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uterine neoplasms/phosphatase
Länken sparas på Urklipp
Sida 1 från 29 resultat
Screening for germline phosphatase and tensin homolog-mutations in suspected Cowden syndrome and Cowden syndrome-like families among uterine cancer patients.
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Cowden syndrome (CS) is an autosomal dominant disorder characterized by multiple hamartomas in the breast, thyroid and endometrium, with a prevalence of 1 per 250,000. Females with CS have a 21-28% lifetime risk of developing uterine cancer. Germline mutations in the phosphatase and tensin homolog
Heat-stable alkaline phosphatase in uterine cancer, with special reference to its histochemical heat-stability and the L-phenylalanine inhibition test.
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We report a histochemical study of alkaline phosphatase (ALP) in normal cells of the female reproductive system, in pre-cancerous and cancerous lesions of the uterine cervix and in endometrial cancer to ascertain the incidence of ALP and its isoenzyme type. For this purpose, serial sections were
[Phosphatases in uterine cancer. IV. Activity and localizations of alkaline phosphatases in the normal and neoplastic uterus; histochemical research].
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[Effects of hormone therapy on acid and alkaline phosphatases in the blood of patients with uterine neoplasms].
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Androgen actions via androgen receptor promote PTEN inactivation induced uterine cancer.
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Haploinsufficient inactivating phosphatase and tensin homolog (Pten) mutations cause Cowden syndrome, an autosomal dominant risk genotype for hormone dependent reproductive cancers. As androgen actions mediated via the androgen receptor (AR) supports uterine growth and may modify uterine cancer
The role of the phosphatidylinositol 3-kinase (PI3K) pathway in the development and treatment of uterine cancer.
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OBJECTIVE
Uterine cancer is the most common gynecologic malignancy in the United States. Although surgery is often curative for women diagnosed in the early stages, prognosis for patients with advanced disease is poor. Alterations in the phosphatidylinositol 3-kinase (PI3K) pathway are known to play
Precision Therapy for Aggressive Endometrial Cancer by Reactivation of Protein Phosphatase 2A.
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Critically important to reducing uterine cancer mortality is the development of more effective therapy for aggressive endometrial cancers, including uterine serous cancer and uterine carcinosarcoma, which together account for over half of deaths due to endometrial cancer. About one-third of these
AKT involvement in cisplatin chemoresistance of human uterine cancer cells.
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OBJECTIVE
The aim of this study was to investigate the possible involvement of Akt activity and specific isoforms (Akt1, Akt2, and Akt3) in the resistance of human uterine cancer cells to cisplatin.
METHODS
Two different endometrial (HEC-1-A and KLE) and one cervical (HeLa) cancer cell lines all
Uterine retiform sertoli-leydig cell tumor: report of a case providing additional evidence that uterine tumors resembling ovarian sex cord tumors have a histologic and immunohistochemical phenotype of genuine sex cord tumors.
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We report a case of a retiform Sertoli-Leydig cell tumor of intermediate differentiation presenting as a uterine intracavity polypoid mass in a 63-year-old woman. In contrast to sertoliform endometrioid carcinoma and to hitherto reported uterine tumors resembling ovarian sex cord tumors (UTROSCTs),
Recurrent PPP2R1A Mutations in Uterine Cancer Act through a Dominant-Negative Mechanism to Promote Malignant Cell Growth.
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Somatic missense mutations in the Ser/Thr protein phosphatase 2A (PP2A) Aα scaffold subunit gene PPP2R1A are among the few genomic alterations that occur frequently in serous endometrial carcinoma (EC) and carcinosarcoma, two clinically aggressive subtypes of uterine cancer with few therapeutic
Comparative clinicopathologic and immunohistochemical analysis of uterine sarcomas diagnosed using the World Health Organization classification system.
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Uterine sarcomas are rare tumors that account for 3% to 7% of uterine cancers. Their histopathologic classification was revised by the World Health Organization (WHO) in 2003. The objectives of this study were to determine the frequency of different subtypes of uterine sarcoma applying the WHO
EM-652 (SCH57068), a pure SERM having complete antiestrogenic activity in the mammary gland and endometrium.
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In order to minimize the risks of endometrial cancer and the development of resistance to antiestrogen therapy, we have synthesized the orally active antiestrogen EM-652 which is the most potent of the known antiestrogens and exerts pure antiestrogenic activity in the mammary gland and endometrium.
PTPH1 immunohistochemical expression and promoter methylation in breast cancer patients from India: A retrospective study.
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Protein Tyrosine Phosphatase H1/Protein Tyrosine Phosphatase Non receptor Type 3 (PTPH1/PTPN3) is upregulated and/or mutated in glioma, ovarian, gastric, and colorectal cancers. Previous studies have documented that PTPH1-associated breast cancers exhibit enhanced sensitivity to tamoxifen and
Significance of serum tumor markers in patients with carcinoma of the ovary.
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A comparison of preoperative serum tumor markers (lactate dehydrogenase, lactate dehydrogenase isoenzymes, alpha-hydroxybutyrate dehydrogenase, alkaline phosphatase, aldolase, leucine aminopeptidase, cholinesterase, erythrocyte sedimentation reaction, carcinoembryonic antigen, alpha-fetoprotein, and
A uterine choriocarcinoma in a virgin Donryu rat.
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A uterine choriocarcinoma was found in a 49-wk-old virgin Donryu rat given intrauterine administration of N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG). The tumor was macroscopically present as a bloody cystic mass and microscopically composed of 2 kinds of cells: small basophilic cells similar to
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