer survival and 2) if a survival disparity remained between black and white patients after adjustment was made for these characteristics. METHODS: This prospective study included 454 blacks and a stratified random sample of 521 whites, aged 20-79 years, with cancer of the colon diagnosed from January 1, 1985, through December 31, 1986, and who were residents of the metropolitan areas of Atlanta, New Orleans, and San Francisco/Oakland. Follow-up was truncated on December 31, 1990. Cox proportional hazards regression was used to estimate the death rate among blacks relative to that among whites after adjustment for potential explanatory factors, including sociodemographic factors, concurrent (comorbid) medical conditions, stage at diagnosis, tumor characteristics, and treatment. All P values were calculated from two-tailed tests of statistical significance. RESULTS: After adjustment for age, sex, and geographic area, the black-to-white mortality hazard ratio (HR) was 1.5 (95% confidence interval [CI] = 1.2-1.9), indicating that the risk of death among black patients was 50% higher than that among white patients. Further adjustment for stage reduced the excess cancer mortality to 20% (HR = 1.2; 95% CI = 1.0-1.5), decreasing the overall racial difference in excess mortality from 50% to 20% or to a 60% reduction in excess mortality. Although adjustment for poverty reduced the excess mortality by 20%, adjusting for both stage and poverty did not further reduce the racial difference. Among patients with stages II and III disease, blacks had lower survival rates than whites (HR = 1.8; 95% CI = 1.0-3.1 and HR - 1.5; 95% CI = 1.0-2.3, respectively). Among those patients with metastatic disease (stage IV), survival was similar for whites and blacks. CONCLUSIONS: Stage at diagnosis accounted for more than half of the excess colon cancer mortality observed among blacks. Poverty and other socioeconomic conditions, general health status, tumor characteristics, and general patterns of treatment did not further explain the remaining survival disadvantage among blacks. IMPLICATIONS: Because the racial disparity was confined to earlier stages, future studies should investigate whether blacks have more advanced disease at diagnosis and whether less aggressive treatment is provided because of understanding.

Adult↗
PubMed1995

The relationship of human papillomavirus to proliferation and ploidy in carcinoma of the anus.

BACKGROUND: Human papillomavirus (HPV) infections have been implicated in anogenital neoplasia in both sexes. In this study, the authors postulated that HPV infections induce squamous epithelium to become hyperproliferative and aneuploid. METHODS: To test this hypothesis, formalin fixed, paraffin embedded tissues were analyzed for the presence of HPV by in situ hybridization. S-phase fraction and DNA content were evaluated by flow cytometry. Proliferative indices also were analyzed using an antibody to proliferating cell nuclear antigen (PCNA). RESULTS: Human papillomavirus DNA was present in 48.1% of the carcinomas. All but one HPV-positive tumor contained HPV 16/18 DNA. The remaining tumor contained only HPV 6/11. No correlation was found between HPV status, patient age, or tumor differentiation. Thirty-three percent of tumors were aneuploid. Only two patients had aneuploid tumors that were HPV-negative; these patients received preoperative radiotherapy. The average S-phase fraction was significantly higher (P < 0.01) in HPV-positive versus HPV-negative lesions. The PCNA index for HPV positive tumors was also significantly higher than that observed in negative tumors (p < 0.003). CONCLUSION: The presence of HPV in tumor cells is significantly associated with an increased proliferative rate and aneuploid status of tumors compared with HPV-negative tumors. These findings are consistent with the fact that viral proteins binding to tumor suppressor gene proteins can deregulate the cell cycle and lead to genomic instability.

Aneuploidy↗
PubMed1995

Anatomic site distribution of colon cancer by race and other colon cancer risk factors.

