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PubMed2003

Cancer survival in Sweden 1960-1998--developments across four decades.

This paper summarizes a comprehensive study of cancer survival in Sweden from 1960 to 1998. A total of 1021421 persons and 40 different cancer sites were included in the analyses. The main outcome measure is the relative survival rate (RSR) for different sites and follow-up times after diagnosis. The 10-year RSR for all sites combined has increased steadily-from 26.6% among men and 41.8% among women in the 1960s, to 44.6% (men) and 57.6% (women) in the 1990s. The expectation of life for a person diagnosed with cancer today is about 7 years longer than that of one diagnosed during the mid-1960s. About 3 years are gained due to changes in the relative distribution of various cancer types and about 4 years due to improved relative survival. During the 1990s substantial survival improvements were observed not only for uncommon types, such as testicular cancer, Hodgkin's lymphoma and some other haematologic malignancies, but also for cancer of the rectum, kidney and malignant melanoma. Survival for breast and cervical cancer also improved during the 1990s, but not that for pancreatic, liver or lung cancer.

Age Factors↗
PubMed1991

Chromogranin A: its role in endocrine function and as an endocrine and neuroendocrine tumor marker.

CgA is a 49 kilodalton protein that is present in the secretory granules of most endocrine and many neuroendocrine cells. Detection of CgA in cells by immunocytochemistry and measurement of CgA in serum by immunoassay can serve as tissue and serum markers for CgA-producing tumors. CgA is of diagnostic value in classical endocrine tumors, in hormone-negative tumors, and in endocrine tumors in which other diagnostic procedures have their limitations. Although the biological function of CgA is yet unknown, it may serve as a precursor molecule, like POMC, for a family of biologically active peptides. CgA is an important new tool for the endocrinologist in the diagnosis and management of patients with endocrine and neuroendocrine tumors.

Amino Acid Sequence↗
PubMed1986

Divergent differentiation in neoplasms. Pathologic, biologic, and clinical considerations.

In this rather brief review, we have illustrated and discussed selected examples of dual or multiple differentiation within certain neoplasms. In so doing, we have attempted to present those cases which highlight common diagnostic problems and which have important biologic and clinical implications. We have shown how tumors arising in many organs such as the lung, gastrointestinal tract, and thyroid can simultaneously manifest combined endocrine-nonendocrine differentiation, and we have addressed this phenomenon in relation to the "parent cell of origin" theory. We have emphasized that while many tumors do in fact resemble the tissues in which they arise, the possession of a particular phenotype, such as endocrine, does not necessarily imply that the tumor in question was derived from an endocrine progenitor cell. To reinforce the concept that the histomorphologic, biochemical, and functional properties of tumor cells reflect ongoing differentiation events rather than a static situation, we have presented examples of tumors in which changes in phenotype have been observed during the course of disease, e.g., small cell carcinomas of the lung and prostate, as well as tumors in which divergent differentiation reflects similar lines of differentiation occurring in normal tissues, e.g., certain neurogenic tumors. Finally we have considered important clinical implications of mixed differentiation and changing phenotype and their impact on the pathologist.

Carcinoid Tumor↗
PubMedDate not supplied

Management of intracranial neoplasms in children with neurofibromatosis type 1 and 2. The Children's Cancer Study Group.

The association of central nervous system neoplasms in neurofibromatosis is common and children are at particular risk. Recent advances in neurodiagnostic techniques allow for non-invasive detection of these tumors, and often these tumors are found in asymptomatic patients. Due to the diversity of neoplasms, varying grades of malignancy, variable growth patterns, and the occupancy of non-neoplastic hamartomatous lesions, the clinician often has difficulty determining which patient should have a diagnostic biopsy or resection, or if therapy should be started without pathologic confirmation. Following a review of the neuroradiology and more common intracranial tumors, recommendations regarding management are proposed.

Brain↗
PubMed1986

Immunocytochemical demonstration of intermediate filament cytoskeleton proteins in human endocrine tissues and (neuro-) endocrine tumours.

