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PubMed2003

Immunohistochemical markers of melanocytic tumors.

While historically detection of premelanosomes by electron microscopic studies was the only means possible of confirming melanocytic lineage of a neoplastic process, advances in the field of immunohistochemistry have allowed for accurate and reliable diagnosis using antibodies to 1 of a number of melanocyte-restricted proteins. S-100 was the first such marker exploited by immunohistochemistry; subsequently, the HMB45 monoclonal antibody to gp100 became widely used as a sensitive and specific melanocytic marker. More recently, antibodies to other melanocytic proteins have become available, inciuding the MART-1 gene product and microphthalmia transcription factor. This article provides a brief overview of these markers in terms of their specificity and sensitivity and offers a discussion of tumors with partial melanocytic differentiation.

Biomarkers, Tumor↗

PubMed2004

Interferons and interferon inhibitory activity in disease and therapy.

Interferon (IFN) resistance is an important factor in the pathophysiology of neoplastic disorders, certain viral infections (e.g., AIDS), and autoimmune diseases (e.g., lupus erythematosus and Wegner's granulomatosis). In addition, in some of these disorders, there is also decreased ability to produce IFNs. The capacity of viruses and neoplastic processes to interfere with the IFN system are thought to represent a "virus-against-host" or "cancer-against-host" defense mechanism. Four resistance factors have been identified: 1) release of free IFN-alpha/beta type 1 receptors into the circulation that, at appropriate concentrations, capture and inactivate IFNs; 2) a new IFN inhibitory protein has been isolated and its chemical structure is under study; 3) prostaglandin E2, which is produced by certain tumor cells, inhibits IFN production; and 4) high levels of cAMP phosphodiesterases present, for example in certain tumor cells, reduces cAMP, an important second messenger in IFN synthesis. Studies are under way to reverse these inhibitory effects and to increase endogenous interferon production.

Acquired Immunodeficiency Syndrome↗

PubMed2004

alpha1-antitrypsin and its C-terminal fragment attenuate effects of degranulated neutrophil-conditioned medium on lung cancer HCC cells, in vitro.

BACKGROUND: Tumor microenvironment, which is largely affected by inflammatory cells, is a crucial participant in the neoplastic process through promotion of cell proliferation, survival and migration. We measured the effects of polymorphonuclear neutrophil (PMN) conditioned medium alone, and supplemented with serine proteinase inhibitor alpha-1 antitrypsin (AAT) or its C-terminal fragment (C-36 peptide), on cultured lung cancer cells. METHODS: Lung cancer HCC cells were grown in a regular medium or in a PMN-conditioned medium in the presence or absence of AAT (0.5 mg/ml) or its C-36 peptide (0.06 mg/ml) for 24 h. Cell proliferation, invasiveness and release of IL-8 and VEGF were analyzed by [3H]-thymidine incorporation, Matrigel invasion and ELISA methods, respectively. RESULTS: Cells exposed to PMN-conditioned medium show decreased proliferation and IL-8 release by 3.9-fold, p < 0.001 and 1.3-fold, p < 0.05, respectively, and increased invasiveness by 2-fold (p < 0.001) compared to non-treated controls. In the presence of AAT, PMN-conditioned medium loses its effects on cell proliferation, invasiveness and IL-8 release, whereas VEGF is up-regulated by 3.7-fold (p < 0.001) compared to controls. Similarly, C-36 peptide abolishes the effects of PMN-conditioned medium on cell invasiveness, but does not alter its effects on cell proliferation, IL-8 and VEGF release. Direct HCC cell exposure to AAT enhances VEGF, but inhibits IL-8 release by 1.7-fold (p < 0.001) and 1.4-fold (p < 0.01) respectively, and reduces proliferation 2.5-fold (p < 0.01). In contrast, C-36 peptide alone did not affect these parameters, but inhibited cell invasiveness by 51.4% (p < 0.001), when compared with non-treated controls. CONCLUSIONS: Our data provide evidence that neutrophil derived factors decrease lung cancer HCC cell proliferation and IL-8 release, but increase cell invasiveness. These effects were found to be modulated by exogenously present serine proteinase inhibitor, AAT, and its C-terminal fragment, which points to a complexity of the relationships between tumor cell biological activities and local microenvironment.

