Class III β‐Tubulin isotype (β III) in the adrenal medulla: II. Localization in primary human pheochromocytomas

Karkavelas, George; Katsetos, Christos D.; Geddes, J. F.; Herman, Mary M.; Vinores, Stanley A.; Cooper, Harry S.; Provencio, J. Javier; Frankfurter, Anthony

doi:10.1002/(sici)1097-0185(199803)250:3<344::aid-ar9>3.0.co;2-#

Cited by 10 publications

(9 citation statements)

References 28 publications

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“…They are mostly, but not invariably, innocuous neoplasms characterized by an excessive catecholamine secretion producing the clinical syndrome of paroxysmal hypertension [reviewed in Karkavelas et al, 1998]. Increased ␤III expression is present in these tumors but its distribution is heterogeneous, closely resembling that observed in the normal adrenal medulla [Katsetos et al, 1998a].…”

Section: Class III ␤-Tubulin In Adrenal Pheochromocytomasmentioning

confidence: 99%

“…Tumor cells expressing ␤III have a tendency to acquire a neuronal morphology and to elaborate neurites. ␤III is absent in the stromal sustentacular cells [Karkavelas et al, 1998]. Studies on the PC12 rat pheochromocytoma cell line with or without treatment with differentiation-promoting agents have shown the presence of ␤III in both immature (neuroblast-like) and neuronally differentiating cells [Asai and Remolona, 1989;Katsetos et al, 1998b].…”

Section: Class III ␤-Tubulin In Adrenal Pheochromocytomasmentioning

confidence: 99%

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Class III β‐tubulin in human development and cancer

Katsetos

Herman²,

Mörk

2003

Cell Motil. Cytoskeleton

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The differential cellular expression of class III ␤-tubulin isotype (␤III) is reviewed in the context of human embryological development and neoplasia. As compared to somatic organs and tissues, ␤III is abundant in the central and peripheral nervous systems (CNS and PNS) where it is prominently expressed during fetal and postnatal development. As exemplified in cerebellar and sympathoadrenal neurogenesis, the distribution of ␤III is neuron-associated, exhibiting distinct temporospatial gradients according to the regional neuroepithelia of origin. However, transient expression of this protein is also present in the subventricular zones of the CNS comprising putative neuronal-and/or glial precursor cells, as well as in Kulchitsky neuroendocrine cells of the fetal respiratory epithelium. This temporally restricted, potentially non-neuronal expression may have implications in the identification of presumptive neurons derived from embryonic stem cells. In adult tissues, the distribution of ␤III is almost exclusively neuron-specific. Altered patterns of expression are noted in cancer. In "embryonal"-and "adult-type" neuronal tumors of the CNS and PNS, ␤III is associated with neuronal differen- Abbreviations: bHLH, basic helix-loop-helix; ␤III, class III ␤-tubulin isotype, CNE , central nervous system enhancer; CNS, central nervous system; EGL, external granule layer; MAP, microtubule-associated protein; NCAM, neural cell adhesion molecule; OPC, oligodendrocyte precursor cell; PCNA, proliferating cell nuclear antigen; PNS, peripheral nervous system; pRb, retinoblastoma tumor suppressor protein; PSA, polysialated; SVZ, subventricular zone; WHO, World Health Organization. tiation and decreased cell proliferation. In contrast, the presence of ␤III in gliomas and lung cancer is associated with an ascending histological grade of malignancy. Thus, ␤III expression in neuronal tumors is differentiation-dependent, while in non-neuronal tumors it is aberrant and/or represents "dedifferentiation" associated with the acquisition of progenitor-like phenotypic properties. Increased expression in various epithelial cancer cell lines is associated with chemoresistance to taxanes. Because ␤III is present in subpopulations of neoplastic, but not in normal differentiated glial or somatic epithelial cells, the elucidation of mechanisms responsible for the altered expression of this isotype may provide insights into the role of the microtubule cytoskeleton in tumorigenesis and tumor progression. Cell Motil. Cytoskeleton 55: 77-96, 2003.

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Section: Class III ␤-Tubulin In Adrenal Pheochromocytomasmentioning

confidence: 99%

Section: Class III ␤-Tubulin In Adrenal Pheochromocytomasmentioning

confidence: 99%

Class III β‐tubulin in human development and cancer

Katsetos

Herman²,

Mörk

2003

Cell Motil. Cytoskeleton

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257

188

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“…Whereas, peripherin is a type III neuron-specific intermediate filament protein abounding in the neural crestderived element of the peripheral nervous system. Because ß-tubulin and peripherin are expressed in human neuroectodermal and neural crest-derived neoplasms (11,14,18), we considered important to examine the expression of these neuron-associated proteins in rat pheochromocytomas and ganglioneuromas originating in the adrenal medulla.…”

