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PubMed1987

Prevalence of HPV DNA and viral copy numbers in cervical scrapes from women with normal and abnormal cervices.

Cervical scrapes were obtained from 215 women with cytologically normal cervices and 74 women with cervical intraepithelial neoplasia (CIN) and probed for HPV 6, 11, 16, and 18 by dot-blot hybridization. Viral copy numbers were determined by densitometric scanning of autoradiographs. The prevalence of HPV DNA in women with normal smears was as follows: 23 per cent of women attending a Family Planning Clinic (FPC), 16 per cent of women attending a Sexually Transmitted Diseases (STD) clinic, and 48 per cent of women attending a laser follow-up clinic after treatment of CIN. Ten per cent of women with normal cervices harboured HPV 16. Viral copy numbers ranged from 1300 to 52,800 genome equivalents per cell. Twenty-seven HPV-positive women with normal smears (including four patients infected with HPV 16) were followed for up to 3 years. None developed CIN irrespective of copy number. Our results show that HPV is present in normal cervices in the absence of CIN. Copy number has no relation to the development of CIN and factors other than the amount of HPV DNA may trigger the neoplastic process.

Adolescent↗
PubMed1995

Non-Hodgkin's lymphoma, coeliac disease, and Epstein-Barr virus: a study of 13 cases of enteropathy-associated T- and B-cell lymphoma.

A group of 166 patients with coeliac disease was followed for a period of up to 25 years. During this time, 17 patients developed intestinal tumours that were diagnosed as lymphoma, of which 15 cases were available for review. Eleven of the lymphomas were of T-cell type (enteropathy-associated T-cell lymphoma, EATL) and two were of B-cell type. Two cases were reclassified as undifferentiated carcinoma. The interval between the diagnosis of enteropathy and the onset of lymphoma varied from less than 2 months in four patients to more than 5 years in seven. Seven of the T-cell and both B-cell lymphomas were investigated for the presence of Epstein-Barr virus (EBV) by in situ hybridization (ISH) using probes against Epstein-Barr virus-encoded RNAs (EBERs) and by immunohistochemistry with EBV-specific monoclonal antibodies. All EATL cases were negative, suggesting that EBV is not an important factor in these cases. In one of the B-cell cases, EBV was detectable by ISH and immunohistochemistry in most tumour cells in the mesenteric lymph nodes, but not in any of the tumour cells in the primary ileal tumour, indicating that in this case EBV infection was a late event in the neoplastic process. These results show that lymphoma may develop any time after the onset of coeliac disease and that in our cases of EATL, EBV was not an important factor. In some cases of EBV-related neoplasia, virus infection may be a late event.

Adult↗
PubMed1980

Zinc65 absorption in patients with carcinoma of the prostate.

The intestinal absorption of 65 Zn was determined in patients with carcinoma of the prostate prior to treatment and during estrogen therapy. Following an oral tracer dose of 65 ZnCl2, plasma levels and urinary and fecal excretions of 65 Zn were determined. The absorption of 65 Zn was low in six of eight patients, particularly in three patients who had extensive metastatic bone involvement. During estrogen therapy the absorption of 65 Zn increased markedly in these patients, and this increase correlated with the clinical remission of the neoplastic process. In one patient who did not respond to estrogen therapy, 65 Zn absorption was normal prior to treatment and did not increase during estrogen therapy. In patients free of neoplasia estrogen administration did not increase 65 Zn absorption, and even decreased it. These results indicate that the intestinal absorption of 65 Zn is decreased during the active phase of carcinoma of the prostate and improves during clinical remission induced by estrogen therapy.

Aged↗
PubMedDate not supplied

Molecular biology of colon polyps and colon cancer.

From a histologic and endoscopic standpoint, colon and rectal cancer (CRC) begins as a small neoplastic polyp which progressively enlarges and transforms through a dysplasia stage into invasive cancer. Recently, molecular abnormalities underlying the adenomacarcinoma progression have been defined. The adenomatous polyposis coli (APC) gene and mismatch repair genes are found to be dysfunctional early in the neoplastic process; either as inherited or somatic mutations. Subsequently, polyps progress to cancer along one of two paths depending on which gene is abnormal. When the APC gene is the initial mutation tumor development follows the "loss of heterozygocity" (LOH) pathway. If mismatch repair genes are altered, the "replication error" (RER) pathway is followed. Somatic mutations of the K-ras oncogene and the MCC, DCC, and p53 tumor suppressor genes accumulate in the LOH pathway and mark the progression through polyp stages. Microsatellite instability is a characteristic of the RER pathway but the precise genes involved in this pathway currently are not known. Defining these pathways has led to a new classification scheme for CRC with resultant changes in our clinical approach to screening, surveillance, and treatment.

