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)

Pituitary carcinoma is a rare tumor characterized by poor responsiveness to therapy, leading to early death. Reported responses to standard chemotherapy have only been anecdotal, with no single agent or combination demonstrating consistent efficacy in the treatment of patients with this disease. The authors report rare examples of a persistent response to cytotoxic chemotherapy in two patients with pituitary carcinoma. One patient was a 38-year-old man with visual field loss caused by a luteinizing hormone-secreting pituitary carcinoma that had recurred despite multiple surgeries and radiation therapy. Intradural metastases to the spine that had failed to respond to radiation therapy were pathologically confirmed. The second patient was a 26-year-old man with hyperprolactinemia from a prolactin-secreting pituitary tumor. Spine magnetic resonance images obtained to search for causes of neck pain showed a vertebral tumor, which was later confirmed through pathological analysis to be a metastatic pituitary carcinoma. His disease progressed despite radiation therapy, high-dose bromocriptine, and chemotherapy. Both patients were treated monthly with temozolomide, which was administered orally on the first 5 days of a 28-day cycle. The patient in the first case underwent all 12 treatment cycles without serious side effects, and his visual field deficits improved. The patient in the second case had undergone only 10 cycles when the drug was stopped because of his severe fatigue. Nonetheless, his pain disappeared and his serum prolactin concentration decreased. Both patients continue to have partial responses and have been employed full-time for more than 1 year after discontinuing temozolomide therapy. These two examples demonstrate that temozolomide may be effective in treating pituitary carcinomas and thus should be considered in the treatment algorithm for these difficult cases.
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PMID:Long-term response of pituitary carcinoma to temozolomide. Report of two cases. 1704 68

In 1996, the German Registry of Pituitary Tumors was founded by the Pituitary Section of the German Society of Endocrinology as a reference center for collection and consultant pathohistological studies of pituitary tumors. The experiences of the first 10 years of this registry based on 4122 cases will herein be reported. The data supplement former collections of the years 1970-1995 with 3480 surgically removed tumors or lesions of the pituitary region. The cases were studied using histology, immunostainings and in some cases also molecular pathology or electron microscopy. The adenomas were classified according to the current World Health Organization classification in the version of 2004. From 1996 on 3489 adenomas (84.6%), 5 pituitary carcinomas (0.12%), 133 craniopharyngiomas (3.2%), 39 meningiomas (0.94%), 25 metastases (0.6%), 22 chordomas (0.5%), 115 cystic non-neoplastic lesions (2.8%), and 46 inflammatory lesions (1.1%, 248 other lesions or normal tissue (6.0%)) were collected by us. The adenomas (100%) were classified into densely granulated GH cell adenomas (9.2%), sparsely granulated GH cell adenomas (6.3%), sparsely granulated prolactin (PRL) cell adenomas (8.9%), densely granulated PRL cell adenomas (0.3%), mixed GH/PRL cell adenomas (5.2%), mammosomatotropic adenomas (1.1%), acidophilic stem cell adenomas (0.2%), densely granulated ACTH cell adenomas (7.2%), sparsely granulated ACTH cell adenomas (7.9%), Crooke cell adenomas (0.03%), TSH cell adenomas (1.5%), FSH/LH cell adenomas (24.8%), null cell adenomas (19.3%), null cell adenoma, oncocytic variant (5.8%), and plurihormonal adenomas (1.3%). Following the WHO classification of 2004, the new entity 'atypical adenoma' was found in 12 cases in 2005. Various prognostic parameters and clinical implications are discussed.
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PMID:Pathohistological classification of pituitary tumors: 10 years of experience with the German Pituitary Tumor Registry. 1728 10

Symptomatic metastases to the pituitary (MP) from renal cell carcinoma (RCC) are rare. In this largest case series reported, we describe the clinical features, treatment and outcome of 5 patients. Over a 6-year period (2000-2006), we treated 5 patients (3 males; mean age 61 years) with large sellar masses and RCC. Four patients had a history of RCC, while in one, RCC was diagnosed after surgery. RCC was diagnosed a median of 11 years prior to diagnosis of MP (range 0-27 years). Four patients had previously developed distant metastases. Clinical presentation included bitemporal hemianopia (3 patients), lethargy (3), headaches (2) and diabetes insipidus (DI) (2). Panhypopituitarism was present in 3 patients and the other two had deficiency of at least ACTH and gonadotropin axes. Elevated prolactin was seen in 3 patients. MRI showed an enhancing sellar mass with suprasellar extension and chiasmal compression in all; prominent vascular flow voids were seen in 2. Three patients underwent transsphenoidal surgery and radiation, while 2 underwent radiotherapy alone. Four patients are alive (follow up 6-46 months); 1 patient died due to systemic metastases at 12 months. Metastases to the pituitary from RCC cause more severe hypopituitarism and visual dysfunction compared to those from other primaries, whereas DI is less common. MRI shows contrast enhancement, stalk involvement, sclerosis and/or erosion of sella and presence of vascular flow voids. Combined treatment using decompressive surgery and stereotactic radiotherapy may result in better outcomes.
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PMID:Symptomatic pituitary metastases from renal cell carcinoma. 1754 48

