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PubMed1995

Superoxide dismutase and lipid-bound sialic acid in sera from children with cancers and juvenile chronic arthritis.

Both experimental and epidemiological studies suggest that patients with autoimmune and other chronic inflammatory diseases are more prone to develop cancer. The aim of the present investigation is to find some typical differences between the content of lipid-bound sialic acid (LSA) and the activity of superoxide dismutase (SOD) in sera from children with neoplastic diseases and juvenile chronic arthritis (JCA). Our results show 30% lower SOD activity in the sera from children with cancer compared with the sera from children with JCA. LSA levels 102% and 166% higher than in children with JCA were observed in the sera from children with blood and solid cancers, respectively. The relation LSA/SOD is about fivefold higher in children with cancers. A negative correlation (r = 0.720, P < 0.001) exists between LSA and SOD in sera from children with cancers. No such correlation was established in the group of children with JCA. We suppose that such differentiation disappears in the beginning of neoplastic process during prolonged therapy of autoimmune diseases. From our findings SOD and LSA appear to be putative markers of malignant disease with potential usefulness not only in JCA but also in other conditions associated with an increased risk of neoplastic development.

Adolescent↗
PubMed2002

[Why do tumor cells avoid immune surveillance?].

Why does cancer develop? What is the essence of premalignant lesions? My answer to these sacramental questions follows. I found out that hyperplastic and tumor nodules are immunologically privileged sites, like the anterior chamber of the eye or the hamster's retrobuccal sac. The antigens from the nodules do not provoke the body's immune reactions, unlike the same antigens from the extranodular tissue. On the other hand, both the autoantibodies and the killer-cells sensitized to this antigens are unable to react with that part of the cells possessing antigens, which are situated within the nodules and completely destroy the same cells in the extranodular tissue. Hyperplastic and tumor nodules are special sites where immunological surveillance is absent. It is because they have no lymphatic and so recirculation of immunocompetent cells through its territory is impossible. Thus, newborn malignant cells in these precancerous formations avoid the immunological control and survive, in contrast to the tissue with the normal structure. So, neoplastic processes will be free from immunological surveillance in the precancerous sites and will therefore be more likely to progress.

Antibody Formation↗
PubMed1985

Relationship between cervical condylomata, pregnancy and subclinical papillomavirus infection.

From a retrospective study of 415 sets of colpophotographs, 25 clinically obvious condylomata of the cervix were identified. Two morphologically distinct forms were found and termed erythrocondylomata and leukocondylomata on the basis of their colposcopic appearance. Erythrocondylomata are red, raised lesions with diagnostic large capillary loops. Those lesions were found in young women (mean age, 22 years) and associated with pregnancy in 72% of cases. They were observed to involute and disappear to the naked eye within a few months of the diagnosis. Colposcopic and histologic studies, however, indicated that the lesions could persist in subclinical form. Of eight such lesions studied, five showed histologic and colposcopic features of subclinical papillomavirus infection, and two showed histologic features compatible with cervical intraepithelial neoplasia (CIN). Leukocondylomata are brilliant white lesions associated histologically with a thick layer of keratin over a typical condylomatous base. Those lesions occurred at a later age (mean, 32 years), were not associated with pregnancy and tended to increase rather than involute with time. Epidemiologic studies have indicated that it is the young and sexually active who are at most risk of developing cervical cancer. This study indicated that it is this same group that is also at highest risk of developing erythrocondylomata of the cervix. Such lesions have been shown to involve the squamocolumnar junction and transformation zone when that area is most active and vulnerable. The progression of such lesions to subclinical papillomavirus infection and CIN suggests that they may be involved in the initiation of the cervical neoplastic process.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Elastofibroma: clonal fibrous proliferation with predominant CD34-positive cells.