The presence and distribution of intermediate filament proteins, such as cytokeratins, vimentin, neurofilament proteins and glial fibrillary acidic protein were assessed immunohistochemically in pituitary adenomas, medullary thyroid carcinomas, endocrine pancreatic tumours, gastric, intestinal and bronchial carcinoids, parathyroid adenomas, pheochromocytomas, paragangliomas and related non-neoplastic tissues. In some cases, immunohistochemical results were correlated with cytoskeletal proteins as analysed by SDS-polyacrylamide gel electrophoresis. Cytokeratin antibodies with broad range of immunoreactivity (i.e. to murine liver cytokeratin component D) reacted with epithelial cells in all non-neoplastic endocrine tissues and related neuroendocrine tumours studied, except for adrenal medulla, pheochromocytoma and paraganglioma, independently of hormone production and biological behaviour. In contrast, antibodies to epidermis-derived cytokeratins failed to stain endocrine tissues and tumours. Paranuclear cytokeratin accumulations were seen in bronchial, gastric, and intestinal carcinoids and seem to be a common feature of neuroendocrine tumours. One- and two-dimensional SDS-polyacrylamide gel electrophoresis of non-neoplastic endocrine tissues and related tumours revealed two major keratin polypeptides corresponding to cytokeratins No. 8 and 18 of the cytokeratin catalog of human cells (Moll et al. 1982). According to this cytokeratin polypeptide composition, endocrine tissues and related tumours conform to the "simple type" of epithelia. Vimentin-related immunoreactivity was restricted to stromal cells and to folliculo-stellate cells in normal pituitary gland, Schwann cells in carcinoids and satellite cells in normal adrenal medulla and in pheochromocytomas. Neurofilament protein- (70 kD)-antibodies only stained nerve fibers in normal tissues and at the periphery of carcinoid tumour cell complexes, and to a variable degree, cells in nontumorous adrenal medulla, pheochromocytomas and paragangliomas. Furthermore, neurofilament reactivity was observed along with cytokeratin expression in two bronchial carcinoids.

Electrophoresis, Polyacrylamide Gel↗
PubMed1980

Cerebral neuroblastoma with elevated nerve growth factor.

Cerebral neuroblastoma is often difficult to differentiate by clinical criteria from other central nervous system neoplasm. This report is of a young child with cerebral neuroblastoma and elevated nerve growth factor. This case illustrates the need for further studies into the usefulness of nerve growth factor in differentiating cerebral neuroblastoma from other central nervous system tumors.

Brain Neoplasms↗
PubMed1984

Primary neoplasms of the central nervous system in Trinidad.

The incidence of primary neoplasms of the central nervous system in Trinidad is less than 1 case per 100.000 population per year. There is no significant difference in the sex and age distribution of the cases, but a definite racial difference is seen in the frequency of different CNS neoplasms.

Adult↗
PubMedDate not supplied

Application of silver stains to cytologic specimens of neuroendocrine tumors metastatic to the liver.

Cytologic specimens of neuroendocrine tumors metastatic to the liver were examined with regard to their silver staining properties after the application of argentaffin and argyrophil staining techniques (Masson, Grimelius and Sevier-Munger). In tumors with a content of serotonin (small intestine carcinoids), the presence of this substance was demonstrated cytologically as an argentaffin reaction in individual tumor cells; however, formalin fixation was a prerequisite for positive staining. Melanin in malignant melanoma cells displayed a positive argentaffin reaction, irrespective of the fixation used (air drying, formalin, Bouin's fluid or acetone-alcohol). Thus, serotonin and melanin can be distinguished in cytologic samples of neuroendocrine tumors by the use of the Masson argentaffin reaction with different fixatives. The nonargentaffin-positive neuroendocrine tumor cells were weakly stained or unreactive with the Grimelius argyrophil technique. The Sevier-Munger argyrophil technique was negative or gave a disturbing nonspecific background staining reaction that was difficult to interpret in the cytologic samples. Thus, the Grimelius method appears to be the most useful silver stain for identifying neuroendocrine tumor cells in cytologic material, irrespective of their hormone content, since both argentaffin-positive and argentaffin-negative cell samples were stained at least to some degree.

Adenocarcinoma↗
PubMed1987

Fat soluble vitamins and cancer localization associated to an abnormal ketone derivative of D3 vitamin: carcinomedin.

