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Results for “Neoplastic Processes”

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PubMed1999

Copper, zinc and superoxide dismutase in precancerous, benign diseases and gastric, colorectal and breast cancer.

The aim of the present study was to assess serum levels of copper and zinc levels and erythrocytes Cu,Zn-SOD activity and to determine probable changes in gastric and colorectal precancerous diseases, benign breast diseases, gastric, colorectal and breast cancer. The study included 165 subjects with cancer, 348 subjects with precancerous (atrophic gastritis, gastric adenoma, colon adenoma, rectal adenoma) and/or benign diseases (weak dysplasia, severe dysplasia, fibroadenoma, cystic disease) and 161 randomly selected healthy controls. Our results suggest that while in gastric and colorectal cancer there were mostly increased copper levels, in breast cancer they were not changed. Zinc levels were weakly decreased in atrophic gastritis, gastric adenoma and breast cancer. There was a strong positive correlation between zinc levels and SOD activity in fibroadenoma and a weak positive correlation in colorectal adenoma and colorectal cancer without any correlation between SOD activity and copper in these groups. In gastric precancerous disease there was a positive correlation between SOD and copper. The results of this study suggest that serum trace element levels and activity of related enzymes might be different in various neoplastic processes. This variation in neoplastic processes might be influenced by other factors that have to be considered in complex relationships between the whole body and neoplastic cells.

Adult↗

PubMedDate not supplied

Enzymes in benign and malignant effusions.

A critical review of the work done in this area indicates that, of the available enzyme systems now used in clinical diagnosis, the LDH system is the only one of significant value in the examination of pleural and peritoneal effusions. In terms of differential diagnosis, estimation of pleural or peritoneal fluid LDH levels will enable the examiner to distinguish between poorly cellular vs. abundantly cellular effusions. In the abundantly cellular effusions, estimation of levels of LDH do not distinguish with any degree of accuracy between those effusions due to inflammatory processes vs. neoplastic processes. Results of studies of LDH isoenzymes are at variance and require more study.

Ascitic Fluid↗

PubMed2000

The expression of fatty acid synthase (FASE) is an early event in the development and progression of squamous cell carcinoma of the lung.

Correlation of elevated levels of the lipogenic enzyme, fatty acid synthase (FASE), with advanced stages of some cancers has drawn attention to this enzyme as a possible marker of poor prognosis. Because recent studies have shown that cancer cells are dependent on fatty acid synthetic activity and pharmacologic inhibitors of this enzyme are selectively cytotoxic to cancer cells, expression of FASE also may provide a potential target for intervention in the neoplastic process. To determine the potential usefulness of expression of FASE in the neoplastic process of the lung, we evaluated its pattern of expression immunohistochemically in archival specimens from 60 human lung specimens with squamous cell cancer (SCC) and associated "preneoplastic" lesions compared with its expression in the normal bronchial epithelium of 60 noncancer specimens. The expression of FASE was significantly higher in SCC associated uninvolved bronchial epithelium (mean = 0.40+/-0.03, median = 0.38) compared with its expression in the bronchial epithelium of noncancer specimens (mean = 0.18+/-0.02, median = 0.16) indicating its early expression. We also observed a statistically significant step-wise increase in FASE expression from SCC associated uninvolved bronchial epithelium (mean = 0.40+/-0.03, median = 0.38) to epithelial hyperplasia (0.58+/-0.04, median = 0.57) to SCC (1.53+/-0.06, median = 1.50). The results suggested that expression of FASE is an early event in the development and progression of SCC of the lung. The inhibition of fatty acid synthesis by inhibiting enzymatic function with metabolic analogues may be a useful strategy in the treatment of SCCs. The expression of FASE in early lesions such as SCC associated uninvolved bronchial epithelium and epithelial hyperplasia might also provide a potential means for intervention early in the neoplastic process in the lung or even preventing their malignant transformation to invasive carcinomas.

Biomarkers, Tumor↗

PubMed1985

Assay for beta-glucuronidase in cerebrospinal fluid: usefulness for the detection of neoplastic meningitis.