PURPOSE: Black patients with colon cancer are more likely to have poorer survival from colon cancer than are white patients. To determine whether anatomic site differences might contribute to survival differences, we compared anatomic site distributions of black and white patients. METHODS: As part of the Black/White Cancer Survival Study, we collected medical record data for 1,045 patients from Atlanta, New Orleans, and San Francisco/Oakland, newly diagnosed in 1985 or 1986 and interviewed 745 of them. RESULTS: In polychotomous logistic regression analysis, site was related to stage, grade, and histologic type and among women with age, parity, and possibly smoking. However, it was not related to race, except perhaps among men age 65 and older, among whom blacks were somewhat likely to have more transverse and distal, not proximal, cancer. These relations were consistent across subgroups and were independent of other factors examined. CONCLUSION: Results suggest that site differences are unlikely to contribute to poorer survival commonly observed among black colon cancer patients in the United States.

Adult↗
PubMed1995

Esophageal heterotopic pancreas presenting as an inflammatory mass.

A 47-year-old female presented with complaints of epigastric pain, poor appetite, and dysphagia. Abdominal CT and esophagogastroduodenoscopy revealed a 9-cm mass extrinsic to the distal esophagus. Esophagogastrectomy was performed. The distal esophagus contained multiple foci of heterotopic pancreatic tissue. There was associated inflammation and fat necrosis in the surrounding periesophageal soft tissue. Heterotopic pancreas is uncommon in the esophagus, with only a few reports appearing in the English literature. The clinical features of heterotopic pancreas, and the pathophysiology of the associated inflammatory lesion is discussed.

Choristoma↗
PubMed1995

Malignant mixed müllerian tumor of the extraovarian secondary müllerian system. Report of two cases and review of the English literature.

OBJECTIVE: To report two cases of malignant mixed müllerian tumor of the extraovarian secondary müllerian system and to identify cases reported in the English literature. DESIGN: Two cases are described and discussed along with cases reported previously in the English literature. SETTING: The University of Cincinnati Medical Center. PATIENTS: (1) A 62-year-old woman with a bilateral ovarian poorly differentiated endometrioid adenocarcinoma with multiple peritoneal metastasis and a malignant mixed müllerian tumor with heterologous elements arising from the pelvic peritoneum. (2) An 83-year-old woman with a malignant mixed müllerian tumor with heterologous elements arising from the cecal peritoneum. RESULTS: Seventeen previously reported cases were identified in the English literature. CONCLUSIONS: The malignant mixed müllerian tumor of the extraovarian secondary müllerian system is a rare disease with only 17 cases reported to date to our knowledge. The prognosis is poor. Of 12 patients with follow-up information available, 10 died within 1 year and 2 within 2 years after diagnosis. The histogenesis of the tumor remains unclear; however, data exist that support transformation of epithelial neoplastic cells into sarcomatous cells (metaplastic theory) and origin from a single totipotential cell. It is possible that both situations may occur.

Adenocarcinoma↗
PubMed1995

Differential sensitivities of E6 type-specific and L1 consensus primers in the detection of human papillomavirus in anal carcinoma.

Anogenital malignancy has been increasing in incidence in recent decades. There is strong evidence in the literature suggesting that human papillomavirus (HPV) plays a role in the genesis of anogenital neoplasia. In addition, identification of oncogenic HPV types in anogenital carcinomas may have prognostic significance. The method used to detect HPV infection, however, affects the frequency with which viral DNA is identified. We examined tissues from 56 patients with anal squamous cell carcinoma for the presence of HPV DNA by in situ hybridization and polymerase chain reaction using both consensus and type-specific primers to determine if HPV detection varies when different methods are used. In situ hybridization identified the presence of HPV DNA in 41.1% of patients. Polymerase chain reaction using type-specific probes for the HPV E6 gene demonstrated HPV DNA in 46% of anal carcinomas, whereas polymerase chain reaction with consensus primers detected HPV DNA in only 16.3% of cases. All cases containing HPV type 6 were identified with L1 primers, whereas only three of 23 cases containing HPV type 16 were identified. The differences in the rate of HPV detection by the two polymerase chain reactions methods are most likely related to L1 gene loss in cells containing integrated HPV type 16.

Adult↗
PubMed1994

The molecular biology of esophageal and gastric cancer and their precursors: oncogenes, tumor suppressor genes, and growth factors.

