Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is presented of delayed radiation necrosis of the pituitary gland region which appeared 2 years after tonsillar carcinoma surgery, followed by radiotherapy, in a 62-year old woman. Magnetic resonance imaging suggested the presence of an adenoma, metastases or craniopharyngioma, of the pituitary gland region. The lesion was resected, totally, using the fronto-orbital approach. Histopathological examination showed radionecrosis of the neurohypophysis. The patient was released from the hospital in a good health condition without neurologic deficits. On the basis of our case and reports of other authors, we can conclude that complications may arise as a result of radiation damage to neighbouring structures and there is also potential to induce malignant disease.
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PMID:[A case of radionecrosis of the pituitary gland region mimicking brain tumor. Case report]. 1159 31

We report a case of suprasellar papillary craniopharyngioma metastatic to the temporoparietal region 2 years after its initial resection. The literature documents examples of craniopharyngioma recurrences along the surgical tract, as well as remote ipsi- and contralateral metastases via cerebrospinal fluid seeding. Ours is the second report of a craniopharyngioma of papillary type to exhibit metastatic behavior. The tumor spread opposite the side of craniotomy. Although a rare occurrence, it confirms the limited capacity of histologically benign craniopharyngiomas to undergo meningeal seeding, likely the result of surgical manipulation. Immunohistochemical demonstration of increased microvascular density and vascular endothelial growth factor expression, as well as a high vascular endothelial growth receptor (VEGFR2) signal by in situ hybridization, suggests that tumor vascularity facilitated angiogenesis and may have been involved in the establishment and growth of the metastatic deposit.
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PMID:Metastatic papillary craniopharyngioma: case study and study of tumor angiogenesis. 1191 4

Metastasis of craniopharyngioma is uncommon. Only 10 cases have been reported in the literature. In this report, we describe 3 patients who presented metastases following operative treatment of suprasellar craniopharyngioma. All 3 patients (ages: 32, 11, and 9 years) underwent radical excision of a supradiaphragmatic, retrochiasmatic craniopharyngioma by the right frontopterional approach. Resection was considered as total in all cases. All patients required hormone replacement therapy. Local recurrence was observed in only one case. Metastasis occurred along the surgical route in all three patients. The interval between surgery and metastasis was 5 and 3 years in the first two cases. The third patient presented two metastases: one in the temporal space at 3 years and another in the frontal space at 10 years. Repeat surgery was performed in 2 patients. The first case involved a lesion located in the right frontal space, and the second involved local recurrence and metastasis along the surgical route. The third patient was treated by puncture and radiation therapy for the temporal lesion and surveillance for the frontal lesions. No recurrence has been observed at 2 and 7 years after re-operation. Although rare, metastasis of craniopharyngioma has been reported up to 21 years after resection of the primary tumor. Metastasis often occurs along the surgical route, as in our 3 cases, but spreading to distant locations via cerebrospinal fluid has been observed. Regular follow-up is necessary, even after supposedly total resection.
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PMID:[Postoperative intracranial seeding of craniopharyngioma. Three case reports and a review of the literature]. 1240 20

The sellar region is the site of a large number of pathological entities arising from the pituitary and adjacent anatomical structures, including brain, blood vessels, nerves and meninges. The surgical pathology of this area requires the accurate identification of neoplastic lesions, including pituitary adenoma and carcinoma, craniopharyngioma, neurological neoplasms, germ cell tumours, haematological malignancies and metastases, as well as non-neoplastic lesions such as cysts, hyperplasias and inflammatory disorders. This review provides a practical approach to the diagnosis of pituitary specimens that are sent to the pathologist at the time of surgery. The initial examination requires routine haematoxylin and eosin staining to establish whether the lesion is a primary adenohypophysial proliferation or one of the many other pathologies that occurs in this area. The most common lesions resected surgically are pituitary adenomas. These are evaluated with several special stains and immunohistochemical markers that are now available to accurately classify these pathologies. The complex subclassification of pituitary adenomas is now recognised to reflect specific clinical features and genetic changes that predict targeted treatments for patients with pituitary disorders.
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PMID:My approach to pathology of the pituitary gland. 1714 70