Section: Discussionmentioning

confidence: 99%

“…Some authors (2) suggested that Schwann cells in neuroblastomas and ganglioneuromas are of reactive origin rather than neoplastic; therefore, it seems that the neuronal cells are the transformed phenotypes and the glial cells are the reactive or stromal cells that may, however, contribute to the process of neuronal differentiation. Neuronal-glial interactions have been observed in the differentiation of primary human adrenal neuroblastomas, ganglioneuroblastomas, and ganglioneuromas (16), as well as in primary pheochromocytomas originating in the adrenal medulla (14).…”

Section: Discussionmentioning

confidence: 99%

Pheochromocytomas and Ganglioneuromas in the Aging Rats: Morphological and Immunohistochemical Characterization

Pace

Perentes

Germann

2002

Toxicologic Pathology

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We investigated, morphologically and immunohistochemically, 74 medullary adrenal tumors, including 64 pheochromocytomas (14 malignant and 50 benign), 9 ganglioneuromas, and 1 malignant schwannoma. The tumors were detected in 2-year-old Wistar and Sprague-Dawley rats from carcinogenicity studies. Morphologically, benign pheochromocytomas were characterized by monomorphic, small, basophilic cells with almost absence of mitoses. Malignant pheochromocytomas presented a low grade of pleomorphism, higher rate of mitoses, necrosis, infiltrative growth and in 1 case metastases in the lung. Ganglioneuromas were characterized by ganglion and neuron-like cells embedded in an eosinophilic matrix containing neurites, Schwann cells, and scant fibrovascular elements. All pheochromocytomas were strongly immunoreactive for tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine synthesis. Subpopulations of chromaffin cells expressed chromogranin A (CGA) positivity. Matrix and Schwann cells were positive for S-100 and for glial fibrillary acidic protein (GFAP). In focal areas of the tumors, ganglion cells and axons were positive for neurofilament proteins (NFP) and synaptophysin. Ganglion cells exhibited peripherin and ß-tubulin. Proliferative activity of the tumors was assessed by immunostaining the endogenous cell proliferation associated-antigen Ki-67 and the proliferating cell nuclear antigen (PCNA). As expected, cell proliferation indeces were much higher in malignant pheochromocytomas than in benign, yet ganglioneuromas remained immunonegative. Considering that Ki-67 antigen is more specific for cell proliferation, it should be regarded as marker of choice for supporting the differential diagnosis between benign and malignant pheochromocytomas.

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“…ß III expression is observed throughout the lifetime from early development in the central and peripheral nervous systems and in some nerve tumors, such as high-grade gliomas (9), oligodendrogliomas (10), medulloblastomas (11), retinoblastomas (12), and pheochromocytomas (13). ß III expression was also shown in the non-neuronal tissues and their tumors, for example: fetal Kulchitsky cells, which are neuroendocrine cells of the lung; neuroendocrine cell tumors of the lung, such as small cell carcinomas, large cell neuroendocrine cell carcinomas and some of atypical carcinoid tumors (14); certain gastrointestinal carcinoid tumors (15); and various lung carcinomas, especially adenocarcinomas (14).…”

Section: Introductionmentioning

confidence: 99%

Aberrant expression of class III β-tubulin in basal cell carcinoma of the skin

Ishida

Kushima²,

Okabe³

2009

Oncol Rep

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Abstract. Tubulin is a major component of microtubules. Class III ß-tubulin (ß III) is a neuron-associated ß-tubulin isotype and expressed in the normal central and peripheral nervous systems. According to a previous study, ß III is not expressed in normal skin and squamous cell carcinoma. However, its expression has not been examined in basal cell carcinoma (BCC) of the skin. Expression of ß III was analyzed together with neural cell adhesion molecule (NCAM), chromogranin A, synaptophysin, epithelial membrane antigen (EMA) and cytokeratin (CK) 20 by immunohistochemical methods in 10 non-neoplastic skin tissues and 50 BCCs. In the normal skin, immunoreactivity to ß III was restricted to the nerve bundles in the dermis and subcutis, no positivity was shown in epithelial cells of the epidermis and skin appendages. ß III and NCAM were expressed in 50 and 68% of BCCs, respectively, predominantly periphery of tumor nests, although the distribution of both markers was not always identical. Chromogranin A, synaptophysin and CK 20 were not expressed in any of BCCs. EMA was focally expressed in only 8% of BCCs. ß III is a potential candidate for inclusion to the panel of immunohistochemical markers to distinguish small BCCs from non-neoplastic hair buds, because non-neoplastic hair follicles are not positive for ß III.

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Class III β‐Tubulin isotype (β III) in the adrenal medulla: II. Localization in primary human pheochromocytomas

Cited by 10 publications

References 28 publications

Class III β‐tubulin in human development and cancer

Class III β‐tubulin in human development and cancer

Pheochromocytomas and Ganglioneuromas in the Aging Rats: Morphological and Immunohistochemical Characterization

Aberrant expression of class III β-tubulin in basal cell carcinoma of the skin

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