Elastofibroma is a rare fibrous lesion that most commonly occurs in periscapular soft tissues and is characterized by accumulated abnormal elastic fibers. Although the lesion is generally regarded as a reactive process, an unusual fibroblastic pseudotumor, or as a fibroelastic tumor-like lesion, its etiology remains largely unknown. Recent cytogenetic demonstrations of chromosomal instability and some recurrent or clonal chromosomal changes have raised the possibility that the lesion represents a neoplastic process. We analyzed 14 cases of elastofibroma to further explore, morphologically and genetically, the characteristics of its cellular composition. The interspersed spindle or stellate cells showed a fibroblast-like appearance and were almost consistently positive for vimentin and frequently positive for CD34 and lysozyme immunohistochemically. No spindle cells of myofibroblastic phenotype were recognized. To assess the clonality of the lesions in female patients, the X-linked polymorphic human androgen receptor gene assay was performed using formalin-fixed, paraffin-embedded tissues. A nonrandom inactivation of the androgen receptor gene was detected in two informative cases. Thus, these findings suggest that CD34-positive mesenchymal cells are an integral component of elastofibroma, which represents a clonal fibrous proliferation.

Aged↗
PubMedDate not supplied

Neoplastic masquerade syndromes.

Masquerade syndromes are classically defined as entities which emulate inflammatory conditions but which are in fact due to a neoplastic process. Careful history and examination in concert with appropriate ancillary investigations and histopathologic evaluation of tissue specimens are required in order to make the correct diagnosis. Many conditions may result in an appearance mimicking an inflammatory condition. The authors review neoplastic conditions which may be considered masquerades. The most common of these is primary intraocular lymphoma or primary central nervous system lymphoma, occurring predominately in older individuals. Diagnostic strategies, therapy, and prognosis are reviewed in detail. Other conditions that can be considered masquerade syndromes are reviewed as well, including lymphomatous and nonlymphomatous conditions, such as melanoma, retinoblastoma, juvenile xanthogranuloma, metastatic lesions, and paraneoplastic syndromes, among others.

Central Nervous System Neoplasms↗
PubMedDate not supplied

[Recovery processes in damage to rats by 252Cf].

The types of recovery processes were demonstrated in experiments on albino rats damaged with 252Cf. The frequency and the degree of manifestation of both pathological and recovery processes were function of radiation dose and time of its formation. The results obtained indicate that changes induced by the incorporation of 252Cf, within a wide range of doses, are compensated incompletely to be manifested later by sklerotic, hyperplastic and neoplastic processes.

Adrenal Glands↗
PubMed1995

The internal auditory canal revisited. The high-definition approach.

The internal auditory canal (IAC) is a bony canal that contains nerves and vessels and is lined by meninges. Pathologic processes may arise from each of these structures. Congenital, developmental, and acquired pathologic conditions may involve the bone of the canal and lead to excessive narrowing or expansion. Lesions formed within the canal include hemangiomas, vascular malformations, and inflammatory and neoplastic processes arising from the facial and acoustic nerves and meninges. Finally, other rare lesions, such as choristomas and metastases, may occur within the IAC, which are not related to its normal content. High-definition computed tomography, MR imaging, and MR angiography allow diagnoses of IAC or cerebellopontine-angle cistern lesions, some of which could not be identified by older techniques.

Ear, Inner↗
PubMedDate not supplied

The pineal gland and cancer.

The pineal gland is considered today as one of the main organs involved in the transduction process which converts environmental light information into an endocrine response. The gland and its hormone melatonin seem to be important chronoimmunomodulators, and a reduction of the latter was associated with experimental and clinical immunodeficiencies and over the control of the neoplastic process. Moreover, melatonin can be an oncostatic or oncostimulating hormone, depending on the timing of its administration. The melatonin circadian rhythm is altered in cancer patients, and this rhythm could be modified as a consequence of certain therapies. Also Electromagnetic Fields (EMF) can affect the pineal function, perhaps working as synchronizers or, as this paper proposes, also through action of the "antenna effect" suggested for artificial human models, with a major energetic transfer over the cephalic area. The pineal could play an important role in the appearance and development of some forms of apparently EMF-related cancers.

