Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and pathologic features of 43 dogs with neoplasia of the rostral cerebrum were reviewed. Primary brain tumors included meningioma, astrocytoma, neuroblastoma, oligodendroglioma, and ependymoma. Other tumors that secondarily affected these areas included solitary hemangiosarcoma, nasal neuroendocrine carcinoma, nasal cell adenocarcinoma, nasal squamous cell carcinoma, and nasal neurofibrosarcoma. Older dogs were usually affected (mean, 10 years), and meningioma was the most frequent tumor type. Thirty-one dogs (72% of total) had a late-onset (greater than 5 years of age) of either generalized seizures or behavior abnormalities, or both, with an initially normal neurologic examination. In these 31 dogs, a mean time of 78 days (range, 2 to 400 days) elapsed from the onset of seizures or behavior change to the detection of a persistently abnormal neurologic examination. In all 43 dogs, the time from the detection of neurologic deficits to death or euthanasia and necropsy ranged from 1 to 63 days (mean, 13 days). On the basis of this review, it appears that dogs with late-onset seizures or behavior change, or both, should be suspected of having tumors involving the rostral cerebrum, despite the absence of persistent neurologic deficits commonly associated with cerebral tumors. Further, the onset of abnormalities in the neurologic examination and the time of death seem to occur within predictable time periods.
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PMID:Clinical signs of tumors affecting the rostral cerebrum in 43 dogs. 322 60

The histologic characteristics of 29 nasal tumors previously diagnosed as neuroblastomas, unclassified carcinomas, or unclassified malignant neoplasms were reviewed. Electron microscopy was performed in 17. Nine tumors were neuroblastomas; six of these were classical neuroblastomas while the other three exhibited olfactory differentiation in addition to the classical neuroblastoma component. Areas of ganglioneuroblastoma were found in the metastasis of one of the three olfactory neuroblastomas. Twenty tumors were classified as neuroendocrine carcinoma because all showed a neuroendocrine pattern with remarkably uniform cells growing from benign glandular epithelium; membrane bound granules were present in the cytoplasm of cells of the ten cases in this group examined by electron microscopy. The mean age of the patients with neuroblastomas was 20 years; survival in this group was 75% at five and seven years, respectively, and 67% at ten years. Recurrences, metastasis, and death occurred within 3 years of diagnosis. There was a low percentage (25%) of multiple recurrences. The metastases were located in cervical lymph nodes, brain and spine. The mean age of the patients with neuroendocrine carcinoma was 50 years. Survival was 100% at five years, 88% at seven years, and 77% at ten years. Recurrences and metastasis in 70% of the cases occurred later than the third year. Multiple recurrences were present in 54% of the cases. The metastases affected lymph nodes, brain and spine in all cases except in one in which lungs and femur were involved. In the latter case adenocarcinoma was also present in addition to the neuroendocrine carcinoma. Three patients died, all more than five years from the time of diagnosis. No correlation was found between staging and prognosis in either group, except for Stage I disease.
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PMID:Neuroblastomas and neuroendocrine carcinomas of the nasal cavity: a proposed new classification. 713 32

Olfactory neuroblastoma is an uncommon tumour arising in the nasal cavity or paranasal sinuses. We report the management of nine cases treated with external beam radiotherapy subsequent to surgery, either attempted definitive removal or biopsy only. Recent refinements in pathological evaluation of these tumours are discussed. Seven cases were deemed classical olfactory neuroblastoma whilst two were classified as neuroendocrine carcinoma. The clinical features, radiotherapy technique and variable natural history are presented. Seven of eight patients treated radically were controlled locally, with a minimum follow-up of two years. Three patients developed cervical lymph node disease and three patients died of systemic metastatic disease. Suggestions are made as to which patients should have en-bloc resection rather than definitive radiotherapy.
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PMID:Olfactory neural tumours--the role of external beam radiotherapy. 894 73

The coexistence of pheochromocytoma and other tumor types in a single adrenal gland has been rarely documented. This type of pheochromocytoma is designated "composite" or "mixed," depending on whether the pheochromocytoma and the nonpheochromocytoma components show the same embryologic origin. The nonpheochromocytoma components reported in the composite pheochromocytoma include ganglioneuroma, ganglioneuroblastoma, neuroblastoma, and malignant schwannoma. The components found in the mixed pheochromocytoma include adrenal cortical neoplasms and spindle cell sarcoma. We report a unique case of composite pheochromocytoma in which the nonpheochromocytoma element is a neuroendocrine carcinoma. The histologic and the immunohistochemical profiles of the 2 distinct components of this tumor were typical for those of pheochromocytoma and neuroendocrine carcinoma. This dual differentiation was also supported by ultrastructural findings. This case not only broadens the morphologic spectrum of composite pheochromocytoma but also provides some additional insight into the histogenesis of this rare but fascinating type of tumor.
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PMID:Pheochromocytoma associated with neuroendocrine carcinoma. A new type of composite pheochromocytoma. 1058 35