Journal Article↗

PubMed2004

Venous thromboembolism in patients with cancer. Part I. Survey of oncology nurses' attitudes and treatment practices for ambulatory settings.

Patients with cancer have a higher incidence of venous thromboembolism (VTE). Little information currently exists on VTE and the understanding and beliefs of oncology nurses. Therefore, the attitudes and treatment practices of ambulatory oncology nurses were surveyed to determine the current knowledge base of VTE in patients with cancer. Survey results are presented along with a thorough literature review of thromboembolism and the unique risk factors for this frequent complication in patients with cancer. The causes of VTE in this patient population often are multifactorial and include hypercoagulability, stasis, and vascular endothelial damage from procedures or the neoplastic process itself. In particular, chemotherapy administration can increase the risk of thrombosis considerably. New therapies, including thalidomide, require oncology nurses caring for these patients to have heightened awareness of the potential for thrombogenic complications. This is the first of two articles that address the problem of thromboembolism in patients with cancer, including the survey results. (See part II on page 465.) Oncology nurses are essential in the care of VTE in patients with cancer and can help with patient identification, treatment, and compliance for improved patient outcomes.

Ambulatory Care↗

PubMed1991

Herpes simplex virus infection in the immunocompromised cancer patient.

The development of infection remains a significant source of morbidity and mortality in the oncology patient. This patient population is at increased risk for infection because of alterations in cell-mediated immunity generated by the underlying neoplastic process and/or immunosuppressive therapy. Viral infection, particularly that attributable to herpes simplex virus (HSV), is being seen with increased frequency in the oncology patient. Because effective therapy is available with the early use of antiviral agents, it is important to be aware of the potential for viral infection and to recognize the signs and symptoms that are evident early in its course. An overview of HSV infection is provided here, including discussion of the virus itself, its pathogenesis, its clinical spectrum, and current prophylactic and therapeutic approaches.

Herpes Simplex↗

PubMed2005

Cardiotoxicity of cancer therapy.

Because cancer is a leading cause of mortality in the United States, the number of therapeutic modalities available for the treatment of neoplastic processes has increased. This has resulted in a large number of patients being exposed to a wide variety of cancer therapy. Historically, it has been well recognized that antineoplastic agents may have adverse effects on multiple organs and normal tissues. The most commonly associated toxicities occur in tissues composed of rapidly dividing cells and may spontaneously reverse with minimal long-term toxicity. However, the myocardium consists of cells that have limited regenerative capability, which may render the heart susceptible to permanent or transient adverse effects from chemotherapeutic agents. Such toxicity encompasses a heterogeneous group of disorders, ranging from relatively benign arrhythmias to potentially lethal conditions such as myocardial ischemia/infarction and cardiomyopathy. In some instances, the pathogenesis of these toxic effects has been elucidated, whereas in others the precise etiology remains unknown. We review herein the various syndromes of cardiac toxicity that are reported to be associated with antineoplastic agents and discuss their putative mechanisms and treatment.

Antineoplastic Agents↗

PubMed2000

A protective role of dietary vitamin D3 in rat colon carcinogenesis.