The specificity and sensitivity of the assay for beta-glucuronidase in cerebrospinal fluid were evaluated to determine the usefulness of this test for the detection of neoplastic meningitis. The enzyme activity was first measured in cerebrospinal fluid from 131 patients with various disorders and was then prospectively measured in cerebrospinal fluid from 30 patients with cytologic results that were positive for or suggestive of malignant disease. Within the first group, elevated levels of beta-glucuronidase were found only among patients with neoplastic processes in the central nervous system, including neoplastic meningitis. Among 26 patients with neoplastic processes in the central nervous system, including neoplastic meningitis. Among 26 patients with positive cytologic results, 13 had elevated beta-glucuronidase activities. Elevated values were more frequent among patients with adenocarcinoma (75%) and myelogenous leukemia (60%). The patients with these two disorders also had the highest enzyme activities. The correlation of th beta-glucuronidase level with other cerebrospinal fluid values, including total protein, glucose content, and cell count, was not significant. The findings of this study indicate that measurement of beta-glucuronidase in cerebrospinal fluid can be used as an adjunctive diagnostic test for neoplastic meningitis. The results should be interpreted with caution, however, because of the possibility that the elevated enzyme levels may be due to acute or subacute bacterial or fungal meningitis.

Cerebrospinal Fluid↗

PubMed1997

Hepatic tumor induction in c-myc mono-transgenic and TGF-alpha/c-myc double-transgenic mice.

Double transgenic mice bearing fusion genes consisting of mouse albumin enhancer/promoter-mouse c-myc cDNA and mouse metallothionein 1 promoter-human TGF-alpha cDNA were generated to investigate the interaction of these genes in hepatic oncogenesis and to provide a general paradigm for characterizing both the interaction of nuclear oncogenes and growth factors in tumorigenesis as well as to produce an experimental model to test how environmental chemicals might interact with these genes during the neoplastic process. Coexpression of c-myc and TGF-alpha as transgenes in the mouse liver resulted in a tremendous acceleration of neoplastic development in this organ as compared to expression of either of these transgenes alone. The two distinct cellular reactions that occurred in the liver of the double transgenic mice prior to the appearance of liver tumors were dysplastic and apoptotic changes in the existing hepatocytes followed by emergence of multiple focal lesions composed of both hyperplastic and dysplastic cell populations. These observations suggest that the interaction of c-myc and TGF-alpha, during development of hepatic neoplasia contributes to the selection and expansion of the preneoplastic cell populations which consequently increases the probability of malignant conversion. Treatment of the double transgenic mice with both genotoxic agents such as diethylnitrosamine and IQ as well as the tumor promoter phenobarbital greatly accelerated the neoplastic process. These results suggest that selective transgenic mouse models may provide important tools for testing both the carcinogenic potential of environmental chemicals and the interaction/cooperation of these compounds with specific genes during the neoplastic process.

Animals↗

PubMed1999

Carcinogenicity and mutagenicity of heterocyclic amines in transgenic mouse models.

Double transgenic mice bearing fusion genes consisting of mouse albumin enhancer/promoter-mouse c-myc cDNA and mouse metallothionein1 promoter-human TGFalpha cDNA were generated to investigate the interaction of these genes in hepatic oncogenesis and to provide a general paradigm for characterizing both the interaction of nuclear oncogenes and growth factors in tumorigenesis. In addition, these mice provide an experimental model to test how environmental chemicals might interact with the c-myc and TGFalpha transgenes during the neoplastic process. Treatment of the double transgenic mice with both genotoxic agents such as diethylnitrosamine and 2-amino-3-methylimidazo-[4,5-f]quinoline (IQ) as well as the tumor promoter phenobarbital greatly accelerated the neoplastic process. To investigate the role of mutagenesis in the carcinogenic process, 2-amino-3,8-dimethyl-imidazo[4,5-f]quinoxaline (MeIQx) induced mutagenesis and hepatocarcinogenicity was examined in C57BL/lacZ (Muta Mice) and double transgenic c-myc/lacZ mice that carry the lacZ mutation reporter gene. The MelQx hepatocarcinogenicity was associated with an increase in in vivo mutagenicity as scored by mutations in the lacZ reporter gene. These results suggest that transgenic mouse models may provide important tools for testing both the carcinogenic potential of environmental chemicals and the interaction/cooperation of these compounds with specific genes during the neoplastic process.