Pituitary carcinomas are very rare tumors, nearly always presenting as widely invasive masses, although the hallmark of these lesions is the finding of distant metastases. One third of reported cases are prolactin (PRL)-secreting tumors. We report the case of a fatal pituitary carcinoma evolving within 4 years from a PRL-secreting microadenoma. A 22-year-old woman presented because of galactorrhea. Evaluation of the patient disclosed slight hyperprolactinemia and magnetic resonance imaging (MRI) showed a 7-mm intrapituitary lesion, which responded to treatment with cabergoline. About 4 years after the first evaluation she developed sudden headache, ptosis, and diplopia in the right eye. MRI disclosed the growth of a large pituitary mass, invading the right cavernous sinus. Despite two trans-sphenoidal surgical procedures followed by gamma-knife radiosurgery, the patient showed rapid local progression of the tumor and the occurrence of new lung lesions, probably of metastatic nature. The patient died 7 months after the development of her first neurological symptoms because of tumor apoplexy and subsequent subarachnoid hemorrhage. This case represents the first documented rapid evolution from a microprolactinoma initially responding to dopamine agonists to a fatal pituitary carcinoma.
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PMID:Evolution of a prolactin-secreting pituitary microadenoma into a fatal carcinoma: a case report. 1791 59

Although most pituitary tumors are benign, some are invasive or aggressive. In the absence of specific markers of malignancy, only tumors with metastases are considered malignant. To identify markers of invasion and aggressiveness, we focused on prolactin (PRL) tumors in the human and rat. Using radiology and histological methods, we classified 25 human PRL tumors into three groups (non-invasive, invasive, and aggressive-invasive) and compared them with a model of transplantable rat PRL tumors with benign and malignant lineages. Combining histological(mitoses and labeling for Ki-67, P53, pituitary transforming tumor gene (PTTG), and polysialic acid neural cell adhesion molecule) and transcriptomic (microarrays and q-RTPCR) methods with clinical data (post-surgical outcome with case-control statistical analysis), we found nine genes implicated in invasion (ADAMTS6, CRMP1, and DCAMKL3) proliferation (PTTG, ASK, CCNB1, AURKB, and CENPE), or pituitary differentiation (PITX1) showing differential expression in the three groups of tumors (P = 0.015 to 0.0001). A case-control analysis, comparing patients in remission (9 controls) and patients with persistent or recurrent tumors (14 cases) revealed that eight out of the nine genes were differentially up- or downregulated (P = 0.05 to 0.002), with only PTTG showing no correlation with clinical course (P = 0.258). These combined histological and transcriptomic analyses improve the pathological diagnosis of PRL tumors, indicating a reliable procedure for predicting tumor aggressiveness and recurrence potential. The similar gene profiles found between non-invasive human and benign rat tumors, as well as between aggressive-invasive human and malignant rat tumors provide new insights into malignancy in human pituitary tumors.
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PMID:A diagnostic marker set for invasion, proliferation, and aggressiveness of prolactin pituitary tumors. 1791 17

Pituitary tumors, almost invariably adenomas, are of frequent occurrence, accounting for 10% to 15% of all the intracranial neoplasm. They are classified as microadenomas (< 10 mm) or macroadenomas (> 10 mm) and as secreting or clinically non-secreting (or not functioning) adenomas. These tumors are autonomously capable to release pituitary hormones such as the growth hormone (GH), prolactin (PRL), adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The occurrence of metastases, characterizing a pituitary carcinoma, is exceedingly rare. However tumors with aggressive behavior, leading to local invasion, are relatively common. Although the pathogenesis of pituitary tumors is fully characterized, many molecular mechanisms of pituitary tumorigenesis had already been revealed. This review intends to describe advances in the understanding of the involved advances that have been made in the last decade concerning pituitary tumors progression, including the participation of oncogenes, tumor suppressor genes and growth factors.
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PMID:[Molecular aspects of pituitary tumorigenesis]. 1860 72

