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1. Hannaford PC, Selvaraj S, Elliott AM, Angus V, Iversen L, Lee AJ: Cancer risk among users of oral contraceptives: cohort data from the Royal College of General Practitioner's oral contraception study. BMJ; 2007 Sep 29;335(7621):651
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer risk among users of oral contraceptives: cohort data from the Royal College of General Practitioner's oral contraception study.
  • OBJECTIVE: To examine the absolute risks or benefits on cancer associated with oral contraception, using incident data.
  • MAIN OUTCOME MEASURES: Adjusted relative risks between never and ever users of oral contraceptives for different types of cancer, main gynaecological cancers combined, and any cancer.
  • Standardisation variables were age, smoking, parity, social class, and (for the general practitioner observation dataset) hormone replacement therapy.
  • Subgroup analyses examined whether the relative risks changed with user characteristics, duration of oral contraception usage, and time since last use of oral contraception.
  • Compared with never users ever users had statistically significant lower rates of cancers of the large bowel or rectum, uterine body, and ovaries, tumours of unknown site, and other malignancies; main gynaecological cancers combined; and any cancer.
  • The relative risk for any cancer in the smaller general practitioner observation dataset was not significantly reduced.
  • Statistically significant trends of increasing risk of cervical and central nervous system or pituitary cancer, and decreasing risk of uterine body and ovarian malignancies, were seen with increasing duration of oral contraceptive use.
  • Reduced relative risk estimates were observed for ovarian and uterine body cancer many years after stopping oral contraception, although some were not statistically significant.
  • The estimated absolute rate reduction of any cancer among ever users was 45 or 10 per 100,000 woman years, depending on whether the main or general practitioner observation dataset was used.
  • CONCLUSION: In this UK cohort, oral contraception was not associated with an overall increased risk of cancer; indeed it may even produce a net public health gain.
  • The balance of cancer risks and benefits, however, may vary internationally, depending on patterns of oral contraception usage and the incidence of different cancers.

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  • [CommentIn] BMJ. 2007 Sep 29;335(7621):621-2 [17855281.001]
  • [CommentIn] Natl Med J India. 2008 Sep-Oct;21(5):234-5 [19320323.001]
  • [CommentIn] BMJ. 2008 Jan 12;336(7635):59-60; author reply 60 [18187700.001]
  • [CommentIn] J Fam Pract. 2008 Feb;57(2):83 [18254189.001]
  • (PMID = 17855280.001).
  • [ISSN] 1756-1833
  • [Journal-full-title] BMJ (Clinical research ed.)
  • [ISO-abbreviation] BMJ
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contraceptives, Oral
  • [Other-IDs] NLM/ PMC1995533
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2. Ilkhchoui Y, Appelbaum DE, Pu Y: FDG-PET/CT findings of a metastatic pituitary tumor. Cancer Imaging; 2010;10:114-6
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  • [Title] FDG-PET/CT findings of a metastatic pituitary tumor.
  • The authors report the fluorodeoxyglucose (FDG)-positron emission tomography(PET)/computed tomography (CT) findings of a rare case of growth hormone-secreting pituitary carcinoma with multiple metastatic lesions to the skeleton.
  • A 31-year-old male had presented with acromegaly and had received transsphenoidal resection of a pituitary tumor and adjuvant radiotherapy.
  • However, the tumor recurred with local invasions and the patient underwent more resections and adjuvant chemotherapy.
  • Several months later, the patient developed rising levels of insulin-like growth factor 1 and whole-body FDG-PET/CT scanning revealed multiple hypermetabolic lesions throughout the skeleton compatible with metastasis.
  • [MeSH-major] Fluorodeoxyglucose F18. Pituitary Neoplasms / radionuclide imaging. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adult. Bone Neoplasms / diagnosis. Bone Neoplasms / secondary. Humans. Insulin-Like Growth Factor I / metabolism. Male

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  • (PMID = 20299302.001).
  • [ISSN] 1470-7330
  • [Journal-full-title] Cancer imaging : the official publication of the International Cancer Imaging Society
  • [ISO-abbreviation] Cancer Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18; 67763-96-6 / Insulin-Like Growth Factor I
  • [Other-IDs] NLM/ PMC2842182
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3. Curtò L, Torre ML, Ferraù F, Pitini V, Altavilla G, Granata F, Longo M, Hofland LJ, Trimarchi F, Cannavò S: Temozolomide-induced shrinkage of a pituitary carcinoma causing Cushing's disease--report of a case and literature review. ScientificWorldJournal; 2010;10:2132-8
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  • [Title] Temozolomide-induced shrinkage of a pituitary carcinoma causing Cushing's disease--report of a case and literature review.
  • Temozolomide (TMZ) is an alkylating chemotherapeutic agent that has recently been used in some cases as a new therapeutic tool for pituitary carcinomas and aggressive pituitary adenomas.
  • In this report, we present the case of effective TMZ treatment in a 42-year-old man with ACTH-secreting carcinoma.
  • The tumor grew progressively over 4 years, from 2.2 to 31.1 cm³, despite three surgical approaches and γ-knife treatment.
  • The treatment was well tolerated except for a transient thrombocytopenia (grade 4 WHO).
  • [MeSH-major] Adenoma / drug therapy. Dacarbazine / analogs & derivatives. Pituitary ACTH Hypersecretion / drug therapy. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Adult. Antineoplastic Agents, Alkylating / therapeutic use. Humans. Male. Treatment Outcome

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  • [CommentIn] Turk Neurosurg. 2015;25(4):679-80 [26242353.001]
  • (PMID = 21057727.001).
  • [ISSN] 1537-744X
  • [Journal-full-title] TheScientificWorldJournal
  • [ISO-abbreviation] ScientificWorldJournal
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone
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4. Hagen C, Schroeder HD, Hansen S, Hagen C, Andersen M: Temozolomide treatment of a pituitary carcinoma and two pituitary macroadenomas resistant to conventional therapy. Eur J Endocrinol; 2009 Oct;161(4):631-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temozolomide treatment of a pituitary carcinoma and two pituitary macroadenomas resistant to conventional therapy.
  • OBJECTIVE: Aggressive pituitary tumours may be difficult to treat.
  • In a small number of cases, TMZ therapy has been reported to reduce pituitary tumour size and hormone hypersecretion.
  • DESIGN: We present three patients with pituitary tumours treated with TMZ.
  • One tumour was initially a macroprolactinoma that developed into a mixed GH- and prolactin-secreting carcinoma (patient A).
  • Two adenomas, a macroprolactinoma (patient B) and a clinically non-functioning pituitary adenoma (patient C), were highly invasive.
  • The three patients suffered from extensive tumour mass effects, and all tumours were resistant to conventional treatment.
  • RESULT: During TMZ therapy, tumour sizes were significantly reduced, hormone levels normalized and symptoms of mass effects decreased in all three cases.
  • The carcinoma was treated from 2004 to 2006 (23 months).
  • Three years after the terminating treatment, the tumour has not regrown and hormone levels are normalized.
  • CONCLUSION: TMZ therapy significantly decreased tumour volume, hormone hypersecretion and symptoms in all three patients, corresponding to the pathological findings regarding MGMT.
  • TMZ therapy may be a new option for the treatment of resistant pituitary adenomas.


