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PubMed1982

Environmental modifiers in carcinogenesis.

The natural history of neoplastic development can be divided into at least three distinct stages - initiation, promotion and progression. These stages can be defined by biological experimentation and by histopathological characterization of the lesions involved in the various stages. It is now possible, both in human beings and in experimental animals, to distinguish by morphological techniques all stages from very early 'precursor' lesions to the final malignant state. Although the final stage - progression - of the neoplastic process can be altered by therapeutic intervention, the principal site at which the natural history of neoplastic development can be actually and potentially regulated is that of promotion. Promoting agents that are relatively selective for carcinogenesis in several different tissue types have now been identified both in experimental systems and in human beings. In at least two experimental systems - those of epidermal carcinogenesis and hepatocarcinogenesis - the general characteristics of both initiation and promotion are virtually identical. Such studies have demonstrated that the activity of promoting agents exhibits a threshold level as well as a maximal level and that the action of promoting agents is reversible; the identification of promoting agents in our environment is therefore of considerable importance in understanding the nature of and preventing the development of human cancer. In addition, the interpretation of whole-animal bioassays for carcinogenic agents in the environment must take into account the existence of promoting agents and recognize that their action is distinct from that of complete and incomplete carcinogens, in order rationally to extrapolate to situations of human risk.

Carcinoma, Hepatocellular↗
PubMed1983

Frequent activation of c-kis as a transforming gene in fibrosarcomas induced by methylcholanthrene.

The DNA's from two of four methylcholanthrene-induced mouse fibrosarcomas contained transforming genes that were identical in their pattern of restriction endonuclease resistance to inactivation of biologic activity. This transforming gene was identified as the activated homolog of the Kirsten murine sarcoma virus onc gene, v-kis. The finding that a defined carcinogen reproducibly leads to activation of kis as a transforming gene should be of value in elucidating the role of oncogenes in the neoplastic process.

Animals↗
PubMed2004

Chemotherapy-induced lung disease.

The lung has significant susceptibility to injury from a variety of chemotherapeutic agents. The clinician must be familiar with classic chemotherapeutic agents with well-described pulmonary toxicities and must also be vigilant about a host of new agents that may exert adverse effects on lung function. The diagnosis of chemotherapy-associated lung disease remains an exclusionary process, particularly with respect to considering usual and atypical infections, as well as recurrence of the underlying neoplastic process in these immune compromised patients. In many instances, chemotherapy-associated lung disease may respond to withdrawal of the offending agent and to the judicious application of corticosteroid therapy.

Antibiotics, Antineoplastic↗
PubMed2001

Myeloperoxidase-positive intravascular large B-cell lymphoma.

Intravascular large B-cell lymphoma (IVLBL) is an uncommon form of non-Hodgkin lymphoma that is also known as malignant angioendotheliosis, intravascular lymphomatosis, and angiotropic large-cell lymphoma. The disease is characterized by a bizarre population of neoplastic cells, which are found systemically within vascular lumina. Although originally thought to be a neoplastic process of the endothelial cells, it has since been demonstrated, by molecular techniques and immunohistochemistry, that the neoplastic cells are of lymphoid origin. The differential diagnosis of these lesions includes granulocytic sarcomas that can be distinguished from IVLBL or other lymphomas by the presence of immunohistochemical positivity for myeloperoxidase. We describe a patient with a history of a myelodysplastic syndrome who subsequently developed IVLBL, which demonstrated immunohistochemical positivity for myeloperoxidase. To our knowledge, this represents the first case of a malignant lymphoma to demonstrate such findings.

Diagnosis, Differential↗
PubMed1979

Inhibition of promutagen activation by the antioxidants butylated hydroxyanisole and butylated hydroxytoluene.

Butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) exhibited antimutagenic activity in the Salmonella typhimurium reversion test. Both BHA and BHT reduced reversion induced by chemicals requiring metabolic activation for effectiveness. However, they did not affect reversion induced by direct-acting mutagens. These results suggested that BHA and BHT may inhibit the metabolic activation processes and demonstrated that the S. typhimurium reversion test may be used to identify inhibitors of the neoplastic process.

Animals↗
PubMed1995

Inflammatory pseudotumour of lymph nodes.

AIM: To describe the clinical, histological and immunohistochemical features in four cases of an uncommon benign lymph node lesion which may mimic a neoplastic process. METHODS: Four cases of inflammatory pseudotumour of lymph nodes were studied using conventional staining (haematoxylin and eosin, PAS, Gordon and Sweets reticulin stain, and the Ziehl-Neelsen stain) and with immunohistochemical techniques using a variety of antibodies (CD3, L26, CD15, CD21, CD30, KP1, MAC 387, vimentin, alpha SMA, HHF-35, D33, CD34, and S100). RESULTS: The lesion comprises a proliferation of spindle cells expanding the connective tissue framework of lymph nodes and is associated with a plasma cell and small lymphocyte infiltrate. There are variable numbers of macrophages, neutrophils and eosinophils, and varying degrees of fibrosis. Vascular changes are common but vary in degree and type. CONCLUSIONS: Inflammatory pseudotumour of lymph nodes is an uncommon benign reaction pattern which may be misdiagnosed as a neoplastic or even a malignant process. Increased awareness of its histological features should help prevent such misdiagnoses.

Adult↗
PubMed1993

Expression pattern of metalloproteinases and their inhibitors changes with the progression of human sporadic colorectal neoplasia.

Several studies have implicated the extracellular matrix-degrading metalloproteinases (MMPs) as essential agents in tumor cell invasion and metastasis. In the present study, we have investigated the patterns of expression of a number of MMPs and their specific tissue inhibitors (TIMP-1 and TIMP-2) in human colonic tissue samples that represent various stages of progression from adenomas showing different degrees of dysplasia to adenocarcinomas. We assessed levels of mRNA by Northern blot analysis and the results were measured semiquantitatively by densitometry. In total, we analyzed nine adenomas of varying size and with varying degrees of dysplasia, three adenomas with adenocarcinoma (malignant polyps), and five adenocarcinomas. Although expression of MMP and TIMP mRNA was highly intercorrelated, transcripts for stromelysin 3 and TIMP-2 (high) showed the strongest relation to the neoplastic process. Detection of stromelysin 3 mRNA accompanied a diagnosis of severe dysplasia or malignancy, whereas levels of TIMP-2 (high) mRNA transcripts permitted finer distinctions on the neoplastic continuum. These data indicate changes within extracellular matrix acquired during the process of malignant transformation of human sporadic colorectal neoplasia.

Adolescent↗
PubMed1991

Nerve growth factor receptor expression on dendritic reticulum cells in follicular lymphoid proliferations.

Using an antibody to the nerve growth factor receptor (NGFR), we examined dendritic reticulum cells (DRCs) immunohistochemically in 62 formalin-fixed, paraffin-embedded lymph nodes from patients with reactive follicular hyperplasia or with various types of lymphoma. A dendritic staining pattern within germinal centers was present in 25 of 26 routinely processed lymph nodes with reactive follicular hyperplasia. In contrast, dendritic staining with anti-NGFR was present within neoplastic follicles in only three of 28 follicular lymphomas. Staining of benign, residual germinal centers with anti-NGFR was present in mantle zone lymphoma and Hodgkin's disease. These findings suggest a possible role for the NGFR in the maturation and/or activation of normal DRCs. The loss of NGFR expression in most follicular lymphomas indicates that DRCs are altered as part of the neoplastic process. The possibility that DRCs may play a role in the pathogenesis of follicular lymphoma is suggested.

Dendritic Cells↗
PubMed1976

Neoplastic disease and tumor immunology from the perspective of host-parasite relationships.