Somatostatin (SS) and SS analogues inhibit the growth of various kinds of endocrine and exocrine cells via the SS receptor (SSTR). Carcinoid tumor is representative of the tumors treatable by SS analogues. We examined the expression of SSTR2A by immunohistochemical and in situ hybridization methods with a specific antibody against a synthesized 20-amino acid peptide of the COOH terminus of human SSTR2A and oligonucleotide probes in 62 endocrine tumors of various kinds: pancreatic endocrine tumor; carcinoid; neuroendocrine carcinoma; medullary thyroid carcinoma; pheochromocytoma; and small cell carcinoma of the lung, neuroblastoma, and ganglioneuroma. SSTR2A was expressed in 87% of these tumors and at both primary and metastatic sites. The immunohistochemical reactivity of SSTR2A was strong on the cell membrane and less intense in the cytoplasm of the tumor cells. SSTR2A mRNA was also detected in the tumor cells. The results indicate the usefulness of SSTR2A analogues for the treatment of neuroendocrine tumors, even metastatic ones: metastatic carcinoids, metastatic pheochromocytomas, tumors that adhered to large vessels, and neuroendocrine carcinomas.
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PMID:Immunohistochemical expression of somatostatin type 2A receptor in neuroendocrine tumors. 1058 62

The term "small round-cell tumor" describes a group of highly aggressive malignant tumors composed of relatively small and monotonous undifferentiated cells with high nuclear to cytoplasmic ratios. This group includes Ewing's sarcoma (ES), peripheral neuroepithelioma (aka, primitive neuroectodermal tumor or extraskeletal ES), peripheral neuroblastoma ("classic-type"), rhabdomyosarcoma, desmoplastic small round-cell tumor, lymphoma, leukemia, small-cell osteosarcoma, small-cell carcinoma (either undifferentiated or neuroendocrine), olfactory neuroblastoma, cutaneous neuroendocrine carcinoma (aka, Merkel-cell carcinoma), small-cell melanoma, and mesenchymal chondrosarcoma. Their clinical presentations often overlap, thus making a definitive diagnosis problematic in some cases. Yet, a clear understanding of their clinicopathologic features usually allows for a confident diagnosis, especially if immunohistochemistry is used. The following is a review of the immunohistochemistry of this small round-cell tumor group.
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PMID:Immunohistochemistry of small round-cell tumors. 1096 7

Tumors exhibiting neuroectodermal differentiation occur throughout the body, and the diverse tissues of the head and neck give rise to a wide assortment of these neoplasms. Neuroectodermal neoplasms may be divided into lesions showing primarily epithelial differentiation (Group I, neuroendocrine carcinomas) and a more diverse group (Group II) of nonepithelial neoplasms. This article reviews these neuroectodermal tumors of the head and neck with emphasis on the neuroendocrine carcinomas and their nomenclature. The author believes that with regard to Group I tumors, the older terminology of carcinoid, atypical carcinoid, and small cell carcinoma should be replaced by subclassifications of well-differentiated, moderately differentiated, and poorly differentiated neuroendocrine carcinoma. The latter category should be further subdivided into small cell and large cell variants. Neuroendocrine carcinomas, particularly the moderately differentiated subtype, are often underdiagnosed in the head and neck region. In the larynx, these tumors are the most common form of nonsquamous carcinoma. Poorly differentiated neuroendocrine carcinoma of small cell type is most common in the salivary glands but can occur elsewhere in the region. The large cell subtype of poorly differentiated neuroendocrine carcinoma has not been well documented in this region. However, the most likely candidate for this tumor category is the so-called sinonasal undifferentiated carcinoma. Group II tumors discussed include olfactory neuroblastoma, malignant melanoma, and Ewing's sarcoma. In addition, differential diagnostic problems related to Group I and II tumors are reviewed in detail. This article reviews and updates our understanding of neuroectodermal neoplasms arising in the head and neck. The focus is on tumors that exclusively involve this region or show a strong predilection to occur here.
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PMID:Neuroectodermal neoplasms of the head and neck with emphasis on neuroendocrine carcinomas. 1190 42