Animals↗

PubMed2001

Skeletonizing en bloc esophagectomy for cancer.

OBJECTIVE: To evaluate the long-term outcome of patients with esophageal cancer after resection of the extraesophageal component of the neoplastic process en bloc with the esophageal tube. SUMMARY BACKGROUND DATA: Opinions are conflicting about the addition of extended resection of locoregional lymph nodes and soft tissue to removal of the esophageal tube. METHODS: Esophagectomy performed en bloc with locoregional lymph nodes and resulting in a real skeletonization of the nonresectable anatomical structures adjacent to the esophagus was attempted in 324 patients. The esophagus was removed using a right thoracic (n = 208), transdiaphragmatic (n = 39), or left thoracic (n = 77) approach. Lymphadenectomy was performed in the upper abdomen and lower mediastinum in all patients. It was extended over the upper mediastinum when a right thoracic approach was used and up to the neck in 17 patients. Esophagectomy was carried out flush with the esophageal wall as soon as it became obvious that a macroscopically complete resection was not feasible. Neoplastic processes were classified according to completeness of the resection, depth of wall penetration, and lymph node involvement. RESULTS: Skeletonizing en bloc esophagectomy was feasible in 235 of the 324 patients (73%). The 5-year survival rate, including in-hospital deaths (5%), was 35% (324 patients); it was 64% in the 117 patients with an intramural neoplastic process versus 19% in the 207 patients having neoplastic tissue outside the esophageal wall or surgical margins (P <.0001). The latter 19% represented 12% of the whole series. The 5-year survival rate after skeletonizing en bloc esophagectomy was 49% (235 patients), 49% for squamous cell versus 47% for glandular carcinomas (P =.4599), 64% for patients with an intramural tumor versus 34% for those with extraesophageal neoplastic tissue (P <.0001), and 43% for patients with fewer than five metastatic nodes versus 11% for those with involvement of five or more lymph nodes (P =.0001). CONCLUSIONS: The strategy of attempting skeletonizing en bloc esophagectomy in all patients offers long-term survival to one third of the patients with resectable extraesophageal neoplastic tissues. These patients represent 12% of the patients with esophageal cancer suitable for esophagectomy and 19% of those having neoplastic tissue outside the esophageal wall or surgical margins.

Adenocarcinoma↗

PubMed1981

Studies of neoplastic development in respiratory tract epithelium.

The dynamics of neoplastic development in conducting airways were studied in an animal model using morphologic and tissue culture techniques. Evidence for the regression of many metaplastic-dysplastic lesions, including advanced "preneoplastic" lesions, was provided. This regression of lesions is not synonymous with reversion of the neoplastic process. The number of "carcinogen-altered" cells and the number of cells with neoplastic potential continued to increase as a function of time after carcinogen exposure. With the cell culture methods developed for these studies, it is possible to analyze qualitatively and quantitatively the progression of the neoplastic process as it takes place in vivo and to detect and enumerate the progenitor cells of later-appearing cancers. The investigations also provide strong evidence suggesting that carcinogen-exposed organs contain many more cells with neoplastic potential. This expression may, however, be sharply enhanced when permissive or promoting conditions prevail. The investigations open up new avenues to develop means for detection of preneoplastic cell populations and for therapeutic intervention during early phases of the neoplastic disease process.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1998

Diffuse marrow disorders in children.

This article describes MR imaging findings in neoplastic processes affecting the marrow of children. Differentiation from non-neoplastic processes, such as edema and hematopoietic marrow is described.

Adolescent↗

PubMed1991

Current state-of-the-art in human cell transformation in culture.

The immortalization and transformation of cultured human cells has far-reaching implications for both cell and cancer biology. Human cell transformation studies will increase our understanding of the mechanisms underlying carcinogenesis and differentiation. The neoplastic process can now be studied in a model human cell culture system. The accompanying biochemical and genetic changes, once identified, will help define the relationship between malignancy and differentiation. The present studies indeed demonstrate that the neoplastic process can now be studied in a human cell model system. Primary human cells treated with various carcinogens became immortalized in culture but were not tumorigenic. Additional exposure to either retroviruses, chemical carcinogenes or X-ŗay irradiation to these cells induced morphological alterations associated with the acquisition of neoplastic properties. These findings demonstrate the malignant transformation of human primary cells in culture by the combined action of either a DNA transforming virus and a retrovirus or a DNA virus and a chemical or X-ray irradiation, and support an multistep process for neoplastic conversion. It has been known that normal human cells in culture are remarkably resistant to experimentally induced tumorigenicity. However, as shown above, normal human cells could now be transformed into tumorigenic cells.