Neoplasia is considered within the biologic framework of host-parasite relationships, and the arguments favoring this perspective are discussed. By viewing neoplastic processes as dynamic interactions between transformed clones, host defense mechanisms, and the environmental circumstances impinging directly on the neoplastic event, the experimentalist and clinician are better prepared conceptually for a balanced assessment of all factors determining the development and outcome of confrontations with neoplastic clones. The frame of reference placing progressive neoplasia into the category of host-parasite associations also prepares the ground for techinical approaches to the study and observation of oncologic phenomena appropriate to their essential nature. The correct evaluation and most promising future development of the current emphasis on immunologic parameters of neoplasia demands especially an awareness of the role of immunologic variables in other host-parasite relationships.

Animals↗
PubMed2005

DeltaNp63 expression in pancreas and pancreatic neoplasia.

DeltaNp63 (DNp63) has become widely used, in particular, for distinguishing invasive carcinomas from noninvasive ducts by highlighting the myoepithelial or basal cells in the breast and prostate, respectively. It is not known whether this marker may have any application in another exocrine organ, the pancreas. As the ductal and intraductal proliferations of this organ become better characterized, the need for markers to distinguish among these processes increases. We investigated immunohistochemical expression of DNP63 in 105 cases. A total of 25 cases were non-neoplastic pancreata, 25 were pancreatic intraepithelial neoplasia (PanIN) of various grades, and 50 were examples of pancreatic ductal adenocarcinoma. Sections of non-neoplastic pancreata included various types of non-neoplastic processes such as squamous/transitional metaplasia (five cases), which can be mistaken for high-grade PanINs, as well as various degrees of reactive ductal atypia and incidental microcysts with attenuated lining (five cases). No DNp63 expression was noted in normal pancreatic ducts. On the other hand, all five foci of squamous/transitional metaplasia were strongly and uniformly positive for this marker. DNp63 labeling was also noted in those incidental microcysts lined by attenuated cells, seen amidst normal pancreatic lobules. All PanINs were negative. Among invasive carcinomas, DNp63 expression was detected only in areas of squamous differentiation and was completely absent in ordinary ductal areas. Based on this observation, five additional cases of adenosquamous/squamous carcinoma was retrieved and stained, and the squamous components of all of these were also positive. In conclusion, (I) DNp63 is a reliable marker of squamous differentiation in the pancreas. It is valuable in distinguishing squamous/transitional metaplasia from PanINs, a distinction of importance for both researchers and diagnosticians. Among invasive carcinomas, it seems to be entirely specific for areas of squamous differentiation. (II) Those incidental microcysts seen in acinar lobules and lined by attenuated cells are also positive for DNp63, which suggests that they may be metaplastic in nature, and that they do not represent neoplastic cells. (III) Unlike the ducts of other exocrine organs, breast and prostate, there are no DNp63-expressing cells in the normal pancreatic ducts, and therefore, this marker cannot be used in distinguishing invasive carcinomas from the non-invasive ducts. (IV) No p63-expressing 'stem' cells are present in the pancreas.

Adenocarcinoma↗
PubMed1991

Clinical implications of screening for cervical cancer under Medicare. The natural history of cervical cancer in the elderly: what do we know? What do we need to know?

Despite the recent passage of coverage for Papanicolaou test screening under Medicare, several aspects of the natural history of cervical cancer in the elderly remain uncertain. This article reviews what we know about cervical cancer in elderly women to provide clinicians with the background necessary for assessments of screening recommendations, integration of new data into practice, and development of consensus approaches to screening in the elderly. Two central questions that affect a screening program for the elderly are how long the neoplastic process takes from preinvasive disease to the development of invasive cancer, and how likely is it that a given neoplastic state observed in an elderly woman will, in fact, progress to a more severe state. The ultimate success of the new Medicare benefit will also be affected by the use of Papanicolaou testing, the technique of obtaining the smear, and the adequacy of reporting and follow-up. The expansion of Medicare benefits to include early cervical cancer detection has the potential to improve the quality and the duration of older women's lives.