Animals↗
PubMed2003

Barrett's esophagus: model of neoplastic progression.

Human cancer progression is characterized by clonal expansion of cells with accumulated genetic errors. Invasive carcinomas contain all the genetic errors that were acquired during neoplastic progression and then continue to accumulate further abnormalities, leading to tumor heterogeneity. Many investigations of human cancer have given valuable insights in genetic abnormalities important for tumor biology. Early events responsible for neoplastic progression, however, are often impossible to investigate in invasive cancers because the premalignant tissue in which the tumors develop are often overgrown and the premalignant conditions cannot be studied in vivo because they are either not detected owing to lack of symptoms or are removed before cancer develops. Unlike many other premalignant conditions Barrett's esophagus is often associated with symptoms leading to diagnosis at an early stage before cancer develops, and the premalignant epithelium is seldom removed at an early stage of cancer progression. Furthermore, in patients who present with invasive carcinoma the tumor is often surrounded by premalignant epithelium, which is available for further investigations. Therefore Barrett's esophagus is an excellent model in which to study the early events of neoplastic progression. It may not only contribute to a better understanding of the neoplastic process but also provide a base for safer assessment of cancer risk during surveillance for early detection of esophageal adenocarcinoma.

Adenocarcinoma↗
PubMed2005

Pathogenesis of myelofibrosis with myeloid metaplasia.

The primary disease process in myelofibrosis with myeloid metaplasia (MMM) is clonal myeloproliferation with varying degrees of phenotypic differentiation. This is characteristically accompanied by secondary intramedullary collagen fibrosis, osteosclerosis, angiogenesis, and extramedullary hematopoiesis. Modern clonality studies have confirmed the multipotent stem-cell origin of the neoplastic process in MMM. The nature of the specific oncogenic mutation(s) is currently being unraveled with the recent discovery of an association between a somatic point mutation of JAK2 tyrosine kinase (V617F) and bcr/abl-negative myeloproliferative disorders, including MMM. The pathogenetic mechanisms that underlie the secondary bone marrow stromal changes in MMM are also incompletely understood. Mouse models of this latter disease aspect have been constructed by either in vivo overexpression of thrombopoietin (TPOhigh mice) or megakaryocyte lineage restricted underexpression of the transcription factor GATA-1 (GATA-1low mice). Gene knockout experiments using such animal models have suggested the essential role of hematopoietic cell-derived transforming growth factor beta1 in inducing bone marrow fibrosis and stromal cell-derived osteoprotegerin in promoting osteosclerosis. However, experimental myelofibrosis in mice does not recapitulate clonal myeloproliferation that is fundamental to human MMM. Other cytokines that are implicated in mediating myelofibrosis and angiogenesis in MMM include basic fibroblast, platelet-derived, and vascular endothelial growth factors. It is currently assumed that such cytokines are abnormally released from clonal megakaryocytes as a result of a pathologic interaction with neutrophils (eg, emperipolesis). This latter phenomenon, through neutrophil-derived elastase, could also underlie the abnormal peripheral-blood egress of myeloid progenitors in MMM.

Animals↗
PubMed2000

Cell populations involved in pigmented villonodular synovitis of the knee.