The current study disusses a new approach to the group of small round cell tumors (SRCTs) independently of their primary anatomical location. We perform this analysis supported mainly by morphological means and particularly with the help of immunohistochemistry and electron microscopy; the last of which continues to play a decisive role in their differential diagnosis. The microscopical similarity of many of these tumors often makes the diagnosis in routine histology extremely difficult, due to the varying degree of heterogeneity present, and may have important therapeutic and prognostic implications. Thus a correct final diagnosis is mandatory for the clinic. Within the group of tumors that express a dominant or occasional small round cell pattern "SRCT" (neoplasms of the Central Nervous System excluded) are included: Ewing's sarcoma and peripheral neuroectodermal tumor (Es/pPNET) comprising its varieties, neuroblastoma, desmoplastic small round cell tumor, rhabdomyosarcoma, alveolar, solid and embryonal, small cell osteosarcoma, chondrosarcoma, myxoid and mesenchymal, round cell and myxoid liposarcoma, synovial sarcoma (monophasic undiffentiated), primitive malignant peripheral nerve sheath tumor (malignant small cell schwannoma), malignant non-Hogdkin lymphoma, Merkel cell tumor of the skin (small cell carcinoma including neuroendocrine carcinoma). This study discusses in each case not only the histology, supported by immunohistochemistry, but also the main ultrastructural characteristics. We are conscious that in some cases further cytogenetic or molecular biology support may be necessary, when considering the limits of morphology today. Thus, short references on molecular genetics, complementing the structural findings, are given.
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PMID:Electron microscopy and other ancillary techniques in the diagnosis of small round cell tumors. 1269 73

We describe a distinctive neuroendocrine carcinoma (NEC) that proliferated intra-epithelially. The tumor was 35 mm in diameter and arose from the right superior turbinate of a 46-year-old woman. Histologically, the tumor exhibited papillary growth and the tumor cells were localized in the thickened mucosal epithelium. The tumor cells had round to oval and vesicular or hyperchromatic nuclei, and cohered without any specific structure such as a fibrillary background, rosette or glandular structure. No stromal invasion by the tumor was observed. Immunohistochemically, the tumor cells were positive for neuron-specific enolase focally. In addition, many tumor cells expressed cytokeratin (AE1/AE3 and CAM 5.2), mostly with characteristic perinuclear dot-like patterns. Electron microscopy revealed focal but well-eveloped cytoplasmic processes containing arrays of microtubules and a few dense core granules. The tumor was considered to be a poorly differentiated neuroendocrine carcinomas (NEC) that exhibited exceptional intra-epithelial proliferation. The tumor completely disappeared after the stereotactic radiosurgery and has not recurred for 40 months. It might be difficult to distinguish a poorly differentiated NEC in the sinonasal region from other neuroectodermal tumors, including olfactory neuroblastoma, but the differential diagnosis is important because each tumor has different clinicopathological characteristics.
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PMID:Intra-epithelial neuroendocrine carcinoma of the nasal cavity. 1278 15

The possibility of links between psychosocial factors and cancer incidence and progression has generated considerable scientific and public interest. Tachykinins, including substance P, neurokinin A and B, hemokinin-1 and endokinins, are a family of neuropeptides, acting through three types of transmembrane G-protein coupled receptors denoted NK1, NK2 and NK3. Besides their role as neurotransmitters in peripheral and central nervous system, tachykinins and their receptors are also expressed in several non neuronal cells contributing to the fine connections between nervous systems and peripheral organ system such as respiratory, cardiovascular, immune, endocrine, gastrointestinal and genitourinary. Being so much involved in regulating physiological functions, they, of course, can concur to pathological conditions including cancer. Tachykinins can act on different steps of carcinogenesis. Tumors expressing NK receptors, such as astrocytoma, glioma, neuroblastoma, pancreatic cancer and melanoma, can misuse tachykinin-induced signaling, operating in normal cells, to promote proliferation and survival of cancer cells and to release cytokines and soluble mediators favoring tumor growth. In neuroblastoma, breast and prostate carcinomas tachykinins facilitate tumor metastatic infiltration in the bone marrow. In neuroendocrine carcinoma, tachykinins are responsible of symptoms associated with these pathologies including flushing, diarrhea, wheezing and right heart disease. In addition, regardless tumor histology, tachykinins may favor cancer incidence and metastatic progression by influencing blood flux and neovascularization in tumor formation as well as inducing immunosuppression mediated by neurogenic inflammation due to stress or surgery. However, the precise involvement of tachykinins in cancer pathologies and the potentiality to become effective pharmacological drug targets remain to be fully defined.
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PMID:Tachykinins and their receptors in human malignancies. 1691 32


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