Adenomatous Polyposis Coli↗
PubMed1995

Expression of retinoblastoma tumor suppressor gene protein, epidermal growth factor receptor, and c-erbB-2 oncoprotein in primary vaginal carcinomas.

Forty-six primary vaginal carcinomas were examined immunohistochemically for expression of retinoblastoma (RB) protein, epidermal growth factor receptor (EGFR), and c-erbB-2 oncoprotein. The results demonstrated that RB protein was not lost in any of the cases, suggesting that structural abnormalities of the RB gene may not play an important role in the pathogenesis of vaginal carcinoma. Fifteen and 11% of the cases showed increased expression of EGFR and c-erbB-2 oncoprotein, respectively, indicating that these oncoproteins may be involved in the neoplastic process of a minority of vaginal carcinomas. Overexpression of EGFR and c-erbB-2 oncoprotein had no prognostic significance in vaginal carcinomas.

Adult↗
PubMed1996

Measures of cell replication in risk/safety assessment of xenobiotic-induced, nongenotoxic carcinogenesis.

The phenomena associated with nongenotoxic carcinogenesis are multifaceted and complex. Nongenotoxic carcinogens stimulate cell replication in the presence or the absence of cytotoxicity. Cell proliferation is pivotal in the neoplastic process, but the extent of its contribution to the development of xenobiotic-induced cancer remains an open question. The search for a better understanding of this process has generated considerable interest and effort, often with the objective of obtaining useful predictors of the tumourigenic potential of xenobiotics. Alterations in the natural balance of endogenous humoural agents that maintain replicative homeostasis results in proliferative stimulation (or inhibition) which may be transient or sustained. The bases for the molecular interaction of these mediators with cellular receptors, trans-cytoplasmic message conveyance, and subsequent nuclear responses leading to xenobiotic-induced mitosis are becoming better understood. Assessment of tissue replicative status has now become established and utilizes biochemical and histological methodology in a routine manner. The increasingly challenging international regulatory environment is demanding greater understanding of the mechanisms that underlie fundamental phenomena and the influences exerted by xenobiotics prior to their registration. While the precise mode of action of an individual xenobiotic may not be known, sound interpretation of toxicological data, including the contribution made by cell replication, creates greater confidence of its safety in the scientific, regulatory, and commercial communities. This article offers a view of cell proliferation from molecular interactions at the cellular level, through practical assessment of cell and tissue replicative status to its utility in contributing to the registration of new drugs and chemicals.

Biological Assay↗
PubMed2005

Can animal models help us select specific compounds for cancer prevention trials?

Animal models provide unparalleled mechanistic insights into cancer development and potential opportunity for cancer prevention. Nevertheless, species differ markedly with regard to dietary exposures, cancer development, drug effects, and toxicity thresholds; therefore, testing in a single animal system may not predict human responses. Although replication of human cancer in animal models remains inexact, more than two decades of research have clearly yielded significant gains, as is evident in agents tested--and in certain cases, approved--for the prevention of epithelial cancers. Research efficiencies achievable through preliminary testing in genetically engineered and carcinogen-induced animal models enable us to probe genetic and signaling pathways that drive normal and neoplastic processes, and thereby figure prominently in decision trees for agent development.

Animals↗
PubMed2004

Somatic mitochondrial DNA mutations in oral cancer of betel quid chewers.

Somatic mitochondrial DNA alteration is a general phenomenon that occurs in cancerous cells. Although numerous mtDNA mutations have been identified in various tumors, the pathogenic significance of these mutations remains unclear. In order to better understand the role of mtDNA mutations in the neoplastic process of oral cancer, the occurrence of mtDNA mutations in oral squamous cell carcinomas was screened by temporal temperature gradient gel electrophoresis (TTGE). The entire mitochondrial genome was amplified with 32 pairs of overlapping primers. The DNA fragments showing different banding patterns between normal and tumor mtDNA were sequenced for the identification of the mutations. Fourteen of 18 (77.8%) tumors had somatic mtDNA mutations with a total of 26 mutations. Among them, 6 were in mRNA coding region. Three were missense mutations (C14F, H186R, T173P) in NADH dehydrogenase subunit 2 (ND2). One frameshift mutation, 9485delC, was in cytochrome c oxidase subunit III. Eight (44%) tumors had insertion or deletion mutations in the np303-309 poly C region of the D-loop. Our results demonstrate that somatic mtDNA mutations occur in oral cancer. The missense and frameshift mutations in the evolutionary conserved regions of the mitochondrial genome may have functional significance in the pathogenesis of oral cancer.

Amino Acid Sequence↗
PubMed1990

Spontaneous tumors in dogs and cats: models for the study of cancer biology and treatment.