OBJECTIVE: Pigmented villonodular synovitis (PVNS) of the knee is a tumor-like process of uncertain nature. We analyzed the involved cell populations, iron deposition, and cell proliferation in PVNS to propose a pathogenetic concept of this still elusive disease entity. METHODS: The study was performed on a series of 14 cases of localized PVNS of the knee. Histology and histochemistry were used to evaluate basic morphology and iron deposit distribution. Immunohistochemistry was performed to characterize the inflammatory cell infiltrate and to identify the proliferating cell compartments. In situ hybridization analysis using a cDNA probe against type I collagen was utilized to further characterize the mononuclear cell infiltrate. RESULTS: In addition to the classic features (mononuclear cell infiltrate, multinuclear giant cells, iron deposits, and stromal fibrosis) we observed a chronic inflammatory cell infiltrate in all PVNS samples, in which CD8 positive T cells were conspicuous. A high portion of non-phagocytotic cells resorbed iron and became CD68 positive. A proportion of mononuclear cells expressed type I collagen, thus resembling B synoviocytes. CONCLUSION: Our results suggest that preexisting chronic inflammation plays an important pathogenetic role in the PVNS disease process. Chronic inflammation increases the risk of articular bleeding and probably deranges the iron processing capacity of local synovial macrophages. The resulting iron overload could lead to a shift of iron storing cells from synovial macrophages to B synoviocytes and fibroblasts. A perpetuated proliferation and activation of these cells can explain why PVNS behaves like a neoplastic process.

Adult↗
PubMed1984

Changes in gene expression following neoplastic transformation of rat myogenic cells.

Two malignant sublines, M4 and RMS4 , were previously derived from the recloned L6 line of rat myogenic cells. Comparative studies in tissue culture and inoculation into suckling rats indicated that M4 cells and RMS4 cells may be considered as low-malignant and high-malignant cells, respectively, while L6 cells are not malignant. In the present work, we used extracts from L6 cells, M4 cells, and RMS4 cells collected during the period of exponential growth, to compare their polyadenylic acid-containing messenger RNA (mRNA) populations and the corresponding cell-free translation products. Analysis of the hybridization kinetics between radioactive complementary DNA and homologous or heterologous cellular RNAs indicated that L6 cells contained about 28,000 distinct polyadenylic acid-containing mRNA sequences of 1.8 kilobases each, of which 2,000 to 2,500 and 4,000 to 5,000 were missing (or at least were very infrequent) in M4 cells and RMS4 cells, respectively. Using a minor fraction of the RMS4 cell complementary DNAs, partially purified through repeated complementary DNA-RNA hybridization cycles, it was further shown that RMS4 cells contained at least 700 to 800 distinct mRNA species, mainly belonging to the class of low abundance, which appeared to be absent in L6 cells. Most of these mRNA species were also found with a lower frequency in M4 cells. Bidimensional analysis of the cell-free translation products directed by polyadenylic acid-containing mRNA revealed some remarkable differences, in particular the synthesis in a RMS4 cell extract of at least three major polypeptides, possibly related either to the neoplastic process itself or to the stage of malignant transformation.

Animals↗
PubMed1997

Mutational activation of pp60(c-src) leads to a tumorigenic phenotype in a preneoplastic Syrian hamster embryo cell line.

Previous studies indicated that overexpression of wild-type avian c-src cannot induce neoplastic transformation of NIH 3T3 cells. In this study, we isolated and characterized novel spontaneously derived transforming mutants of avian pp60(c-src) from a Syrian hamster embryo-derived cell line, 10W, transfected with the avian c-src gene. Seventeen independently derived transfected 10W cell clones were injected into athymic nude mice. After a latency period, tumors eventually arose and were established in culture. The tumorigenic phenotype was always accompanied by the presence of the avian c-src DNA and functional expression of pp60(c-src). However, most of the tumor-derived cell lines expressed an electrophoretically altered form of pp60(c-src), suggesting mutations in src. Consistent with this hypothesis, DNAs isolated from the tumor-derived lines, but not the parental 10W cell lines, morphologically transformed NIH 3T3 cells in a focus-forming assay. We characterized pp60(c-src) in detail from three of the tumor-derived lines: 4AT, 4BT, and E2T. Two of these lines contained mutations within the exogenous c-src coding region. Line 4AT has an internal repeat of 29 amino acids immediately following Gln-513, which disrupts the spacing between the end of the kinase domain and Tyr-527, the negative regulatory site in pp60(c-src). Line 4BT has a 5-bp deletion following Phe-520, which results in loss of Tyr-527. However, the DNA sequence of the coding region of pp60(c-src) from a third line, E2T, was completely wild type. Cyanogen bromide cleavage analyses of the altered pp60(c-src) from lines 4AT and 4BT showed that Tyr-527, the site of negative regulation of c-src, is not phosphorylated, but Tyr-416, the site of in vitro autophosphorylation, is phosphorylated. However, in line E2T, Tyr-527 was phosphorylated, and Tyr-416 was phosphorylated to a lesser extent. Additionally, two proteins that indicate activation of src, p85 cortactin and p120(cas), are phosphorylated in at least six of the tumor-derived cell lines, although to a lesser extent in line E2T. These results suggest that dephosphorylation of Tyr-527 and phosphorylation of Tyr-416 correlate with activation of pp60(c-src) in the tumor-derived lines 4AT and 4BT, respectively. However, in line E2T, the high levels of pp60(c-src), in combination with a partial activation of the pp60(c-src) protein as indicated by phosphorylation of Tyr-416, appear to be involved in the neoplastic process, rather than mutation.