Pituitary carcinomas are exceedingly rare. At present, the sole diagnostic criterion is metastatic spread, either craniospinal or systemic. There is no agreement on a histologic, immunohistochemical, and/or ultrastructural definition. We report a clinically and morphologically well-documented example of pituitary thyrotropin cell carcinoma in a man with multiple endocrine neoplasia type 1 syndrome. The tumor produced thyrotropin, alpha-subunit, and prolactin and, through electron microscopy, was found to consist solely of Thyrotroph cells. Over a protracted course, craniospinal and systemic metastases were noted. The primary and metastatic deposits of this aggressive tumor were studied. To our knowledge, this tumor is the first reported case of thyrotropin cell carcinoma occurring in association with the multiple endocrine neoplasia type 1 syndrome. The literature regarding thyrotropin carcinomas is reviewed. Based on the study of several biopsies during disease progression, we believe that the carcinoma originated de novo without an intermediary adenoma phase.
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PMID:Multiple endocrine neoplasia type 1-associated thyrotropin-producing pituitary carcinoma: report of a probable de novo example. 1875 92

Changes in testosterone, prolactin and estradiol levels were evaluated vis-a-vis outcome and different patterns of androgen suppression--continuous androgen blockade or intermittent therapy--for prostate cancer patients. There was a significant difference between pre- (3.4 +/- 0.5 mM/l) and post- (1.0 +/- 0.3 mM/l) treatment levels of testosterone in cases of tumor progression and that in patients with positive response--(9.1 +/- 0.6 mM/l) and (4.3 +/- 0.4 mM/l), respectively. Relatively low levels of testosterone involved tumor progression. Prolactin level was significantly higher in patients with multiple distant metastases--(18.6 +/- 1.2 microg/l) and isolated foci--(9.5 +/- 0.8 microg/l) while tumor progression was associated with enhancing correlation with PSA concentration. It was established that prolactin level can be used as a criterion for resumption or discontinuation of intermittent therapy. Estradiol dynamics was similar to that of prolactin. The difference between pre- (172.9 +/- 9.8 pM/l) and post- (246.5 +/- 12.8 pM/l) treatment levels of estradiol in cases of tumor progression was significantly higher than that in patients with positive response (85.0 +/- 3.8 pM/l) and (76.9 +/- 4.4 pM/l), respectively.
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PMID:[Role of hormonal profile in adjusting therapy for prostate cancer]. 1894

Aggressive pituitary adenomas are notoriously difficult to manage due to their size, invasiveness, speed of growth and high frequency of recurrence. Except for prolactinomas, surgery (usually transsphenoidal but sometimes transcranial) is the first-line option, but re-growth of aggressive tumors is almost inevitable and monitoring and repeat surgery is required to control symptoms. In prolactinomas, dopamine agonists are the first-line treatment and they normalize prolactin levels in most patients even with macroprolactinomas. Somatostatin analogues offer another pharmacotherapy for pituitary adenomas either for primary therapy, pre-operatively to reduce the tumor volume and make it more amenable to surgical removal, or post-surgery to control re-expansion. When surgery and pharmacotherapy fail, radiotherapy is a useful third-line strategy that reduces recurrence, while extreme pituitary adenomas with metastases may potentially be managed with chemotherapy (although more data are needed). A combination of these therapies will be required for aggressive pituitary adenomas and careful follow-up is essential.
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PMID:Management of aggressive pituitary adenomas: current treatment strategies. 1900 40

Spontaneous mammary tumors occur in middle aged or senile dogs and are of three principal pathological types; a diffuse epithelial and connective tissue overgrowth often with associated cartilage and bone; solid masses of epithelial cells; intracystic papillomatous tumors. The metastases in this series were always composed of papillary carcinomatous cysts; this tissue in transplants to abdominal connective tissue induced epithelial osteogenesis. All of the dogs with mammary tumors had lipid-rich suprarenal cortical tumors. The tumors frequently secrete a dilute milk with citric acid content considerably increased above serum levels; large numbers of colostrum corpuscles are present in this fluid. After weaning, normal parturient dogs undergo a complete cessation of mammary secretion; lactation persists considerably longer in dogs with mammary tumor than in normal dogs. Absence of suckling does not eliminate lactation in pseudopregnancy. The failure of the breast to lactate under the stimulus of prolactin signifies a lack of physiological maturity. The breasts of mature dogs have two types of response to ovariectomy; either great physiological involution results or lactation, actual or potential, is retained in areas for at least 3 to 6 months. Those in which excision of the ovaries does not cause prompt and great involution of the breast include all dogs with mammary tumors, all with pseudopregnancy, and certain dogs, presumably normal which we are unable to characterize further at this time. Excision of the suprarenal glands in addition to the ovaries usually did not completely eliminate lactation or the lactational potential.
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PMID:STUDIES ON THE MAMMARY TUMORS OF DOGS : I. LACTATION AND THE INFLUENCE OF OVARIECTOMY AND SUPRARENALECTOMY THEREON. 1987 29


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