5. McCutcheon IE, Pieper DR, Fuller GN, Benjamin RS, Friend KE, Gagel RF: Pituitary carcinoma containing gonadotropins: treatment by radical excision and cytotoxic chemotherapy: case report. Neurosurgery; 2000 May;46(5):1233-9; discussion 1239-40
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  • [Title] Pituitary carcinoma containing gonadotropins: treatment by radical excision and cytotoxic chemotherapy: case report.
  • OBJECTIVE AND IMPORTANCE: Pituitary carcinomas are extremely rare.
  • CLINICAL PRESENTATION: Here we present a 22-year-old woman with a pituitary carcinoma that was immunohistochemically positive for luteinizing hormone and follicle-stimulating hormone at both the primary and metastatic sites.
  • INTERVENTION: The patient had experienced failure of previous treatments, including standard surgery and radiotherapy, and presented to us for radical resection of the tumor, with exenteration of the involved cavernous sinus.
  • She was pretreated with cytotoxic chemotherapy and continued to receive this therapy after surgery.
  • CONCLUSION: This is the only documented case of a gonadotropin-staining pituitary carcinoma for which hormone production was proven in both the primary and metastatic tumors.
  • Many benign "nonsecreting" pituitary adenomas actually produce subclinical amounts of gonadotropins, and malignant nonfunctional pituitary neoplasms may do the same.
  • [MeSH-major] Carcinoma / surgery. Follicle Stimulating Hormone / metabolism. Luteinizing Hormone / metabolism. Neoplasm Recurrence, Local / surgery. Pituitary Neoplasms / surgery
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Combined Modality Therapy. Craniotomy. Female. Humans. Pituitary Gland / pathology. Reoperation

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  • (PMID = 10807257.001).
  • [ISSN] 0148-396X
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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6. Losa M, Mazza E, Terreni MR, McCormack A, Gill AJ, Motta M, Cangi MG, Talarico A, Mortini P, Reni M: Salvage therapy with temozolomide in patients with aggressive or metastatic pituitary adenomas: experience in six cases. Eur J Endocrinol; 2010 Dec;163(6):843-51
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  • [Title] Salvage therapy with temozolomide in patients with aggressive or metastatic pituitary adenomas: experience in six cases.
  • OBJECTIVE: The prognosis of either pituitary carcinoma or aggressive pituitary adenoma resistant to standard therapies is poor.
  • We assessed the efficacy of treatment with temozolomide, an oral second-generation alkylating agent, in a consecutive series of six patients with aggressive pituitary adenomas.
  • DESIGN: This was a 1-year prospective study of temozolomide therapy in six consecutive patients with pituitary carcinoma (one case) or atypical pituitary adenoma (five cases) resistant to standard therapies.
  • RESULTS: Four patients completed the 12 cycles of temozolomide treatment, as planned.
  • Two patients stopped the drug after 3 and 6 months respectively because of the progression of disease.
  • Immunohistochemistry for O(6)-methylguanine-DNA methyltransferase (MGMT) in tumor sample showed a partial association with treatment response.
  • CONCLUSIONS: Temozolomide treatment has a wide range of efficacy in patients with pituitary carcinoma or locally aggressive pituitary adenoma.

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  • (PMID = 20870708.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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7. Widhalm G, Wolfsberger S, Preusser M, Woehrer A, Kotter MR, Czech T, Marosi C, Knosp E: O(6)-methylguanine DNA methyltransferase immunoexpression in nonfunctioning pituitary adenomas: are progressive tumors potential candidates for temozolomide treatment? Cancer; 2009 Mar 1;115(5):1070-80
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  • [Title] O(6)-methylguanine DNA methyltransferase immunoexpression in nonfunctioning pituitary adenomas: are progressive tumors potential candidates for temozolomide treatment?
  • BACKGROUND: Currently, no effective alternative treatment exists for progressive, regrowing, nonfunctioning pituitary adenomas (NFPA) that are resistant to conventional multimodality therapy.
  • Temozolomide (TMZ) was proposed as a treatment option for pituitary carcinomas and aggressive pituitary adenomas.
  • Recently, it was suggested that the responsiveness of pituitary tumors to TMZ depends on the immunoexpression of O(6)-methylguanine DNA methyltransferase (MGMT).
  • Therefore, the authors of this report assessed MGMT expression in a series of patients with progressive, regrowing NFPAs to evaluate whether TMZ may serve as alternative treatment option.
  • RESULTS: At the time of initial surgery, low MGMT expression was observed in 12 of 24 patients (50%) in the study group with progressive, regrowing NFPAs.
  • CONCLUSIONS: The current data has suggested that half of the patients with progressive, regrowing NFPAs exhibit low MGMT expression and are potential candidates for treatment with TMZ.
  • These findings provide a rationale for the use of TMZ as an alternative treatment approach in this subgroup if conventional therapy, including reoperation, radiosurgery, and radiotherapy, fails.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / enzymology. Antineoplastic Agents, Alkylating / therapeutic use. Dacarbazine / analogs & derivatives. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / enzymology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Reoperation. Time Factors