3T3 Cells↗
PubMed2004

Mechanisms and effectors of MIF-dependent promotion of tumourigenesis.

The importance of secreted cytokines and growth factors in the development and promotion of malignancies is often underestimated. Many different soluble, extracellular gene products participate in processes that collectively contribute to the growth and survival of a developing neoplasm. These secreted molecules can, directly or indirectly, play a central role in uncontrolled tumour cell division, angiogenic stimulation or suppression of tumour cell immune surveillance. One of the first cytokine activities ever described, macrophage migration inhibitory factor (MIF), is unique to these soluble mediators in that it participates in all of these pro-tumourigenic processes. Overexpressed in most tumour types examined, MIF has been shown to promote malignant cell transformation, inhibit tumour cell-specific immune cytolytic responses and strongly enhance neovascularization. Despite this broad array of activities, the elucidation of molecular and cellular mechanisms involved in MIF-dependent bioactions has remained elusive. This review will focus on recently characterized phenotypes and mechanistic effectors thought to be associated with MIF-dependent promotion of neoplastic processes and discuss their relative importance in carcinogenesis.

Animals↗
PubMed1997

Orbital compression syndrome in sickle cell disease.

BACKGROUND: Orbital complications are an uncommonly reported finding in sickle cell disease. METHODS: The authors review the reported orbital manifestations of sickle cell disease and discuss a patient with hemoglobin sickle beta(0) thalassemia in whom rapidly progressive bilateral orbital compression developed. RESULTS: Computed tomography of the orbits in a patient with fever, headache, orbital swelling, and optic nerve dysfunction displayed bilateral superior subperiosteal cystic masses. Surgical exploration showed bilateral liquefied hematomas, which were evacuated. Recovery was complete 13 days after surgery. A mild recurrence 14 months later resolved with conservative treatment. The literature contains 11 reports of 16 young patients with sickle cell disease (15 sickle cell disease [Hb SS] and 1 hemoglobin sickle cell disease [Hb SC]) with rapidly developing findings ranging from frontal headache, fever, and eyelid edema to bilateral complete orbital compression syndrome. Including our patient, 60% had orbital hemorrhage on computed tomography. Ten of 12 patients tested were found to have orbital bone marrow infarctions. Sixteen of 17 patients had complete recovery; 13 were treated conservatively and 4 surgically. Only 2 of 17 had recurrence. CONCLUSIONS: Orbital complications in sickle cell disease are unusual manifestations in which a vaso-occlusive process in the marrow space around the orbit results in frontal headache, fever, eyelid edema, and often orbital compression syndrome. Subperiosteal hematomas are common and appear to result from bone marrow infarctions. Appropriate management requires a thorough evaluation to exclude other hemorrhagic, infectious or neoplastic processes, as well as vigilant ophthalmic monitoring. Supportive care is effective, unless optic nerve dysfunction or large hematomas are present, which would indicate that surgical evacuation is warranted to prevent loss of vision and to speed recovery.