Aged↗
PubMed1989

Carcinogenesis and teratogenesis may have common mechanisms.

The specific mechanisms of carcinogenesis and teratogenesis are poorly understood. There are, however, some known or potential common mechanisms, such as gene or chromosome mutations, interference with gene expression, altered membrane properties, or altered intracellular homeostasis. Carcinogenesis is generally regarded as a multistage process, and a carcinogen can act at one or several stages. Agents acting in the early stages of the neoplastic process are DNA-reactive, mutagenic compounds which enable cells to be transformed to malignancy. These agents can also, if acting during critical periods of ontogenesis, induce abnormal development of the embryo. Agents which block gap junctional intercellular communication may act both as tumor-promoting agents and ans teratogens in the developing embryo. Hormones are essential in the control of development and differentiation. Modulation of the intracellular hormone receptors may lead to changes in homeostasis with abnormal cellular proliferation and development as a consequence.

Animals↗
PubMedDate not supplied

[Orbital pseudotumour imitating a proliferative process].

INTRODUCTION: Orbital pseudotumour is a non-specific inflammatory process of the orbit of unknown origin. It is a rarely diagnosed disease particularly in children, which imitates a neoplastic process. Typical clinical picture is a tumour localized in the orbit, causing various degree of exophtalmus and a decrease of globe mobility and vision. The extent of intraorbital changes are revealed by imaging studies (USG, TK, MR). Diagnosis is based on histopathology of tumour sample. In treatment steroid therapy, radiotherapy or chemotherapy in resistant cases are used. Relapse and malignant transformation are observed. CASE REPORT: We present a case of a 5-years old girl with orbital pseudotumour. In the histopathological examination there a small lymphoid cells, immunohistochemically there is mixed lymphocytic T and B infiltration (CD 3 (+), CD 20 (+), bcl (+), CD 43 (-)). She was treated with steroid therapy, and achieved complete regression of the tumour. At present she is regularly oncologically examined because of the possibility of malignant transformation. CONCLUSIONS: 1. Orbital pseudotumour should be included in the differential diagnosis of children with an orbital tumour 2. Corticosteroids seem to be the treatment of choice in orbital pseudotumour 3. Children with orbital pseudotumour should be regularly oncologically examined because of the possibility of malignant transformation.

Child↗
PubMed1996

[Malignant neoplasms and intestinal obstruction in children 3 to 15 years old].

Observations on one of the rare complications in children presenting malignant neoplasms of the abdominal cavity and retroperitoneal space are described. Over a 7-year period, operative treatment is undertaken in 42 children aged 3 to 15 years. In eleven of them (26.42 per cent) it is a matter of mechanical ileus. The type of bowel obstruction in the series of children under study is a follows: obturation-in three and adhesion-in five cases. The obturation involves the large intestine, and is due to pressure of a neoplastic process in advanced stage of development on the colon. Ileus due to adhesions occurs after operative removal of the neoplastic formation. The essential differences in type of intestinal obstruction in children with malignant neoformation in the abdominal region from the one in adult patients justify the report on the observations.

Abdominal Neoplasms↗
PubMedDate not supplied

Spontaneous mutation of RNA tumour viruses.