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  • [Copyright] (c) 2009 American Cancer Society.
  • (PMID = 19156926.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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8. Pickles T, Agranovich A, Berthelet E, Duncan GG, Keyes M, Kwan W, McKenzie MR, Morris WJ, British Columbia Cancer Agency, Prostate Cohort Outcomes Initiative: Testosterone recovery following prolonged adjuvant androgen ablation for prostate carcinoma. Cancer; 2002 Jan 15;94(2):362-7
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  • [Title] Testosterone recovery following prolonged adjuvant androgen ablation for prostate carcinoma.
  • BACKGROUND: This study was conducted to describe the rate and completeness of the recovery of testosterone production following prolonged temporary androgen ablative therapy in men with prostate carcinoma undergoing curative radiation therapy.
  • METHODS: Two-hundred and sixty-seven men treated with between 3 months and 3 years of adjuvant androgen ablation (AA) were followed at 6-month intervals following cessation of their androgen deprivation therapy.
  • RESULTS: Drugs used included low dose cyproterone/stilboestrol (CPA/DES) in combination (56%) and 1 month depot (18%) and 3 month depot (25%) leutinizing hormone releasing hormone agonist (LHRHa).
  • In comparison, men who had never received androgen ablative therapy showed a fall of testosterone, with 17% having sub-normal levels after 3 years.
  • Median time to testosterone recovery was 10 months.
  • Factors associated on multivariate analysis with delayed testosterone recovery included advanced age (P = 0.008), low pre-therapy testosterone (P = 0.04), and the use of 3 month LHRHa preparations as compared with CPA/DES (P = 0.002) or 1 month LHRHa preparations (P = 0.015).
  • The duration of drug use was not significantly associated with time to testosterone recovery.
  • [MeSH-major] Adenocarcinoma / blood. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Neoplasms / blood. Testosterone / blood
  • [MeSH-minor] Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Cohort Studies. Humans. Male. Middle Aged. Pituitary Gland / physiology. Prospective Studies. Radiotherapy, Adjuvant. Testis / physiology. Time Factors. Treatment Outcome

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  • (PMID = 11900222.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 3XMK78S47O / Testosterone
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9. Granata A, Figura M, Gulisano S, Romeo G, Sicurezza E, Failla A, Scuderi R: [Central diabetes insipidus as a first manifestation of lung adenocarcinoma]. Clin Ter; 2007 Nov-Dec;158(6):519-22
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  • [Title] [Central diabetes insipidus as a first manifestation of lung adenocarcinoma].
  • [Transliterated title] Diabete insipido centrale come prima manifestazione di adenocarcinoma polmonare.
  • The pituitary gland and infundibulum can be involved in a variety of medical conditions, including infiltrative diseases, fungal infections, tuberculosis, primary and metastatic tumors.
  • Metastases to the pituitary gland are absolutely rare, and they are generally secondary to pulmonary carcinoma in men and breast carcinoma in women.
  • Pituitary metastases more commonly affect the posterior lobe and the infundibulum than the anterior lobe.
  • The posterior lobe involvement may explain why patients with pituitary metastases frequently present with diabetes insipidus.
  • We are presenting a case report of a 48-year-old male patient with sudden onset of polyuria and persistent thirst.
  • Computed tomography (CT) scan of the brain showed a mass located in the sella turcica and suprasellar region.
  • Bronchoscopy and biopsy demonstrated a pulmonary adenocarcinoma.
  • Thus, we made a diagnosis of lung cancer with local and pituitary metastases.
  • The patient received radiotherapy on the pituitary gland and adjuvant chemotherapy.
  • In conclusion, in patients presenting with sudden onset of diabetes insipidus pituitary metastases should be taken in account in differential diagnosis.
  • [MeSH-major] Adenocarcinoma / diagnosis. Diabetes Insipidus / etiology. Lung Neoplasms / diagnosis. Pituitary Neoplasms / complications. Pituitary Neoplasms / secondary
  • [MeSH-minor] Biopsy. Bronchoscopy. Diagnosis, Differential. Humans. Lymphatic Metastasis. Magnetic Resonance Imaging. Male. Middle Aged. Polyuria / etiology. Thirst. Tomography, X-Ray Computed


10. Suhardja A, Kovacs K, Rutka J: Genetic basis of pituitary adenoma invasiveness: a review. J Neurooncol; 2001 May;52(3):195-204
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  • [Title] Genetic basis of pituitary adenoma invasiveness: a review.
  • Compatible with contemporary paradigms of the role of genetic aberrations in the progression of human tumors, the growth of pituitary tumors into a state of invasiveness appears to be due to genetic alterations.
  • Amplification of H-ras and c-myc oncogenes and mutations of p53, nm23 and Rb genes have been identified disproportionately more in aggressive tumors and, in the case of Rb gene, in pituitary carcinomas, providing evidence that amplification of these oncogenes (H-ras and c-myc) and inactivation of tumor suppressor genes (p53, nm23 and Rb) seem to be at least one mechanism by which pituitary tumors progress.
  • The current level of management of invasive pituitary adenomas should become more comprehensive as the advances in our understanding of genetic basis of pituitary adenoma invasiveness becomes translated into development of novel chemotherapy or gene transfer technique.
  • [MeSH-major] Adenoma / pathology. Genes, Tumor Suppressor. Neoplasm Invasiveness / genetics. Nucleoside-Diphosphate Kinase. Oncogenes. Pituitary Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cell Cycle / genetics. Cell Transformation, Neoplastic / genetics. Chromosomes, Human / genetics. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Drug Design. Gene Expression Regulation, Neoplastic. Genes, Retinoblastoma. Genes, myc. Genes, p53. Genes, ras. Genetic Therapy. Humans. Monomeric GTP-Binding Proteins / deficiency. Monomeric GTP-Binding Proteins / genetics. Monomeric GTP-Binding Proteins / physiology. Mutation. NM23 Nucleoside Diphosphate Kinases. Proto-Oncogene Proteins c-myc / deficiency. Proto-Oncogene Proteins c-myc / physiology. Proto-Oncogene Proteins p21(ras) / deficiency. Proto-Oncogene Proteins p21(ras) / physiology. Retinoblastoma Protein / deficiency. Retinoblastoma Protein / physiology. Transcription Factors / deficiency. Transcription Factors / genetics. Transcription Factors / physiology. Tumor Suppressor Protein p53 / deficiency. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 11519849.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / Proto-Oncogene Proteins c-myc; 0 / Retinoblastoma Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; EC 2.7.4.6 / NME1 protein, human; EC 2.7.4.6 / Nucleoside-Diphosphate Kinase; EC 3.6.5.2 / HRAS protein, human; EC 3.6.5.2 / Monomeric GTP-Binding Proteins; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Number-of-references] 113
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11. Fadul CE, Kominsky AL, Meyer LP, Kingman LS, Kinlaw WB, Rhodes CH, Eskey CJ, Simmons NE: Long-term response of pituitary carcinoma to temozolomide. Report of two cases. J Neurosurg; 2006 Oct;105(4):621-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term response of pituitary carcinoma to temozolomide. Report of two cases.
  • 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.
  • 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.
  • [MeSH-major] Adenoma / drug therapy. Luteinizing Hormone / secretion. Neoplasm Recurrence, Local / drug therapy. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy
  • [MeSH-minor] Adult. Drug Administration Schedule. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Radiosurgery. Retreatment. Spinal Cord / pathology. Spinal Cord Neoplasms / drug therapy. Spinal Cord Neoplasms / secondary. Treatment Failure