Cell Transformation, Neoplastic↗

PubMed1981

Fibrous histiocytomas of the oral mucosa.

The oral lesions reported in this article fall into the first category of benign fibrous histiocytomas analogous to those which occur on sun-exposed skin surfaces of young objects. The ages of the patients, the histologic features and the history of traumatic episodes, as well as their biologic behaviors on follow-up, are all features compatible with those benign lesions which occur in the skin. According to the information presented in these cases, there is stronger evidence that the lesions of the oral mucosa, like their dermatologic counterparts, are representative of reactive inflammatory processes rather than neoplastic processes. It is of considerable interest that in both cases reported here the patients were children whose lesions developed following significantly severe traumatic episodes. Also of interest is the finding that the lesions healed with no recurrences or complications, even though in one of the cases it was not completely removed. These findings are in agreement with other reports of such lesions which have occurred in the head and neck regions of children and young adults. From the over-all information obtained in the literature review regarding the biologic behavior of benign fibro-histiocytic lesions, the collected data seem to indicate that lesions of the skin and superfacial mucosal surfaces which occur in children and young adults are proliferative, reactive lesions and infection, or irradiation. Systemic, visceral, or deep-seated lesions in the lower extremities appear to be true neoplasms and their prognoses must be considered as guarded.

Child↗

PubMed1975

Paget's disease of the breast.

Criteria of the morphological diagnosis as well as the histogenesis of the lesions in Paget's disease are presented; the authors claim that the initial lesion occurs in the lactiferous ducts, the skin being secondarily involved. Likewise, the dyskeratotic lesions are considered as secondary to the neoplastic process, either by neoplastic induction or by mobilization and proliferation of cancerous cells from lactiferous ducts. The utility of biopsies in all cases of nipple eczema, and of the histologic investigation of the profound tissues is pointed out. In this way the canalicular starting point in the vicinity of the nipple can be noticed.

Breast↗

PubMed1997

[Content of haptoglobin in blood serum in patients after thoracic surgery for various indications].

Initial results are presented on the usefulness of haptoglobin content monitoring in blood serum of patients after thoracic operations performed for various indications. 57 patients were analysed and divided into 3 groups based on the type of disease. Group 1 consisted of patients operated for malignant neoplasm. Group 2 consisted of patients with inflammatory changes and purulent complications within the thorax. Group 3 consisted of patients operated from other indications. The experimental samples of further 30 operated patients have not been analysed yet due to a delay in shipment of plates from Boehringer. The control group consisted of 31 healthy volunteers. In the experimental groups blood was taken 1 day before and 1, 3, 7, 10 and 14 days after the surgical intervention and in the case of complications-21 and 30 days after surgery. Erythrocyte sedimentation, leucocyte level, serum haptoglobin content, clinical and radiological data were analysed. Haptoglobin content was measured using the radial immunodiffusion method according to Manchini. Results were analysed statistically. The increase in serum haptoglobin content in patients after thoracic surgeries and after purulent complications, shows that haptoglobin is a sensitive acute phase indicator and its monitoring may be useful in evaluating the disease process. In advanced neoplastic processes haptoglobin content is a reflection of the progression of the disease process.

Adult↗

PubMedDate not supplied

GABA content and GAD activity in gastric cancer.

BACKGROUND: Several recent reports have suggested a connection between the GABA-ergic system and neoplastic processes. It has been confirmed that both GABA content and GAD activity, are increased in neoplastic tissues in colon and breast cancer. In the light of the theory of dynamic balance between stimulating and inhibitory amino acids, disturbances in GABA metabolism may be an expression of the cell's defensive response to the neoplastic process. The aim of the present study was to evaluate GABA content and GAD activity in the tissue from gastric cancer and in the macroscopically unchanged wall of the stomach. MATERIAL AND METHODS: GABA content and GAD activity were evaluated in tissue material obtained from 34 patients operated for gastric cancer. GABA and GAD levels were determined in neoplastic tissue and surrounding unchanged tissue by spectrofluorometric method. RESULTS: The investigations revealed that the GABA content and GAD activity were significantly higher in the neoplastic tissue in comparison to the unchanged tissue of the stomach. CONCLUSION: The results obtained, together with reports from the literature, suggest the possibility of introducing GABA-ergic system agonists into adjuvant therapy in gastric cancer.