The aim of the present work was to gain insight into a putative anticancer effect of dietary vitamin D3 (cholecalciferol) in a rat model of colon carcinogenesis. Male rats were assigned to three different dietary groups. The dietary regimens were based on a standard murine-defined diet (AIN-76A) or a stress diet containing 20% fat, reduced Ca2+ concentration, a high phosphorus-to-Ca2+ ratio, and either low or high vitamin D3 content. Colorectal cancer was induced by administration of the procarcinogen 1,2-dimethylhydrazine (DMH). Blood Ca2+, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], and 25-hydroxyvitamin D3 [25(OH)D3] levels were measured in DMH-treated rats and in respective weight- and age-matched dietary control groups. Colonic epithelial proliferation was assessed by determining thymidine kinase (TK) activity, bromodeoxyuridine (BrdUrd) incorporation into crypt cell DNA, and the mean labeling index along the colonic crypt continuum. Maintenance of rats on the stress diet either unmodified or supplemented with vitamin D3 in the absence of carcinogen treatment provoked a time-dependent rise in colonic TK activity and hyperproliferation of colonic epithelium. DMH treatment of rats maintained on the standard diet caused a marked increase in the proliferative indexes of colonic epithelium and in expansion of the crypt proliferative compartment. TK activity and the crypt mitotic zone were significantly augmented in the animal group fed the stress diet. Supplementary vitamin D3 abrogated the stress diet-enhanced colonic responses to the carcinogenic insult. Colon tumor multiplicity was fourfold higher in animals fed the stress diet than in animals maintained on a standard diet. The marked rise in colonic tumor multiplicity and adenocarcinoma incidence in rats fed the stress diet was obliterated by supplemental dietary vitamin D3. Cumulatively, the present results indicate that dietary vitamin D3 impedes the neoplastic process in murine large intestine and strengthen the view that inappropriate changes in dietary components and micronutrients are contributory determinants of colorectal cancer.

1,2-Dimethylhydrazine↗

PubMed2000

Suppression of azoxymethane-induced preneoplastic lesions and inhibition of cyclooxygenase-2 activity in the colonic mucosa of rats drinking a crude green tea extract.

We determined the effects of a crude green tea extract given as drinking fluid on the promotion/progression phase of colon carcinogenesis in rats after induction of the neoplastic process by azoxymethane. Adult Wistar rats were given azoxymethane (15 mg/kg i.p.) once a week for two weeks. One week after the second injection, the rats were randomly divided into two groups. One group (n = 8) received daily prepared aqueous solutions of green tea extracts (GTE; 0.02%, wt/vol); the control group (n = 8) received tap water. After six weeks, rats receiving GTE showed a 60% reduction in the number of colonic preneoplastic lesions (aberrant crypts). The number of individual crypts per aberrant crypt focus (crypt multiplicity) was significantly reduced in the GTE group; the majority (80%) of the remaining aberrant foci contained only one or two preneoplastic crypts. A significant and selective decrease of cyclooxygenase (COX)-2 activity was observed in the colon of rats receiving GTE (23 +/- 3 vs. 117 +/- 30 mU/mg protein in controls), whereas COX-1 showed no alterations. Our data demonstrate that GTE reduces COX-2 and suppresses the formation of colonic preneoplastic lesions. They provide new insights into the mechanism of chemopreventive and anti-inflammatory properties of green tea.

Animals↗

PubMed2004

The epidermal growth factor-like growth factor amphiregulin is strongly induced by the adenosine 3',5'-monophosphate pathway in various cell types.

We examined the cAMP-mediated regulation of the epidermal growth factor-like growth factor amphiregulin (AR) in T cells and observed a strong cAMP-induced up-regulation of AR mRNA in a time- and concentration-dependent manner independent of T cell activation. This regulation may be mediated in part through activation of a cAMP-responsive element in the AR promoter, because the cAMP-responsive element conferred cAMP responsiveness to a luciferase reporter in Jurkat TAg cells. Similar effects of AR mRNA induction were seen in T cells treated with cAMP-elevating agents such as prostaglandin E(2) and forskolin as well as with the phosphodiesterase inhibitors rolipram and isobutylmethylxanthine. Furthermore, the induction of AR mRNA by cAMP was strongly suppressed by a protein kinase A type I-selective inhibitor, whereas treatment with an exchange protein directly activated by cAMP-specific agonist did not increase AR levels. In addition, an increase in AR gene transcripts by cAMP was seen in MCF-7 mammary carcinoma cells and H295R adrenal cells. Moreover, the potent cAMP-mediated induction of AR mRNA resulted in increased secretion (5-fold) of AR from T cells. Furthermore, supernatants from cAMP-stimulated T cells containing secreted AR induced phosphorylated MAPK in OVCAR-3 carcinoma cells. In conclusion, our data suggest that AR is under strong regulation by the cAMP pathway in various cell types, and that prostaglandin E(2)- and cAMP-induced AR secretion from T cells may be highly relevant in a microenvironment consisting of tumor cells and infiltrated immune cells, because AR by activating the MAPK pathway through a paracrine route may contribute to proliferation of tumor cells and thus add to neoplastic processes.