Spontaneous tumors in dogs and cats are appropriate and valid model tumor systems available for testing cancer therapeutic agents or studying cancer biology. The pet population is a vastly underutilized resource of animals available for study. Dogs and cats develop spontaneous tumors with histopathologic and biologic behavior similar to tumors that occur in humans. The tumors with potential relevance for human cancer biology include osteosarcoma, mammary carcinoma, oral melanoma, oral squamous cell carcinoma, nasal tumors, lung carcinoma, soft tissue sarcomas, and malignant non-Hodgkin's lymphoma. Canine osteosarcoma is a malignant aggressive bone tumor with a 90% metastasis rate after surgical amputation. Its predictable metastatic rate and pattern and its relative resistance to chemotherapy make this tumor particularly attractive for studying anti-metastasis approaches. Canine and feline malignant mammary tumors are fairly common in middle-aged animals and have a metastatic pattern similar to that in women; that is, primarily to regional lymph nodes and lungs. Chemotherapy has been minimally effective, and these tumors may be better models for testing biological response modifiers. Oral tumors, especially melanomas, are the most common canine malignant tumor in the oral cavity. Metastasis is frequent, and the response to chemotherapy and radiation has been disappointing. This tumor can be treated with anti-metastatic approaches or biological response modifiers. Squamous cell carcinomas, especially in the gum, are excellent models for radiation therapy studies. Nasal carcinomas are commonly treated with radiation therapy. They tend to metastasize slowly, but have a high local recurrence rate. This tumor is suitable for studying radiation therapy approaches. Primary lung tumors and soft tissue sarcomas are excellent models for studying combined modality therapy such as surgery with chemotherapy or biological response modifiers. Finally, non-Hodgkin's lymphoma is a common neoplastic process seen in the dog. These tumors respond to combination chemotherapy and have great potential as a model for newer chemotherapeutic agents and biological response modifiers. This paper will further elaborate on the relative merits of each tumor type as a model for human cancer therapy and biology.

Animals↗
PubMed1993

erbB-3, a third member of the erbB/epidermal growth factor receptor gene family: its expression in head and neck cancer cell lines.

Proto-oncogenes encoding growth factor receptors constitute several distinct families with close overall structural homology. The highest degree of homology can be observed in their catalytic domains, which are essential for intrinsic tyrosine kinase activity. Growth factor receptors in several of these families play critical roles in the regulation of normal cell growth and development. Some of these molecules have been implicated in the neoplastic process as well. A related DNA fragment distinct from epidermal growth factor receptor and erbB-2 genes was detected by reduced stringency hybridization of v-erbB to normal genomic human DNA. The expression of erbB-3 was studied by southern and northern blot technique in a subset of nine head and neck tumor cell lines, as well as in three immortalized cultures established from normal human salivary glands. No gene amplification of erb-B-3 was noted in any of the head and neck cell lines. The 6.2 kb transcript of erbB-3 was elevated significantly in an epidermoid carcinoma of the larynx (A388) and an esophageal carcinoma (HA 114).

Blotting, Northern↗
PubMed1996

Immunohistochemically demonstrated variation in expression of cathepsin E between uracil-induced papillomatosis and N-butyl-N-(4-hydroxybutyl)nitrosamine-induced preneoplastic and neoplastic changes in rat urinary bladder.

Expression of rat urinary bladder cathepsin E in benign papillomatosis induced by uracil and various stages of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN)-induced carcinogenesis was investigated immunohistochemically. Seven-week-old, male F344/DuCrj rats were used. In the normal urothelium of control rats, cathepsin E stained in all layers of cells, although in umbrella cells and some basal cells the reaction was relatively weak. In rats given a diet containing 3% uracil for 5 weeks immunoreactivity of cathepsin E in uracil-induced papillomatosis was consistently homogeneous in all layers, but weaker than in normal urothelium. In rats given 0.05% BBN in drinking water for 12 weeks and subsequently maintained without treatment for 48 weeks cells with little cathepsin E, never observed in normal urothelium, appeared at 5 weeks above the basement membrane in the earliest stage of BBN-induced urinary bladder cancer (simple hyperplasia). Throughout the neoplastic process, groups of cells with a little cathepsin E were randomly distributed, with expression in the urothelium being markedly unstable. Almost all areas of squamous cell proliferation in TCC were negative for cathepsin E. Instability of cathepsin E expression in rat urothelium therefore appears characteristic for carcinogenesis and offers the possibility of using this feature as an early biomarker for urinary bladder carcinogenesis.

Animals↗
PubMed1992

Chromosome 1 in human colorectal tumors. Cytogenetic research on structural changes and their significance.