The evolution of sequential histological changes from normal cells through invasive cancer affords the cancer biologist the opportunity to identify separate molecular steps involved in cancer progression. As one studies the development of human carcinoma, it becomes apparent that multiple genetic alterations affecting both cellular proto-oncogenes and tumor suppressor genes are involved during the development and progression of both esophageal and gastric cancers. The different histological forms of both esophageal and gastric carcinomas as well as their differing etiologies result in the possibility that a spectrum of genetic changes is involved in different tumor types. p53 abnormalities occur frequently in tumors arising in both organs, and in both sites p53 abnormalities can be observed in precancerous lesions as well as in overt cancer. Subsequent abnormalities affecting other genes (eg, epithelial growth factor receptors [EGFRs]) potentially enhance the growth potential of tumors. This review focuses on abnormalities of oncogenes, tumor suppressor genes, and growth factors commonly found in cancers of the esophagus and stomach.

Carcinoma, Squamous Cell↗
PubMed1993

Effect of streptozotocin diabetes on development of nitrosamine-induced pancreatic carcinoma when diabetes induction occurs after nitrosamine exposure.

Diabetes mellitus has been suggested as a possible risk factor for the development of pancreatic cancer in humans. Previous studies in our laboratory have shown, however, that streptozotocin (STZ) diabetes inhibits the development of cancer of the exocrine pancreas in hamsters when STZ is administered prior to treatment with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). It has been reported by others that the concurrent administration of BOP and STZ enhances pancreatic carcinogenesis in hamsters. The purpose of the present study was to determine the effect of STZ diabetes on the development of BOP-induced pancreatic carcinoma when STZ is given following exposure to BOP. Groups of Syrian golden hamsters were treated with either BOP only (single s.c. injection, 40 mg/kg body wt at week 0), BOP (single s.c. injection, 40 mg/kg body wt at week 0) plus STZ (50 mg/kg body wt x3 daily i.p. doses at weeks 10, 20 or 30), STZ only (50 mg/kg body wt x3 daily i.p. doses at weeks 10, 20 or 30), or neither BOP nor STZ. The experiment was terminated at 40 weeks after BOP treatment. No significant difference was seen in the incidence of pancreatic cancer between those animals receiving BOP only at week 0 and those receiving BOP at week 0 plus STZ at weeks 10, 20 or 30 of the study. The results would appear to indicate that STZ diabetes, established after BOP tumor initiation, plays no apparent role in the modulation of pancreatic carcinogenesis.

Animals↗
PubMed1992

The future of prognostic factors in outcome prediction for patients with cancer.

The anatomic description of the extent of tumor spread (tumor staging) assists clinical management, facilitates communication among physicians, is an essential part of randomized controlled trials, and may help in the counseling patients and their families. However, in recent years, additional "prognostic factors" have been defined, many of which assess or reflect the biologic behavior of malignant neoplasms. Other measures of tumor biochemistry address the natural history of neoplastic development and often are included in a discussion of new prognostic factors. This review article summarizes current knowledge and thinking related to tumor prognostic factors in four areas by providing: (1) a definition and principles of anatomic spread of tumor (staging) and some suggestions for improvement, (2) a description of some examples of additional factors of prognostic significance, (3) some statistical methods to evaluate prognostic factors, and (4) an examination of the possible future of summary statements of outcome (i.e., prognostic indexes).

Biomarkers↗
PubMed1992

The relationship of human papillomaviruses to anorectal neoplasia.

This review begins with an overview of the anatomy of the anal canal, which is followed by a discussion of human papillomavirus (HPV) infections in the anogenital tract. The organization of the HPV genome and the function of the encoded proteins is discussed in relation to the oncogenic potential of these viruses. Particularly stressed are interactions with known tumor suppressor genes. Then the interaction of HPV with the host cells and some growth factors is reviewed. An important consideration is the synergy between this virus and other known carcinogenic factors. These include smoking, immunologic status, and other factors. Finally, the pathologic features of anal warts and malignant lesions are summarized with respect to their histologic findings and expression of viral subtypes.

Anus Neoplasms↗