Adenylyl Cyclases↗

PubMed2002

Galectin-3 messenger ribonucleic acid and protein are expressed in benign thyroid tumors.

Galectin-3 is a protein of the lectin family that has been associated with neoplastic processes in various tissues. In the thyroid, expression of this protein has been described in differentiated follicular cancer, suggesting that the immunohistochemical study of galectin-3 may be a potential marker of malignancy in thyroid neoplasms. The confirmation of these results may represent an extremely useful tool for presurgical diagnosis and medical conduct. In this study, galectin-3 protein and mRNA expression were analyzed in the thyroid tissues from 87 patients with histomorphological diagnosis of multinodular goiter (MNG) (n = 24), follicular adenoma (n = 31), follicular carcinoma (n = 20), papillary carcinoma (n = 12), and five normal tissues. Galectin-3 protein expression was detected by immunohistochemical method in light, fluorescence, and confocal microscopy, using monoclonal antibody. Galectin-3 mRNA expression was detected by the RT-PCR method. Our results showed that the majority of carcinomas expressed galectin-3 protein (follicular, 90%; papillary, 100%). However, in contrast to the previously published data, benign lesions also expressed galectin-3 (adenoma, 45%; MNG, 17%). We further demonstrated by RT-PCR that thyroid tissues with diagnosis of adenoma and MNG-expressed galectin-3 mRNA. Although the galectin-3 immunostaining demonstrated a sensitivity of 93.8% in the identification of cancer, the accuracy in the distinction between benign and malignant tissues was 77.0%. This accuracy was even lower (68.6%) when the galectin-3 expression in follicular adenoma was compared with follicular carcinoma. Thus, the use of galectin-3 immunodetection as a molecular marker for thyroid carcinoma must be interpreted with caution, particularly in the differentiation between thyroid follicular carcinoma and follicular adenoma.

Adenocarcinoma, Follicular↗

PubMed2004

Cytoplasmic expression of fibroblast growth factor receptor-4 in human pituitary adenomas: relation to tumor type, size, proliferation, and invasiveness.

The pathogenesis of pituitary adenomas remains unknown. A pituitary tumor-derived (ptd) isoform of fibroblast growth factor receptor-4 (ptd-FGFR4) has been implicated in the neoplastic process. To further understand the expression of FGFR4 in sporadic human pituitary adenomas, we studied 137 pituitary adenomas of various types (102 adenomas from Japanese patients and 35 adenomas from Canadian patients) and 10 nontumorous pituitaries using a polyclonal antiserum that recognizes the C terminus of FGFR4 and analyzed possible relationships among expression of FGFR4, patient nationality, tumor type, size, invasion, and the labeling index of the proliferation marker Ki-67 using the MIB-1 antibody. Cytoplasmic expression of FGFR4 protein was observed in 57.8% of Japanese cases and 62.8% of Canadian cases. FGFR4 reactivity was absent in all 10 normal adenohypophysial tissues examined. FGFR4 expression in pituitary adenomas was restricted mainly to the cytoplasm, a pattern similar to that seen in rat pituitary cells transfected with human ptd-FGFR4 but different from that of cells transfected with wild-type FGFR4, which displayed membrane localization of staining. Protein from primary human adenomas migrated as a 65-kDa species consistent with the predicted size of ptd-FGFR4. FGFR4 protein expression was frequently found in adenomas containing GH, ACTH, or FSH/LH and was also found in null cell adenomas, but reactivity was relatively rare in prolactin-containing adenomas in both Japanese and Canadian groups. The expression of FGFR4 protein was stronger in macroadenomas than in microadenomas (P = 0.02) and high levels of FGFR4 expression (moderate or greater density staining) were more frequently observed in macroadenomas than in microadenomas (P < 0.05). High levels of FGFR4 expression also correlated significantly with the proliferation marker Ki-67 (P = 0.002) and tended (but not significantly) to be found in invasive tumors. These data are consistent with a role for ptd-FGFR4 in pituitary tumorigenesis in a majority of human pituitary adenomas. Moreover, detection of FGFR4 cytoplasmic staining may provide an ancillary diagnostic tool in the diagnosis of pituitary adenoma, particularly in equivocal cases.