Many investigations suggested relations between fat soluble vitamin levels in blood and incidence of cancer. These studies are concerning both therapeutical efficiency of vitamins intake, seric levels and cancer risk, and the supposed correlation between blood fat soluble vitamin levels and the cancer localization. The purpose of the present study was to investigate whether the alterations of fat soluble vitamin levels (A-vitamin, beta-carotene and alpha-tocopherol) were correlated not only to carcinogenic processes but also to the localizations of their developments. In a former article, we have found that an abnormal ketone derivative of D3 vitamin (1-keto-24-methyl-25-hydroxycholecalciferol) or carcinomedin was present in the serum of all cancer patients and absent in that of healthy control subjects. Serum levels of the four above substances were determined in 1068 subjects suffering from differently localized cancers and in 880 healthy subjects. A statistical multidimensional analysis of data led a separate five groups of cancer types (p less than 0.001). Within each group alterations of vitamin spectra, compared to controls, were identical; between groups they were significantly different. These groups were: anal and intestinal cancer; pancreatic, hepatic, oesophageal and gastric cancer; laryngeal and lung cancer; uro-genital and breast cancer; brain cancer. All these groups are statistically different from the reference one (p less than 0.001). This grouping roughly corresponds to the embryologic origin of affected organs. This suggests that carcinogenesis may alter fat soluble vitamin metabolism, specifically in various forms of cancer, or these alterations of vitamin metabolism are in some way involved in the carcinogenic process.

Adult↗
PubMed1989

Exposure of newborn mice to adenosine causes neural crest dysplasia and tumor formation.

In the first part of this paper, we show that intraperitoneal injection of adenosine into newborn mice causes multiple neural crest tumors, neural crest hyperplasia, and heterotopic melanin pigmentation. In the second part, we review published data to propose (1) that microtubule proteins, phosphorylated through the action of calmodulin-dependent kinase and cyclic adenosine monophosphate and the adenosine A2 receptor of neural crest cells, may participate in neurotransmission and (2) that at least some neural crest tumors may be associated with disorders of neurotransmission in embryonic neural crest cells.

Adenosine↗
PubMed1986

Monoclonal antibody HISL-19 as an immunocytochemical probe for neuroendocrine differentiation. Its application in diagnostic pathology.

The monoclonal islet cell antibody HISL-19 was generated after immunization of BALB/c mice with human islet cell preparations. Besides reactivity with all cells of the human pancreatic islet, MAb HISL-19 also reacted with other cells of the diffuse neuroendocrine system, including anterior pituitary cells, C cells of the thyroid, endocrine cells of the gut and bronchus, the adrenal medulla, and central and peripheral neurons. In this study the authors screened a series of 53 neuroendocrine and 71 nonneuroendocrine tumors for their reactivity with MAb HISL-19 using an indirect immunoperoxidase technique on formalin-fixed and Paraplast-embedded sections. MAb HISL-19 reacted strongly with all insulomas (10), carcinoids (8), C-cell carcinomas of the thyroid (8), pituitary adenomas (6), neuroendocrine carcinomas of the skin (4), paragangliomas of the carotid body (3), and pheochromocytomas (2) tested. Neuroblastomas (3), oat-cell carcinomas of the lung (2), and melanomas (4) exhibited only very few immunoreactive cells scattered throughout the tumor or remained unstained with MAb HISL-19. With the exception of one lobular carcinoma of the breast (1/3), one adenocarcinoma of the endometrium (1/4), and one adenocarcinoma of the stomach (1/6), nonneuroendocrine tumors were negative with MAb HISL-19. Biochemical findings obtained by SDS-PAGE, "Western" immunoblotting, immunoaffinity chromatography, and absorption experiments indicate that the MAb HISL-19-defined antigen is not related to neuron specific enolase. Because the epitope recognized by MAb HISL-19 is well preserved in formalin-fixed and routinely processed tissues, this monoclonal antibody finds potential applications in diagnostic pathology as an indicator for neuroendocrine cells and their neoplasms.

Antibodies, Monoclonal↗
PubMed1999

Gene transfer technologies for malignant gliomas.

Although early clinical gene therapy trials for recurrent central nervous system neoplasms showed the proof-of-principle, they did not fulfill the high expectations suggested by the preclinical experimental data. Insufficient distribution of vectors in human brain tumors and very low transduction efficiency require that we reevaluate gene transfer concepts for brain tumor treatment. Major steps to improve gene transfer into the central nervous system and the efficacy of gene therapy for malignant brain tumors include: 1) the design of more effective vector systems; 2) the development of new or improved prodrug/suicide systems, gene replacement approaches, or strategies targeting the immune response or tumor angiogenesis; 3) the study of new techniques to enhance delivery of genetic vectors into brain tumors and for monitoring gene delivery into tumors; and 4) assessment of the role of gene therapy as part of a combined treatment approach.

Animals↗