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  • (PMID = 17044568.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-67-9 / Luteinizing Hormone
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12. Kaltsas GA, Nomikos P, Kontogeorgos G, Buchfelder M, Grossman AB: Clinical review: Diagnosis and management of pituitary carcinomas. J Clin Endocrinol Metab; 2005 May;90(5):3089-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical review: Diagnosis and management of pituitary carcinomas.
  • Pituitary carcinomas are rare, making up some 0.2% of all pituitary tumors, but represent a particular challenge to clinical practice.
  • The diagnosis of a pituitary carcinoma requires evidence of metastatic disease, either outside the central nervous system (CNS) or as separate noncontiguous foci within the CNS.
  • They may present as typical pituitary adenomas, which reveal their malignant character only as time progresses, or as peculiarly aggressive tumors ab initio.
  • The majority of carcinomas are secretory, usually arising from corticotroph tumors or prolactinomas, but all histological types and secretory patterns are represented.
  • Treatment is by surgery, transsphenoidal wherever possible, and conventional and stereotactic radiotherapy, but ultimately, a plethora of therapies may be required, including various attempts at medical therapy.
  • Chemotherapy in some instances probably prolongs survival, but, in general, their progress from the diagnosis of carcinomatous changes is progressive and inexorable.
  • However, we do not believe there will be any real prospect of long-term survival until the development and use of therapies targeted at specific molecular abnormalities.
  • [MeSH-major] Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy

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  • (PMID = 15741248.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 116
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13. Colao A, Ochoa AS, Auriemma RS, Faggiano A, Pivonello R, Lombardi G: Pituitary carcinomas. Front Horm Res; 2010;38:94-108
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary carcinomas.
  • Pituitary carcinoma is a extremely rare and is characterized by a very poor prognosis.
  • Even if at diagnosis the presence of metastases is required to define a pituitary carcinoma, the lesion was almost invariably diagnosed first as a benign pituitary tumor, that after a variable period of latency, ranging from few months to many years, changed its natural course to an aggressive pituitary tumor poorly responsive to therapy.
  • Recent studies have partially clarified its molecular pathogenesis and found possible markers of aggressiveness in order to make an earlier diagnosis, when still treatment could improve their prognosis.
  • Most pituitary carcinomas are functioning, and ACTH- and PRL-secreting carcinomas are the most frequent.
  • Treatment includes surgery, radiotherapy, medical therapy and chemotherapy, but the poor results with current therapies should prompt all investigators to better understand its pathogenesis and searching new molecular targets for treatments.
  • [MeSH-major] Pituitary Neoplasms / therapy

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  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20616500.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 88
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14. Maïza JC, Caron P: [Pituitary carcinomas and aggressive adenomas: an overview and new therapeutic options]. Ann Endocrinol (Paris); 2009 Sep;70 Suppl 1:S12-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pituitary carcinomas and aggressive adenomas: an overview and new therapeutic options].
  • Pituitary carcinomas are a rare disease with an estimated prevalence around 0.2 % of the pituitary tumours.
  • They are defined by the presence of intra or extra-cranial metastases but initially they can share the same features as aggressive pituitary adenomas.
  • Indeed there are some indicators that help to differentiate adenomas and carcinomas such as histological findings and immunohistochemical characteristics.
  • Usually in carcinomas, mitotic activity is higher, proliferative index Ki-67 is higher, p53 expression is positive and microvascular density is mostly increased.
  • The majority of carcinomas are prolactin or ACTH-secreting tumors.
  • Dopamine and somatostatin-receptor agonists are not as effective as for the treatment of adenomas.
  • Carcinomas require often repeated surgery and radiotherapy fail to control the tumor.
  • Conventional chemotherapy is poorly effective, but recent case reports with the alkylating agent temozolomide have provided better results at least in the short term.
  • The effects of temozolomide are reversed by the enzyme MGMT and the treatment's response can be predicted by the study of MGMT's expression : tumours lacking MGMT are especially sensitive to temozolomide.
  • [MeSH-major] Adenoma / therapy. Pituitary Neoplasms / therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Humans

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  • (PMID = 19878763.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents
  • [Number-of-references] 36
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15. Sansur CA, Oldfield EH: Pituitary carcinoma. Semin Oncol; 2010 Dec;37(6):591-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary carcinoma.
  • Pituitary carcinoma is defined by metastasis of a pituitary tumor to a distant location.
  • Although rare, pituitary carcinoma is becoming an increasingly recognized entity among pituitary surgeons.
  • Most pituitary carcinomas have endocrine activity, and as such these lesions may be associated with signs of excess endocrine function.
  • Surgical debulking is the standard treatment for the sellar component of disease.
  • An important recent development has been the discovery that these lesions may significantly respond to systemic chemotherapy.
  • In this review, we will discuss the diagnosis and clinical features of pituitary carcinomas, immunohistochemistry with cytogenetics, and treatment.
  • [MeSH-major] Carcinoma / pathology. Carcinoma / therapy. Pituitary Neoplasms / pathology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Biomarkers, Tumor. Combined Modality Therapy. Humans. Mitotic Index. Neoplasm Metastasis

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21167378.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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16. Granata A, Viola G, Privitera C, Romeo G, Cacciaguerra S, Gaeta M, Sicurezza E, Figuera M: Smoking, polyuria and impaired vision. Clin Nephrol; 2007 Jan;67(1):49-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The pituitary gland can be involved in a variety of medical conditions, including metastatic tumors.
  • Metastases to the pituitary gland, although absolutely rare, more commonly affect the posterior pituitary lobe and so frequently present with diabetes insipidus.
  • Computed tomography (CT) scan of the brain showed a mass located in the sella turcica and in the suprasellar region.
  • CT scan of the chest showed a mass in the right superior lobe with mediastinal lymphadenopathy, with bronchoscopy and biopsy features of pulmonary adenocarcinoma.
  • The patient received radiotherapy on the pituitary gland and adjuvant chemotherapy, and as intrasellar and suprasellar mass decreased in size, urinary output was accordingly reduced.
  • Therefore, is that in patients with risk factors for cancer and sudden onset of diabetes insipidus pituitary metastasis should be taken into account in differential diagnosis.
  • [MeSH-major] Adenocarcinoma / secondary. Diabetes Insipidus, Neurogenic / etiology. Hemianopsia / etiology. Lung Neoplasms / pathology. Pituitary Neoplasms / secondary. Polyuria / etiology. Smoking / adverse effects