Adult↗

PubMedDate not supplied

Fine needle aspiration cytology of a dedifferentiated liposarcoma: report of a case with histologic and immunohistochemical follow-up.

BACKGROUND: Dedifferentiation is a histologic progression of a neoplasm from low grade to high grade histology. It occurs in tumors of the retroperitoneum and in those undergoing treatment. This usually occurs in the setting of radiation or chemotherapy or as a spontaneous process over a long period. The features of dedifferentiation can be toward any mesenchymal element of the underlying neoplastic process. CASE: We report the cytologic features of a dedifferentiated liposarcoma arising in a 76-year-old man who had a history of well-differentiated liposarcoma. Papanicolaou- and Diff-Quik-stained smears from a radiologically guided fine needle aspiration biopsy showed a hypercellular sample. The smears showed a mixed population of cells. There were multinucleated, pleomorphic giant cells with abundant cytoplasm, smaller clusters of cells with a high nuclear/cytoplasmic ratio and cells with spindled and elongated nuclear features. The follow-up surgical resection specimen showed a dedifferentiated liposarcoma with strong and diffuse immunoreactivity to vimentin, desmin and CD68 in the large, pleomorphic cells; focal and weak immunoreactivity to smooth muscle actin and S-100 in these cells; and strong and focal immunoreactivity to desmin, smooth muscle actin and muscle-specific actin in the spindle cells. This supports the dedifferentiated components of this tumor to be of fibrohistiocytic and leiomyosarcomatous differentiation. CONCLUSION: Dedifferentiation of a well-differentiated liposarcoma should be entertained in the setting of a mass lesion in the retroperitoneum in patients with prior histories of well-differentiated liposarcoma. The radiologic features of a particular neoplastic process can be very helpful in determining the nature of this process.

Aged↗

PubMed1991

[The association of myasthenia gravis and hairy-cell leukemia].

Myasthenia gravis (MG) and tricholeucemia (TL) produce an important immune alteration favoring the appearance of neoplastic and autoimmune disorders. The case of a 53 years old patient who developed type B TL 5 years after the diagnosis of MG is reported. Upon revision of the literature, 37 cases of association of MG and malignant hemopathies, fundamentally lymphoproliferative were found. In general, MG precedes the appearance of the neoplastic process. The autoimmunity and immunodeficiency characteristic of MG probably constitute the pathogenic mechanism leading to the appearance of the neoplastic process.

Bone Marrow↗

PubMed1991

Free-radical processes in multistage carcinogenesis.

Rodent and human cells in culture, transformed in vitro by radiation or chemicals into malignant cells, afford us the opportunity to probe into early and late events in the neoplastic process at a cellular and molecular level. Transformation can be regarded as an abnormal expression of cellular genes. The initiating agents disrupt the integrity of the genetic apparatus altering DNA in ways that result in the activation of cellular transforming genes (oncogenes) during some stage of the neoplastic process. Events associated with initiation and promotion may overlap to some degree, but in order for them to occur, cellular permissive conditions prevail. Permissive and potentiating factors include free radicals, and thyroid hormone, and inadequate antioxidants. Protective factors which suppress the carcinogenic process include enzymatic and dietary antioxidants. These are constitutive under normal circumstances and can be induced under conditions of oxidative stress produced by a wide range of carcinogens.

Animals↗

PubMed1999

Hypermethylation of tumor suppressor genes in cancer.

Hypermethylation of tumor suppressor genes and other genes functionally important in the neoplastic process is a recently recognized process. This epigenetic process is characterized by loss of function of these genes associated with transcriptional loss in the absence of structural alterations. The growing list of genes inactivated by promoter region hypermethylation provide an opportunity to examine the patterns of inactivation of such genes and provide clues as to the roles these events play in the neoplastic process.

Cell Transformation, Neoplastic↗