There are 2 categories of spontaneously occurring avian and mammalian RNA tumour virus mutants: conditional and non-conditional. 1) Conditional mutants are able to replicate in or transform cells only under certain physiological conditions or in certain cells. RNA tumour virus temperature-sensitive mutants, focus-morphology mutants, and host range mutants are spontaneously formed. Some of these conditional mutants probably arise by point mutations in the viral genome. 2) Non-conditional mutants have genetic lesions that render them inactive under all conditions. There are non-conditional spontaneous RNA tumour virus mutants that are missing either the virion envelope glycoprotein or both the envelope glycoprotein and the virion DNA polymerase. These mutants cannot replicate or transform cells. Other spontaneous non-conditional mutants can replicate but are defective in their ability to transform fibroblastoid cells. These spontaneous transformation-defective mutants can have deletions in 10-20% of the genomic RNA. Conditional mutants with an altered host range occur at a high rate of approximately 1 mutation/50 infected cell generations during DNA-to-DNA information transfer. This type of conditional mutation requires cell replication but does not occur frequently either during the original synthesis of viral DNA (RNA-to-DNA information transfer) or during the transcription of progeny viral RNA from the (RNA-to-DNA information transfer) or during the transcription of progeny viral RNA from the DNA (DNA-to-RNA information transfer). Temperature-sensitive and focus-morphology mutants also have a high rate of spontaneous formation. Non-conditional mutants missing the viral envelope glycoprotein, DNA polymerase, or transformation gene, also appear to be spontaneously formed at a high rate. Normal avian and mammalian cells contain RNA tumour virus-related genes in their DNA. It is hypothesized that these endogenous RNA tumour virus-related genes in normal cells also have a high rate of spontaneous mutation and are involved in neoplastic processes.

Animals↗
PubMed1986

Glycosyltransferase levels in familial polyposis coli.

Glycosyltransferase levels have been reported to be decreased in the tumor mucosa of adenocarcinoma of the colon. The purpose of this study was to determine if similar changes are present in the polyp mucosa of patients with Familial Polyposis Coli (FPC). The levels of eight glycosyltransferases were determined by measuring transfer of a radiolabeled sugar from a nucleotide sugar donor to a glycoprotein acceptor. The levels of four of the enzymes were significantly different in the mucosa of tumors and the polyp mucosa of patients with FPC as compared to the colonic mucosa of persons without known neoplastic disease. The changes were specific for these four enzymes and occurred to the same degree in tumor mucosa and the polyp mucosa. These changes in glycosyltransferase levels are a marker of the malignant transformation of the cell and since they occur in the histologically benign cells of FPC may serve as a key to understanding the neoplastic process.

Adenocarcinoma↗
PubMed2005

Dehydroepiandrosterone inhibits the progression phase of mammary carcinogenesis by inducing cellular senescence via a p16-dependent but p53-independent mechanism.

INTRODUCTION: Dehydroepiandrosterone (DHEA), an adrenal 17-ketosteroid, is a precursor of testosterone and 17beta-estradiol. Studies have shown that DHEA inhibits carcinogenesis in mammary gland and prostate as well as other organs, a process that is not hormone dependent. Little is known about the molecular mechanisms of DHEA-mediated inhibition of the neoplastic process. Here we examine whether DHEA and its analog DHEA 8354 can suppress the progression of hyperplastic and premalignant (carcinoma in situ) lesions in mammary gland toward malignant tumors and the cellular mechanisms involved. METHODS: Rats were treated with N-nitroso-N-methylurea and allowed to develop mammary hyperplastic and premalignant lesions with a maximum frequency 6 weeks after carcinogen administration. The animals were then given DHEA or DHEA 8354 in the diet at 125 or 1,000 mg/kg diet for 6 weeks. The effect of these agents on induction of apoptosis, senescence, cell proliferation, tumor burden and various effectors of cellular signaling were determined. RESULTS: Both agents induced a dose-dependent decrease in tumor multiplicity and in tumor burden. In addition they induced a senescent phenotype in tumor cells, inhibited cell proliferation and increased the number of apoptotic cells. The DHEA-induced cellular effects were associated with increased expression of p16 and p21, but not p53 expression, implicating a p53-independent mechanism in their action. CONCLUSION: We provide evidence that DHEA and DHEA 8354 can suppress mammary carcinogenesis by altering various cellular functions, inducing cellular senescence, in tumor cells with the potential involvement of p16 and p21 in mediating these effects.

Adjuvants, Immunologic↗