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  • (PMID = 17269600.001).
  • [ISSN] 0301-0430
  • [Journal-full-title] Clinical nephrology
  • [ISO-abbreviation] Clin. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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17. Ragel BT, Couldwell WT: Pituitary carcinoma: a review of the literature. Neurosurg Focus; 2004 Apr 15;16(4):E7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pituitary carcinoma: a review of the literature.
  • Pituitary carcinomas, defined as distant metastases of a pituitary neoplasm, are rare; fewer than 140 reports exist in the English literature.
  • The initial presenting pituitary tumor is usually a secreting, invasive macroadenoma, with adrenocorticotropic hormone (ACTH)--and prolactin (PRL)--secreting tumors being the most common.
  • The latency period between the diagnosis of a pituitary tumor and the diagnosis of a pituitary carcinoma is 9.5 years for ACTH-producing lesions and 4.7 years for PRL-secreting tumors.
  • Treatment options include additional surgery, radiotherapy, and chemotherapy, all of which are associated with poor results.
  • Future studies will focus on identifying those invasive pituitary tumors most likely to metastasize and treating them aggressively before they progress to pituitary carcinomas.
  • [MeSH-major] Carcinoma / diagnosis. Carcinoma / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / therapy
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Biomarkers, Tumor / analysis. Gene Expression Regulation, Neoplastic. Genes, p53. Genes, ras / genetics. Humans. Pituitary Gland / pathology. Pituitary Gland / ultrastructure. Point Mutation. Prolactin / secretion

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  • [CommentIn] Neurosurg Focus. 2005 Sep 15;19(3):E11; author reply E11 [16196164.001]
  • (PMID = 15191336.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
  • [Number-of-references] 122
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18. Bode H, Seiz M, Lammert A, Brockmann MA, Back W, Hammes HP, Thomé C: SOM230 (pasireotide) and temozolomide achieve sustained control of tumour progression and ACTH secretion in pituitary carcinoma with widespread metastases. Exp Clin Endocrinol Diabetes; 2010 Nov;118(10):760-3
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  • [Title] SOM230 (pasireotide) and temozolomide achieve sustained control of tumour progression and ACTH secretion in pituitary carcinoma with widespread metastases.
  • Pituitary carcinomas are rare and neurosurgically challenging lesions, as they commonly relapse after surgical removal.
  • Their prognosis is dismal due to their limited response to radiotherapy and chemotherapy.
  • We report a patient with an ACTH-secreting pituitary carcinoma and widespread intracranial, spinal and systemic metastases despite repeated surgical treatment, bilateral adrenalectomy, medical treatment and radiotherapy.
  • Additionally to chemotherapy with temozolomide, the patient received SOM230 as salvage therapy with an improvement of the patient's clinical status, and a reduction of ACTH levels.
  • After 12 months of combination therapy a sustained tumor control was achieved and persisted upon monotherapy with SOM230 for more than 9 months thereafter.
  • Thus, temozolomide in combination with SOM230 seems to be promising in patients with ACTH-secreting metastasized pituitary carcinoma.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / drug therapy. Carcinoma / secondary. Dacarbazine / analogs & derivatives. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / therapeutic use. Female. Humans. Middle Aged. Salvage Therapy. Treatment Outcome

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  • [Copyright] © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20496311.001).
  • [ISSN] 1439-3646
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Hormonal; 51110-01-1 / Somatostatin; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide
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19. Raverot G, Sturm N, de Fraipont F, Muller M, Salenave S, Caron P, Chabre O, Chanson P, Cortet-Rudelli C, Assaker R, Dufour H, Gaillard S, François P, Jouanneau E, Passagia JG, Bernier M, Cornélius A, Figarella-Branger D, Trouillas J, Borson-Chazot F, Brue T: Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience. J Clin Endocrinol Metab; 2010 Oct;95(10):4592-9
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  • [Title] Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience.
  • CONTEXT: To date only 18 patients with aggressive pituitary tumors or carcinomas treated with temozolomide have been reported.
  • OBJECTIVES: The objective of the study was to describe the antitumoral efficacy and toxicity of temozolomide in patients with aggressive pituitary tumors or carcinomas and evaluate the possible prognostic value of MGMT promoter methylation and protein expression.
  • PATIENTS: Eight patients, five with pituitary carcinomas (three prolactin (PRL) and two ACTH) and three with aggressive pituitary tumors (one PRL and two ACTH), all treated with temozolomide administered orally for four to 24 cycles, were included in our French multicenter study.
  • RESULTS: Three of the eight patients (two ACTH adenomas and one PRL carcinoma) responded to temozolomide as demonstrated by significant tumor shrinkage and reduced hormone secretion.
  • Three cycles of temozolomide were sufficient to identify treatment-responsive patients.
  • Additional cycles did not improve treatment efficacy in those not responding, even when associated with carboplatin and vepeside.
  • CONCLUSION: Temozolomide treatment may be an effective option for some aggressive pituitary tumors or carcinomas.
  • Response to a trial of three cycles of treatment seems sufficient to identify responders and more reliable than patient MGMT status.
  • [MeSH-major] Carcinoma / drug therapy. Dacarbazine / analogs & derivatives. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / drug therapy. ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Antineoplastic Agents, Alkylating / therapeutic use. DNA Methylation. Female. France. Humans. Male. Middle Aged. Neoplasm Invasiveness. O(6)-Methylguanine-DNA Methyltransferase / genetics. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Prolactinoma / drug therapy. Prolactinoma / genetics. Prolactinoma / pathology. Retrospective Studies. Sequence Analysis, DNA