Anemia, Sickle Cell↗
PubMed2001

Bizarre epithelial atypia of the sinonasal tract after chemotherapy.

Certain chemotherapeutic agents can induce bizarre epithelial atypia. The lower respiratory tract is a frequently targeted site, but similar changes have not been described adequately in the sinonasal tract. Unfamiliarity with these changes could potentially cause confusion with an infectious or neoplastic process. All biopsies of the sinonasal tract at The Johns Hopkins Hospital were reviewed prospectively over a 54-month period. Eleven cases with bizarre atypia of the respiratory epithelium formed the basis of this study. The medical records of these patients were reviewed. The specimens were from 11 patients who had previously undergone chemotherapy and bone marrow transplantation for acute myelocytic leukemia (n = 5), multiple myeloma (n = 3), acute lymphocytic leukemia (n = 2), and chronic myelocytic leukemia (n = 1). Although the chemotherapy regimens were highly variable, all included one or more of the alkylating agents (cyclophosphamide, n = 11; busulfan, n = 5; melphalan, n = 1). In all 11 patients, biopsies were acquired to rule out invasive fungal sinusitis. The atypical epithelial changes included striking nuclear enlargement, hyperchromasia, and pleomorphism. Sometimes these changes were full thickness and were associated with squamous metaplasia. Two of eight cases evaluated by frozen section were misinterpreted initially as high-grade epithelial dysplasia. Certain chemotherapeutic agents can induce striking epithelial atypia in the sinonasal tract. These changes should not be interpreted as neoplastic in nature, a potential pitfall in the frozen section evaluation of a destructive nasal process in oncology patients.

Adolescent↗
PubMed1984

Expression of normal and tumor-associated antigens in human breast carcinoma.

The expression of six cytoplasmic/membrane antigens (beta 2-microglobulin, HLA, HLA-DR, carcinoembryonic antigen, and two breast tumor-associated antigens (TAAs), B6.2 and B72.3) was investigated in serial sections of 28 human breast carcinomas using monoclonal antibodies and the avidin-biotin complex immunoperoxidase technique. The frequency of expression and linkage between these antigens was determined, and antigenic expression was related to patient age, morphologic differentiation, cytologic grade, and estrogen receptor/progesterone receptor content of the tumor. The expression of beta 2-microglobulin and HLA correlated with morphologic differentiation, well-differentiated and moderately well-differentiated tumors expressing these antigens more often than poorly differentiated tumors. Expression of the TAAs, however, was not related to differentiation. There was no linkage between beta 2-microglobulin/HLA and the TAAs. Carcinoembryonic antigen was found to be linked to the TAA, B6.2. Expression of the TAA, B72.3, correlated with patient age. Eighty percent (23 of 28) of the tumors were positive for carcinoembryonic antigen or at least one of the TAAs. The estrogen receptor/progesterone receptor status of the tumor was not statistically related to the expression of any of the antigens studied. Analysis of tumor antigen profiles may provide important information relevant to prognosis, therapy, and early detection of cancer, as well as insights into the nature of the neoplastic process.

Adult↗
PubMed1983

[Role of exogenous and endogenous factors in the etiology of human tumors].

The factors of major importance in the development of human tumors: exogenous chemical carcinogens, endogenous carcinogens, hormones, radiation, immunity disorders, heredity, nutrition, harmful habits are analysed on the basis of epidemiological and experimental evidence. Close interaction of exogenous and endogenous factors in the process of tumor development is demonstrated. Occupational carcinogens affecting at high doses small human contingents are frequently the major etiological cause of tumor development. In the general population exposed to the effect of quite low doses of carcinogens the latter are probably only initiators of neoplastic process completed by specific and nonspecific stimulators of carcinogenesis (cocarcinogens, promoters). The mechanisms of action of modifying factors on carcinogenesis (the effect of carcinogens on endogenous synthesis and metabolism, their interaction with cell macromolecules, tumor growth) are discussed.

Air Pollutants, Occupational↗