Adenoma↗

PubMed1983

Xanthogranuloma of the dura in systemic Weber-Christian disease.

A 51-year-old woman who had systemic Weber-Christian disease (WCD) displayed multiple xanthomatous lesions and a large xanthogranuloma of the tentorium cerebelli with signs of brainstem and cerebellar compression. Three other cases of dural xanthomatous lesions associated with systemic WCD have been reported. These dural and leptomeningeal xanthomatous lesions in WCD, a nonsuppurative inflammatory condition, are similar to those of Hand-Schüller-Christian disease, a quasi-neoplastic process.

Dura Mater↗

PubMed1988

Spontaneous remission of paraneoplastic ocular flutter and saccadic intrusions.

We report two women with ocular flutter and saccadic intrusions, documented by electro-oculography, who had complete spontaneous remission of their ocular motor findings prior to the appearance of a primary neoplastic process remote from the nervous system. Transient elevation of blood HVA and VMA levels was detected in one patient who subsequently had breast cancer. These cases indicate that spontaneous remission of saccadic oscillations does not necessarily imply a benign outcome. Patients with this ocular motor abnormality should be followed closely for signs of a remote neoplasm even if initial investigation is negative.

Adult↗

PubMed1990

Autonomic function and human immunodeficiency virus infection.

We compared autonomic function in 26 patients infected by the human immunodeficiency virus (HIV) (18 AIDS and 8 ARC) to 22 controls. A significant decline in autonomic function was present across groups. Autonomic dysfunction correlated strongly with signs of HIV-associated nervous system disease. We observed significant differences across groups in tests of heart rate variation (expiratory-inspiratory ratio, maximum minus minimum heart rate difference, and mean square successive difference), the mean arterial blood pressure fall to tilting, and the blood pressure response to isometric exercise. A trend of declining autonomic function from controls to AIDS was present in the 30:15 ratio, the Valsalva ration, the systolic blood pressure fall to standing and tilt, and the cold pressor test. We did not observe any correlation between autonomic dysfunction and individual neurologic signs, prior therapeutic agents, and concurrent HIV-associated inflammatory or neoplastic processes. This study provides support for the presence of autonomic dysfunction in association with HIV infection. Autonomic dysfunction occurs more frequently and with greater severity in patients with AIDS; however, it may be present in the early stages of HIV infection and appears to progress during the illness.

AIDS-Related Complex↗

PubMed1998

Neuropathy in diffuse infiltrative lymphocytosis syndrome: an HIV neuropathy, not a lymphoma.