20. Nasr C, Mason A, Mayberg M, Staugaitis SM, Asa SL: Acromegaly and somatotroph hyperplasia with adenomatous transformation due to pituitary metastasis of a growth hormone-releasing hormone-secreting pulmonary endocrine carcinoma. J Clin Endocrinol Metab; 2006 Dec;91(12):4776-80
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  • [Title] Acromegaly and somatotroph hyperplasia with adenomatous transformation due to pituitary metastasis of a growth hormone-releasing hormone-secreting pulmonary endocrine carcinoma.
  • Hypothalamic gangliocytomas producing GHRH are also known to be associated with pituitary adenomas causing acromegaly.
  • OBJECTIVES: The objective of this study was to describe a case of acromegaly due to a pulmonary GHRH-secreting endocrine carcinoma with metastasis to the pituitary gland and to look at the peculiar histological features of this case.
  • SUBJECT: The patient was a 44-yr-old woman who was diagnosed with a biopsy-proven metastatic pulmonary endocrine tumor during pregnancy.
  • After delivery, she underwent radiation and chemotherapy for pulmonary and skeletal metastases.
  • Her disease was clinically stable for 7 yr until she developed bitemporal hemianopia.
  • RESULTS: Magnetic resonance imaging (MRI) of the brain confirmed the presence of a 2.6-cm lesion within the sella turcica extending above the sella and compressing the optic chiasm.
  • Histological examination confirmed metastatic endocrine carcinoma to the pituitary, and immunohistochemistry localized GHRH to the tumor cells.
  • The adjacent pituitary exhibited somatotroph hyperplasia with abundant reactivity for GH and alpha-subunit.
  • CONCLUSION: This is the first report of a GHRH-producing endocrine tumor metastasizing to the pituitary and causing local hyperstimulation with somatotroph hyperplasia and adenomatous transformation.
  • [MeSH-major] Acromegaly / complications. Acromegaly / etiology. Adenoma / etiology. Carcinoma / complications. Growth Hormone-Releasing Hormone / secretion. Lung Neoplasms / complications. Paraneoplastic Endocrine Syndromes / complications. Pituitary Neoplasms / secondary. Somatotrophs / pathology

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  • (PMID = 16968791.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones, Ectopic; 0 / Indium Radioisotopes; 9034-39-3 / Growth Hormone-Releasing Hormone
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21. Lau Q, Scheithauer B, Kovacs K, Horvath E, Syro LV, Lloyd R: MGMT immunoexpression in aggressive pituitary adenoma and carcinoma. Pituitary; 2010 Dec;13(4):367-79
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  • [Title] MGMT immunoexpression in aggressive pituitary adenoma and carcinoma.
  • Recent case reports have documented the efficacy of temozolomide therapy in some aggressive pituitary adenomas and pituitary carcinomas resistant to multimodality therapy.
  • Evidence suggests that low O6-methylguanine-DNA methyltransferase (MGMT) immunoexpression correlates with response to temozolomide chemotherapy.
  • Herein, we aimed to study MGMT immunoexpression in a spectrum of pituitary tumors, indolent, aggressive and malignant.
  • A literature review of the use of temozolomide in pituitary tumors was also performed.
  • Immunohistochemistry for MGMT was performed on 60 pituitary tumors identified in the Mayo Clinic Tissue Registry and the consultation files of one of us (BWS).
  • The group included 30 pituitary carcinomas (15 ACTH, 10 PRL, 1 FSH/LH, 1 TSH, 1 silent subtype 3 and 2 null cell).
  • Tissue from recurrences was available in 17 cases.
  • In addition, 30 functionally different pituitary adenomas were studied, including 15 invasive and 15 non-invasive adenomas.
  • Overall, 32 cases of pituitary tumors (54%) demonstrated low MGMT immunoexpression.
  • This included 17 of 30 (57%) carcinomas, 9 of 15 (60%) invasive adenomas, and 6 of 15 cases (40%) of non-invasive pituitary adenomas.
  • Prolactin-producing carcinomas had the highest proportion of tumors (80%) with low expression.
  • A significant proportion of pituitary adenomas and carcinomas demonstrate low MGMT immunoexpression.
  • In an effort to anticipate the likelihood of a temozolomide response, all cases of aggressive pituitary tumors should be assessed for MGMT expression.
  • [MeSH-major] DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Pituitary Neoplasms / immunology. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Alkylating / therapeutic use. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Humans. Immunohistochemistry. Immunosuppression. Male

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  • (PMID = 20740317.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; YF1K15M17Y / temozolomide
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22. Guzel A, Tatli M, Senturk S, Guzel E, Cayli SR, Sav A: Pituitary carcinoma presenting with multiple metastases: case report. J Child Neurol; 2008 Dec;23(12):1467-71
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  • [Title] Pituitary carcinoma presenting with multiple metastases: case report.
  • Pituitary carcinoma, an uncommon tumor in adults, generally presents with craniospinal and systemic metastases.
  • We report a case of pituitary carcinoma with multiple craniospinal metastases in a child.
  • Histopathological and immunohistochemical examination of the excised left frontal mass revealed pituitary carcinoma.
  • Treatment with cyclic temozolomide was started after the operation, but the patient died after 2 months without response to medical therapy.
  • This is the first pediatric case, to the authors' knowledge, of a pituitary carcinoma with widespread intracranial and intraspinal metastases.
  • [MeSH-major] Brain Neoplasms / secondary. Pituitary Neoplasms / complications. Pituitary Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Child. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Female. Humans. Magnetic Resonance Imaging. Papilledema / drug therapy. Papilledema / etiology. Tomography, X-Ray Computed

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  • (PMID = 19073854.001).
  • [ISSN] 1708-8283
  • [Journal-full-title] Journal of child neurology
  • [ISO-abbreviation] J. Child Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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23. Autorino R, Zito A, Di Giacomo F, Cosentino L, Quarto G, Di Lorenzo G, Mordente S, Pane U, Giordano A, D'Armiento M: Orbital metastasis as a first indication of prostate cancer: a case report. Arch Ital Urol Androl; 2005 Jun;77(2):109-10
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  • [Title] Orbital metastasis as a first indication of prostate cancer: a case report.
  • Prostatic carcinoma accounts for only 3.6% of orbital metastases encountered in clinical practice.
  • We report the clinical presentation and response to treatment of a patient with metastatic prostatic carcinoma to the sella turcica.
  • A 73-year-old man presented with a three-months history of progressive right proptosis associated with increasing diplopia in down-gaze and slightly decreased visual acuity.
  • Gadolinium-MRI scans of the head revealed a left osteoblastic intrasellar mass, displacing the pituitary gland.
  • Transrectal ultrasound-guided biopsy revealed prostatic adenocarcinoma (Gleason score 4+3) in both lobes of the prostate.
  • The visual complaints regressed dramatically within the first month of the treatment.
  • However the disease subsequently progressed and the patient died 22 months after diagnosis.