Central diabetes insipidus is the end result of a number of different diseases that affect the hypothalamic-neurohypophyseal system. In many patients, especially children and young adults, it is caused by the destruction or degeneration of neurons that originate in the supraoptic and paraventricular nuclei of the hypothalamus. The known causes of these lesions include germinoma or craniopharyngioma; Langerhans cell histiocytosis; local inflammatory, autoimmune or vascular diseases; trauma resulting from surgery or an accident; sarcoidosis; metastases; and midline cerebral and cranial malformations. In rare cases, genetic defects in AVP synthesis that are inherited as autosomal dominant, autosomal recessive or X-linked recessive traits are the underlying cause. Accurate diagnostic differentiation is essential for both safe and effective disease management. Proper etiological diagnosis can be achieved via a series of steps that start with clinical observations and then progress, as needed, to more sophisticated methods. Indeed, magnetic resonance imaging (MRI) represents the examination method of choice for evaluating hypothalamic-pituitary-related endocrine diseases due to its ability to provide strongly-contrasted high-resolution multi-planar and spatial images. Specifically, MRI allows a detailed and precise anatomical study of the pituitary gland by differentiating between the anterior and posterior pituitary lobes. MRI identification of pituitary hyperintensity in the posterior part of the sella, now considered to be a clear marker of neurohypophyseal functional integrity, together with careful analysis of pituitary stalk shape and size, have provided the most striking recent findings contributing to the diagnosis and understanding of some forms of 'idiopathic' central diabetes insipidus.
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PMID:The diagnosis of children with central diabetes insipidus. 1745 Oct 74

Craniopharyngiomas (CP) are benign epithelial tumors of the sellar region and can be clinicopathologically distinguished into adamantinomatous (adaCP) and papillary (papCP) variants. Both subtypes are classified according to the World Health Organization grade I, but their irregular digitate brain infiltration makes any complete surgical resection difficult to obtain. Herein, we characterized the cellular interface between the tumor and the surrounding brain tissue in 48 CP (41 adaCP and seven papCP) compared to non-neuroepithelial tumors, i.e., 12 cavernous hemangiomas, 10 meningiomas, and 14 metastases using antibodies directed against glial fibrillary acid protein (GFAP), vimentin, nestin, microtubule-associated protein 2 (MAP2) splice variants, and tenascin-C. We identified a specific cell population characterized by the coexpression of nestin, MAP2, and GFAP within the invasion niche of the adamantinomatous subtype. This was especially prominent along the finger-like protrusions. A similar population of presumably astroglial precursors was not visible in other lesions under study, which characterize them as distinct histopathological feature of adaCP. Furthermore, the outer tumor cell layer of adaCP showed a distinct expression of MAP2, a novel finding helpful in the differential diagnosis of epithelial tumors in the sellar region. Our data support the hypothesis that adaCP, unlike other non-neuroepithelial tumors of the central nervous system, create a tumor-specific cellular environment at the tumor-brain junction. Whether this facilitates the characteristic infiltrative growth pattern or is the consequence of an activated Wnt signaling pathway, detectable in 90% of these tumors, will need further consideration.
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PMID:A tumor-specific cellular environment at the brain invasion border of adamantinomatous craniopharyngiomas. 2006 32

We report the case of a 31-year-old male who presented to the ER with a 1-week history of progressively worsening, throbbing, left retro-orbital headache, ptosis, and subjective worsening of short-term memory function. Initial review of systems and laboratory data were noncontributory. Non-contrasted CT demonstrated a large hyperdense mass centered in the suprasellar cistern without evidence of dissecting extra-axial hemorrhage. Though the initial appearance mimicked a basilar tip aneurysm or another primary extra-axial suprasellar pathology such as a hemorrhagic or proteinaceous craniopharyngioma, germinoma, or optic glioma, a second smaller, clearly intra-axial, hyperdense lesion was observed in the left periventricular forceps major white matter. Consideration for multiple cavernomas versus hypervascular metastatic disease such as renal malignancy, thyroid malignancy, or melanoma was raised. CTA confirmed normal intracranial vasculature. Subsequent MRI images showed an acutely hemorrhagic mass centered at the left paramedian hypothalamus and tuber cinereum with numerous secondary foci, demonstrating mature hemorrhagic elements and confirming the diagnosis of multiple cavernomas.
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PMID:Exophytic hypothalamic cavernous malformation mimicking an extra-axial suprasellar mass. 2130 32