OBJECTIVE: To determine whether CD8 lymphoid infiltrates in nerves of patients with HIV-associated diffuse infiltrative lymphocytosis syndrome (DILS) corresponds to a lymphomatous neoplastic process or to a proliferation of T cells reactional to HIV. BACKGROUND: DILS is characterized by persistent CD8 hyperlymphocytosis and multivisceral CD8 T-cell infiltration, which may affect peripheral nerves. METHODS: Presence of monoclonal T cells and HIV-1 proviral load were evaluated by polymerase chain reaction (PCR) techniques in frozen peripheral nerve samples from six patients with DILS neuropathy and 22 patients with other HIV-associated peripheral neuropathies, including mononeuritis multiplex (MM:6), inflammatory demyelinating polyneuropathies (IDP:6), distal sensory polyneuropathy (DSP:5), and toxic distal sensory polyneuropathy (TDSP:5). RESULTS: Five of six patients with DILS showed no detectable monoclonal T-cell clones in their nerves. Nerve proviral load in DILS (6.8 +/- 0.2 log/10(5) cells) was much higher than in MM (p < 0.008), IDP (p < 0.001), DSP (p < 0.001), and TDSP (p < 0.005). CONCLUSIONS: DILS neuropathy represents a separate entity among HIV-associated neuropathies. It is associated with massive HIV proviral load in nerve and must not be confused with a peripheral nerve T-cell lymphoma.

Biopsy↗

PubMed1998

The functional role of tumor suppressor genes in gliomas: clues for future therapeutic strategies.

The ability to transfer exogenous genes to cancer cells has yielded a wealth of information about the neoplastic processes that occur at molecular and cellular levels. Current research focuses on defining the biochemical factors that govern the interplay between cell growth and cell death in gliomas. The identification of tumor suppressor genes has greatly enhanced our understanding of the molecular mechanism of brain tumors. Accomplishing the transition from basic science to clinical practice is a major challenge for the future of brain tumor research. The concept of tumor suppressor genes is examined, with particular emphasis on the functional studies of the role of the p53, p16, Rb, and PTEN/MMAC1 genes in gliomas. Moreover, recent advances linking tumor suppressor genes, apoptosis, and cell-cycle control pathways in brain tumors are reviewed. The ability to detect mutations in tumor suppressor genes plays an important role in cancer diagnosis and prognosis. Perhaps of greatest significance has been the realization that tumor suppressor genes may provide novel targets for development of specific anticancer therapies for brain tumors.

Apoptosis↗

PubMed2001

Inflammatory pseudotumour involving the skull base and cervical spine.

Inflammatory pseudotumour (IPT) is an idiopathic condition characterized by sclerosing inflammation, which mimics a neoplastic process. IPT involving the skull base and cervical spine is distinctly rare and usually indistinguishable from aggressive neoplasms or infection. We report a case of IPT involving the skull base and cervical spine. Initially the patient complained of headache and hearing loss without other neurological dysfunction. Two cycles of oral systemic steroid therapy resulted in only partial responses. Low dose radiotherapy was followed by quadriparesis as the lesion infiltrated into the cervical vertebral bodies. Subsequently a second course of radiation was administered to the whole cervical spine. Marked improvement was observed clinically and radiologically; however, the patient gradually deteriorated and died of sepsis. Given the aggressive nature of disease and the complications related to the long-term treatment, we suggest that a more aggressive therapeutic approach is suitable in extensive IPT of the skull base.

Cervical Vertebrae↗

PubMed2003

Primary sinonasal non-Hodgkin's lymphoma masquerading as chronic rhinosinusitis: an issue of routine histopathological examination.

Primary non-Hodgkin's lymphoma (NHL) of the sinonasal tract is uncommon. Morphologically and radiographically, sinonasal lymphomas are difficult to distinguish from other malignant neoplasms or non-neoplastic processes. However, there is no general consensus about the need of routine histopathological examination for nasal polyps among otolaryngologists. We present a case of primary sinonasal NHL mimicking chronic rhinosinusitis and debate the issue of routine histopathological examination. We suggest that all tissues removed from the sinonasal tract during surgery must be submitted for histopathological examination. Failure to do so may miss diagnosis and delay appropriate treatment.

Diagnosis, Differential↗