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  • (PMID = 16146273.001).
  • [ISSN] 1124-3562
  • [Journal-full-title] Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
  • [ISO-abbreviation] Arch Ital Urol Androl
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Fertility Agents, Female; 33515-09-2 / Gonadotropin-Releasing Hormone; EC 3.4.21.77 / Prostate-Specific Antigen
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24. Leung G, Tsao SW, Wong YC: The effect of flutamide and tamoxifen on sex hormone-induced mammary carcinogenesis and pituitary adenoma. Breast Cancer Res Treat; 2002 Mar;72(2):153-62
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  • [Title] The effect of flutamide and tamoxifen on sex hormone-induced mammary carcinogenesis and pituitary adenoma.
  • Based on the previous finding that the dose of testosterone affects only the latency period of mammary cancer, not the final incidence and that androgen upregulates apoptotic activity in pre-malignant mammary glands, we hypothesised that estrogen is the initiator and androgen the promoter for hormonal mammary carcinogenesis of the rats.
  • We showed that tamoxifen could totally inhibit mammary carcinogenesis while flutamide cause a delay and reduction in tumour incidence in the 12 months treatment term.
  • Blocking effect of flutamide and tamoxifen on T + E2 (testosterone and 17beta-estradiol) short-terms treatment was demonstrated by the similar histological changes identified in the mammary glands of the T + E2 and drug treated rats to that of the age matched E2 and T controls, respectively.
  • Autopsy of the tumour bearing rats showed presence of pituitary macroadenoma causing compression and atrophy of the brain stem.
  • Tamoxifen was also effective in blocking the formation of pituitary adenoma in the sex hormone treated rats.
  • Pituitary size and level of prolactin were higher in the T + E2 + flutamide group than the T + E2 group in both short-term and long-term treatments.
  • It suggests that testosterone may have a role in counteracting estradiol stimulation on the pituitary lactotropes although it is synergistic to estrogen in mammary carcinogenesis.
  • Pituitary adenomas were found in all rats that developed mammary adenocarcinoma but not vice versa suggesting that prolactin level elevation alone cannot lead to mammary tumorigenesis.
  • The animal model, in addition to mammary carcinogenesis, may be useful for investigation of anti-estrogen therapy in pituitary adenomas.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Breast / drug effects. Breast Neoplasms / prevention & control. Flutamide / pharmacology. Pituitary Gland / drug effects. Prolactinoma / prevention & control. Tamoxifen / pharmacology

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  • (PMID = 12038706.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Gonadal Steroid Hormones; 094ZI81Y45 / Tamoxifen; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 76W6J0943E / Flutamide
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25. Massoud W, Paparel P, Lopez JG, Perrin P, Daumont M, Ruffion A: Discovery of a pituitary adenoma following treatment with a gonadotropin-releasing hormone agonist in a patient with prostate cancer. Int J Urol; 2006 Jan;13(1):87-8
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  • [Title] Discovery of a pituitary adenoma following treatment with a gonadotropin-releasing hormone agonist in a patient with prostate cancer.
  • We report the case of a T3 prostate cancer in a 70-year-old white man.
  • Hormone therapy represents a prominent branch in the treatment of locally advanced and metastatic prostate cancer.
  • Gonadotropin-releasing hormone agonists have been proven to have a double effect on androgen metabolism: an initially stimulating, followed by an inhibitory, effect on the pituitary gland.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenoma / chemically induced. Antineoplastic Agents, Hormonal / adverse effects. Gonadotropin-Releasing Hormone / agonists. Leuprolide / adverse effects. Pituitary Neoplasms / chemically induced. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Biopsy. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed

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  • (PMID = 16448441.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 33515-09-2 / Gonadotropin-Releasing Hormone; EFY6W0M8TG / Leuprolide
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26. Guastamacchia E, Triggiani V, Tafaro E, De Tommasi A, De Tommasi C, Luzzi S, Sabbà C, Resta F, Terreni MR, Losa M: Evolution of a prolactin-secreting pituitary microadenoma into a fatal carcinoma: a case report. Minerva Endocrinol; 2007 Sep;32(3):231-6
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  • [Title] Evolution of a prolactin-secreting pituitary microadenoma into a fatal carcinoma: a case report.
  • 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.
  • We report the case of a fatal pituitary carcinoma evolving within 4 years from a PRL-secreting microadenoma.
  • 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.
  • This case represents the first documented rapid evolution from a microprolactinoma initially responding to dopamine agonists to a fatal pituitary carcinoma.
  • [MeSH-major] Carcinoma / pathology. Pituitary Neoplasms / pathology. Prolactinoma / pathology
  • [MeSH-minor] Adult. Combined Modality Therapy. Disease Progression. Dopamine Agonists / therapeutic use. Drug Resistance. Ergolines / therapeutic use. Fatal Outcome. Female. Humans. Octreotide / therapeutic use. Pituitary Apoplexy / etiology. Radiosurgery. Subarachnoid Hemorrhage / etiology

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  • (PMID = 17912159.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
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27. Sturm I, Kirschke S, Krahl D, Dörken B: Panhypopituitarism in a patient with breast cancer. Onkologie; 2004 Oct;27(5):480-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Panhypopituitarism in a patient with breast cancer.
  • Nevertheless, a specific cause--requiring specified treatment--for this symptom should be ruled out.
  • We report on a patient with a complex endocrine dysfunction that developed due to a tiny metastasis of a breast carcinoma in the pituitary stalk.
  • CASE REPORT: A 46- year-old woman presented with general ill feeling 3 years after operation for a breast carcinoma.
  • For the application of chemotherapy, an i.v.
  • In the postoperative period, an emergency situation developed due to demasked cortisol deficiency and hypernatremia.
  • Careful laboratory investigations revealed hypofunction of the anterior lobe of the pituitary gland and diabetes insipidus centralis.
  • By MRI imaging of the parasellar region, a 4 x 5 mm metastatic lesion in the pituitary stalk was found--notable only in knowledge of the clinical diagnosis.
  • The patient's condition and quality of life improved markedly with hormone replacement therapy.
  • CONCLUSION: Metastatic cancer may present as endocrine disease, either by release of hormone-like substances or by tumorous destruction of endocrine structures.
  • Metastases of solid tumors to the pituitary gland are often asymptomatic or present with diabetes insipidus.
  • The presentation with a hypofunction of the anterior and posterior lobe of the pituitary gland is a rare event.
  • It is recommended to consider endocrine dysfunction as potential cause of 'malaise' in a cancer patient.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma, Ductal / diagnosis. Carcinoma, Ductal / secondary. Hypopituitarism / diagnosis. Hypopituitarism / etiology. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secondary
  • [MeSH-minor] Fatigue / diagnosis. Fatigue / etiology. Female. Hormone Replacement Therapy / methods. Humans. Middle Aged. Treatment Outcome