Central diabetes insipidus (CDI) is the end result of a number of conditions that affect the hypothalamic-neurohypophyseal system. The known causes include germinoma/craniopharyngioma, Langerhans cell histiocytosis (LCH), local inflammatory, autoimmune or vascular diseases, trauma resulting from surgery or an accident, sarcoidosis, metastases and midline cerebral and cranial malformations. In rare cases, the underlying cause can be genetic defects in vasopressin synthesis that are inherited as autosomal dominant, autosomal recessive or X-linked recessive traits. The diagnosis of the underlying condition is challenging and raises several concerns for patients and parents as it requires long-term follow-up. Proper etiological diagnosis can be achieved via a series of steps that start with clinical observations and then progress to more sophisticated tools. Specifically, MRI identification of pituitary hyperintensity in the posterior part of the sella, now considered a clear marker of neurohypophyseal functional integrity, together with the careful analysis of pituitary stalk shape and size, have provided the most striking findings contributing to the diagnosis and understanding of some forms of 'idiopathic' CDI. MRI STIR (short-inversion-time inversion recovery sequencing) is a promising technology for the early identification of LCH-dependent CDI.
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PMID:Diabetes insipidus--diagnosis and management. 2243 47

A major challenge in the routine practice of surgical neuropathology is the distinction between reactive astrocytosis, which may be because of non-neoplastic and neoplastic conditions, and a low-grade infiltrating diffuse astrocytoma [World Health Organization (WHO) grade II]. This can be particularly challenging with small biopsies that often yield limited amounts of tissue for pathologic study, especially considering the marked differences in prognosis and therapy after a pathologic diagnosis. This paper will review some basic principles of gliosis as an astrocytic reaction to a wide range of central nervous system insults and focus on some common diagnostic pitfalls such as (1) gliosis associated with brain tumor mimics, including demyelinating disease and infections, (2) gliosis associated with nonglial tumors such as craniopharyngioma, hemangioblastoma, metastases, and central nervous system lymphoma. New diagnostic methods have facilitated the differentiation between reactive astrocytosis and the diffuse gliomas. Of these, the use of mutated isocitrate dehydrogenase-1 (IDH-1) as a marker of diffuse infiltrating astroctomas, oligodendrogliomas, and a subset of glioblastomas (secondary glioblastomas) is particularly exciting for tissue diagnosis and patient prognosis. In addition IDH-1 may be useful to distinguish a diffuse infiltrating glioma from low-grade "focal" neoplasms such as the pilocytic astocytoma in histologically ambiguous cases. The discovery of BRAF mutations as molecular signatures of some pilocytic astrocytomas, gangliogliomas, and pleomorphic xanthoastrocytomas has provided another diagnostic tool for the pathologist. Only after a definitive diagnosis of a diffuse infiltrating glioma or a focal glioma is made should a tumor grade be applied and some practical issues in current glioma grading are provided.
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PMID:Gliosis versus glioma?: don't grade until you know. 2269 87

Pituitary adenomas have to be studied in detail for structural characteristics, especially regarding the degree of granulation and immunohistochemical hormone expression, such as growth hormone (GH), prolactin, adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH), luteinizing hormone (LH) and proliferation markers (e.g. Ki-67 and p53) for correlation to clinical data and assessment of the prognosis. If histological and immunostaining data do not correlate to the patient data, explanations for the discrepancies must be found. All active adenoma types can also be present as inactive, so-called silent adenomas showing the same features. An increased Ki-67 index (> 3%), significant nuclear expression of protein p53 and mitoses are characteristic of atypical adenomas. Up to now the biological relevance of these atypical adenomas, especially their role as preneoplasms for pituitary carcinomas has not been fully elucidated. The only proof of a pituitary carcinoma is the existence of metastases. Extensive local invasion and a greatly increased Ki-67 index are not sufficient for this diagnosis. Craniopharyngiomas have to be classified into adamantinomatous types (intrasellar and suprasellar) and papillary types (only suprasellar). Regressive changes are found in adamantinomatous types only. Strong regression may lead to difficulties in the differential diagnosis of Rathke's cleft cysts with squamous metaplasia. Demonstration of nuclear expression of beta-catenin in these cases enables the diagnosis of craniopharyngioma. Papillary craniopharyngiomas are characterized by BRAF mutations that may be helpful in the differential diagnosis. All pituicytomas of the neurohypophysis, all spindle cell oncocytomas of the anterior pituitary and all granular cell tumors of the posterior pituitary express thyroid transcription factor 1 (TTF-1) and are thought to be variants of a common uniform spindle cell tumor of the pituitary.
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PMID:[New aspects of tumor pathology of the pituitary]. 2594 24


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