The significance of short and long arm anomalies of chromosome 1 was investigated in 55 colorectal tumors comprising 41 carcinomas and 14 adenomas. The tumors were at various stages of transformation from adenoma to carcinoma. Our investigation was prompted by the observation of a p32-pter deletion on the short arm of chromosome 1 in a case of benign tubulovillous adenoma with mild dysplasia, as well as by frequent reports that chromosome 1 is involved in many neoplastic processes. Long arm anomalies were found in seven of the 41 carcinomas, six of which were in stage B2, and short arm anomalies in ten carcinomas at various stages. Three of the adenomas exhibited chromosome 1 anomalies, which in one case comprised a 1p32-pter deletion only. Overall, short arm anomalies especially concerned the p32-36 region. These results suggest that the cytogenetic anomalies respectively located on the short and long arms of chromosome 1 should be considered separately. Damage to the long arm might constitute a late non-specific event, whereas damage to the p32-pter region of the short arm might be involved in triggering colorectal tumor development.

Adenocarcinoma↗
PubMed1977

Persistently abnormal brain scintigraphy after cerebral infarction.

The current literature indicates nuclear brain images typically return to normal within two to three months following an episode of cerebral infarction. In this report, two patients are described who demonstrated no significant change in their brain scan abnormalities 11 and 17 months following their strokes. Computed tomography confirmed the clinical impression that the persistent brain scan abnormalities were due to cerebral infarction rather than to neoplastic process.

Aged↗
PubMed1984

Primary cystic arthrosis of the hip.

Subchondral cysts can mimic the radiographic features of intra-osseous ganglia or a variety of neoplastic processes. This case demonstrates the development of a massive subarticular cyst in the supra-acetabular bone. The unique pathogenesis of subchondral cysts is illustrated by the evolution of radiographic features that may be useful in planning treatment.

Bone Cysts↗
PubMed1981

HISTOSCAN: computer program for cytophotometry in tissue sections and its application in the evaluation of nuclear atypia.

The grading of nuclear atypia has a great and well recognized value when predicting the malignancy of neoplastic processes. Although the basic criteria for the grading are generally agreed upon, in the individual case, the final judgement is to some extent still a matter of subjectivity, which naturally impairs reproducibility. The present paper describes a method for quantification of variability of nuclear size and Feulgen-stainability. By plotting the mean optical density against the area value in a scatter-diagram, a cluster is obtained, the size of which reflects the degree of nuclear atypia. The measurements are performed in tissue sections using stage scanning cytophotometry. A computer program--HISTOSCAN--has been developed which enables measurements in highly cellular tissues. The system is also insensitive to the influence of light scattering, a factor of importance when measuring in tissue sections. The performance of the program is tested in both imprints and tissue sections.

Animals↗
PubMed1995

Ruptured spinal dermoid cyst with chemical arachnoiditis and disseminated intracranial lipid droplets.

A 33-year-old man presented with a 3-month history of gradually progressive leg weakness. Spinal MRI and myelography with CT demonstrated an extensive intradural abnormality suggesting a diffuse inflammatory or neoplastic process. Only after cranial CT and MRI demonstrated lipid droplets was the diagnosis of a ruptured spinal dermoid cyst suggested. Subsequent laminectomy revealed a ruptured intradural dermoid cyst in the lumbar spine, with chemical arachnoiditis.

Adult↗
PubMed1985

Immunohistological evidences of cortical and medullary differentiation in thymoma.

The phenotypical characteristics of human epithelial and lymphoid cells have been studied with immunohistochemical methods on frozen sections of 12 thymomas. On the basis of the cytohistological characteristics of thymoma epithelial cells (EC) the thymomas were divided in cortical, medullary and mixed types, according to recently developed light microscopical criteria. When tested with a series of monoclonal antibodies, thymoma EC were all stained by the antibody Ki-M3 (as in the thymus), but reacted with anti-HLA-DR, anti-HLA-A,B,C and with a new monoclonal antibody to cortical EC, 21A6, to a lesser extent and with weaker, variable intensity in comparison with the normal thymus. Cortical type thymomas were most reactive and the medullary type almost negative. Thymomas, like normal thymus showed different immunoreactivity patterns with antibodies to prekeratins of different specificities. Cortical type thymomas and areas in mixed thymoma showed an EC staining with the antibody to non-squamous type keratin (35 beta H11) whereas medullary type thymomas and areas showed staining with antibodies to squamous-type keratin (34 beta E12-IV/82) in addition. Lymphoid cells with cortical (OKT6+, Leu 1 weakly+, Leu 2a+, Leu 3a+) or mature medullary (OKT6-, Leu 1 strongly+, Leu 2a or Leu 3a+) phenotype were found to colonize tumours with different EC types. These immunohistochemical findings largely confirm our earlier cytological distinction of thymoma EC. In addition important differences have been observed in neoplastic cortical EC concerning the HLA-DR and 21A6 immunoreactivity that may be intimately related to the neoplastic process and paraneoplastic immune phenomena.

Antibodies, Monoclonal↗