28. Cos S, Sánchez-Barceló EJ: Melatonin and mammary pathological growth. Front Neuroendocrinol; 2000 Apr;21(2):133-70
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  • In this article we review the state of the art on the role of the pineal gland and melatonin in mammary cancer tumorigenesis in vivo as well as in vitro.
  • The former hypothesis of a possible role of the pineal gland in mammary cancer development was based on the evidence that the pineal, via its main secretory product, melatonin, downregulates some of the pituitary and gonadal hormones which control mammary gland development and are also responsible for the growth of hormone-dependent mammary tumors.
  • The working hypotheses of most experiments were that the activation of the pineal gland, or the administration of melatonin, should give rise to antitumoral behavior; conversely, suppression of the pineal gland or melatonin deficits should stimulate mammary tumorigenesis.
  • From in vivo studies on animal models of tumorigenesis, the general conclusion is that experimental manipulations activating the pineal gland, or the administration of melatonin, enlarge the latency and reduce the incidence and growth rate of chemically induced mammary tumors, while pinealectomy usually has the opposite effects.
  • The direct actions of melatonin on mammary tumors have been suggested because of its ability to inhibit, at physiological doses (1 nM), the in vitro proliferation and invasiveness of MCF-7 human breast cancer cells.
  • The fact that most studies have been performed on two models, chemically induced mammary adenocarcinoma in rats (in vivo studies) and the cell tumor line MCF-7 (in vitro studies), makes the generalization of the results somewhat difficult.
  • On the strength of these data, the small number of clinical studies focusing on the possible therapeutic value of melatonin on breast cancer is surprising.
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Division / drug effects. Female. Humans. Pineal Gland / physiopathology. Tumor Cells, Cultured

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  • [Copyright] Copyright 2000 Academic Press.
  • (PMID = 10764528.001).
  • [ISSN] 0091-3022
  • [Journal-full-title] Frontiers in neuroendocrinology
  • [ISO-abbreviation] Front Neuroendocrinol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] JL5DK93RCL / Melatonin
  • [Number-of-references] 181
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29. Vomachka AJ, Pratt SL, Lockefeer JA, Horseman ND: Prolactin gene-disruption arrests mammary gland development and retards T-antigen-induced tumor growth. Oncogene; 2000 Feb 21;19(8):1077-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolactin gene-disruption arrests mammary gland development and retards T-antigen-induced tumor growth.
  • Prolactin (PRL), interacting with other hormones from the pituitary, gonad, and placenta, activates specific signals that drive the appropriately timed morphological and functional development of the mammary gland.
  • A mouse model of isolated PRL deficiency (PRL-/-) was created by gene disruption in an effort to further understand the molecular basis of mammary gland development and breast cancer.
  • Replacement therapy with PRL injections stimulated a modest degree of lobular budding and ductal arborization (3.75+/-0.9).
  • Pituitary transplants to the kidney capsule of PRL-/- mice restored lobular budding and ductal arborization, to the full extent of that seen in control animals (20. 3+/-5.5).
  • Pregnancy, established by mating progesterone-treated PRL-/- females with PRL-/- males, led to complete morphological development of the mammary gland, appropriate to the gestational stage.
  • PRL treatment stimulated tyrosine phosphorylation and DNA binding activity of Stat5a, but not Stat1 in PRL-/- or PRL+/- females, and Stat5a, but not Stat1, was elevated by estradiol within 24 h.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. DNA-Binding Proteins / drug effects. DNA-Binding Proteins / metabolism. Female. Mice. Mice, Mutant Strains. Mice, Transgenic. Phosphorylation / drug effects. Pituitary Gland / transplantation. Pregnancy. STAT1 Transcription Factor. STAT5 Transcription Factor. Trans-Activators / drug effects. Trans-Activators / metabolism. Tyrosine / metabolism

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  • (PMID = 10713693.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / DNA-Binding Proteins; 0 / Milk Proteins; 0 / STAT1 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / Stat1 protein, mouse; 0 / Stat5a protein, mouse; 0 / Trans-Activators; 42HK56048U / Tyrosine; 9002-62-4 / Prolactin
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30. Gessl A, Vierhapper H, Feichtinger H: Non-suppressible TSH in a patient thyroidectomized due to follicular thyroid carcinoma. Exp Clin Endocrinol Diabetes; 2006 Jul;114(7):389-92
MedlinePlus Health Information. consumer health - Thyroid Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-suppressible TSH in a patient thyroidectomized due to follicular thyroid carcinoma.
  • Poor compliance or drug malabsorption are the most common reasons why an adequate TSH suppression is not achieved with oral levothyroxin in patients with hypothyroidism or thyroid carcinoma.
  • We report a female patient with follicular thyroid carcinoma in whom, under intended levothyroxin suppression therapy, a TSH-PRL-producing pituitary adenoma manifested by failure to achieve adequate TSH suppression, subtle signs of hyperthyroidism,and finally symptoms of elevated PRL.
  • [MeSH-minor] Adenocarcinoma, Follicular / blood. Adenocarcinoma, Follicular / diagnosis. Adenocarcinoma, Follicular / pathology. Adenocarcinoma, Follicular / surgery. Adult. Female. Humans. Pituitary Gland / pathology. Treatment Outcome

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  • (PMID = 16915543.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 9002-71-5 / Thyrotropin
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31. Lim S, Shahinian H, Maya MM, Yong W, Heaney AP: Temozolomide: a novel treatment for pituitary carcinoma. Lancet Oncol; 2006 Jun;7(6):518-20
Hazardous Substances Data Bank. DACARBAZINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temozolomide: a novel treatment for pituitary carcinoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Carcinoma / drug therapy. Dacarbazine / analogs & derivatives. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Aged. Combined Modality Therapy. Humans. Magnetic Resonance Imaging. Male. Treatment Outcome






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