RESUMO
OBJECTIVE: Patients with prolactinoma seem to be at high risk for osteopenia. However, whether patients with various pathological sellar tumors have risk for osteopenia remains unclear. The aim of the present study is to assess the bone mass alteration in patients with various sellar tumors and further to investigate the risk factors of bone mass alteration. MATERIALS AND METHODS: 65 premenopausal female patients with diverse sellar tumors and 325 normal controls were enrolled in this study. Bone mineral density (BMD) of lumbar spine and comprehensive endocrinological evaluations were undergone. RESULTS: Compared to the matched controls, BMD of patients with prolactinoma or craniopharyngioma significantly decreased. Patients with sellar meningioma and nonfunctioning adenoma are with a decreasing tendency and patients with growth hormone-secreting adenoma are with an increasing tendency compared to controls. Univariate and multivariate regression analysis indicated that the bone loss in prolactinomas was significantly correlated to disease duration and hypogonadism. CONCLUSION: In the premenopausal women, patients with prolactinoma or craniopharyngioma are often accompanied with osteopenia or osteoporosis, and disease duration and hypogonadism are the risk factors of bone loss in prolactinoma. Continuous surveillance of BMD is recommended in patients with meningioma or nonfunctioning adenoma.
Assuntos
Doenças Ósseas Metabólicas/epidemiologia , Craniofaringioma/complicações , Neoplasias Hipofisárias/complicações , Prolactinoma/complicações , Neoplasias da Base do Crânio/complicações , Adenoma/complicações , Adenoma/fisiopatologia , Adolescente , Adulto , Densidade Óssea , Doenças Ósseas Metabólicas/complicações , Doenças Ósseas Metabólicas/etiologia , China/epidemiologia , Craniofaringioma/fisiopatologia , Feminino , Adenoma Hipofisário Secretor de Hormônio do Crescimento/complicações , Adenoma Hipofisário Secretor de Hormônio do Crescimento/fisiopatologia , Humanos , Hipogonadismo/etiologia , Neoplasias Meníngeas/complicações , Neoplasias Meníngeas/fisiopatologia , Meningioma/complicações , Meningioma/fisiopatologia , Pessoa de Meia-Idade , Osteoporose/complicações , Osteoporose/epidemiologia , Osteoporose/etiologia , Neoplasias Hipofisárias/fisiopatologia , Pré-Menopausa , Prolactinoma/fisiopatologia , Fatores de Risco , Neoplasias da Base do Crânio/fisiopatologia , Fatores de Tempo , Adulto JovemRESUMO
In the centrosymmetric dinuclear title compound, [Ag(2)(C(36)H(26)N(8))(2)](PF(6))(2)·2C(2)H(3)N, the Ag(+) ion is bound to four N atoms from two 1,2-diphenyl-N,N'-bis-(di-2-pyridyl-methyl-eneamino)ethane-1,2-diimine ligands in a distorted tetra-hedral geometry. The ligand adopts a twist conformation, coordinating two metal centers by three pyridyl N atoms and one imine N atom and spanning two Ag(+) ions, resulting in the formation of a helical dimeric structure.
RESUMO
Hepatoma-derived growth factor (HDGF) plays an important role in tumor progression. Highly expressed HDGF has been found to indicate poor prognosis in many cancers. However, no information is available regarding the prognostic value of nuclear or cytoplasmic HDGF staining level in breast cancer. In the present study, the nuclear or cytoplasmic HDGF staining level was investigated in 86 patients with primary breast cancer by immunohistochemistry; the relationship between nuclear or cytoplasmic HDGF staining level and clinicopathological parameters was examined by Two-tailed Mann-Whitney U-test or Krustal-Wallis. The prognostic value of nuclear or cytoplasmic HDGF staining level in disease-free survival and overall survival was analyzed by Kaplan-Meier methods and log-rank test. We found that the percentage of cases with strong nuclear HDGF staining level was significantly higher in the cases with high tumor grade, high stage, high proliferation index (Ki-67 index>20%), as well as in those with lymph node invasion and recurrence (p<0.05) compared to those without. No significant correlation was found between cytoplasmic HDGF expression and any clinicopathological variables. In addition, disease-free survival and overall survival were significantly lower in patients with high nuclear HDGF expression (level 2) than in those with low nuclear HDGF expression (level 0 and level 1). Further Cox multivariate analysis showed that high nuclear HDGF expression is an independent factor for indicating poor prognosis in breast cancer patients. No significant difference in disease-free survival rate and overall survival was found between different cytoplasmic HDGF staining levels. All these findings suggest that increased nuclear HDGF expression is involved in tumor progression and might be used as a new prognosticator for breast cancer.
Assuntos
Adenocarcinoma/metabolismo , Neoplasias da Mama/metabolismo , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Adenocarcinoma/diagnóstico , Adenocarcinoma/mortalidade , Neoplasias da Mama/diagnóstico , Neoplasias da Mama/mortalidade , Núcleo Celular/metabolismo , Núcleo Celular/patologia , China/epidemiologia , Citoplasma/metabolismo , Citoplasma/patologia , Intervalo Livre de Doença , Feminino , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Metástase Linfática , Pessoa de Meia-Idade , Estadiamento de Neoplasias , PrognósticoRESUMO
ADAM10 is a metalloproteinase that regulates invasiveness in many tumors. Here, we found that ADAM10 expression correlates with the invasiveness of pituitary adenomas and contributes to invasion by cleaving L1 and CD44. In high-grade pituitary adenoma patients, ADAM10 expression levels were found to be elevated compared with low-grade pituitary adenomas. In a phorbol 12-myristate 13-acetate (PMA)-stimulated pituitary adenoma cell line, AtT-20 cells, we found that the cleavage of L1 was correspondingly enhanced with the increased interaction between Src and Shc. Increases in PMA-induced L1 cleavage and the phosphorylation of residue 418 of Src (418Src) were promoted by overexpression of ADAM10. Inversely, knockdown of Adam10 suppressed PMA-induced L1 cleavage and the phosphorylation of Src, which was blocked by the Src inhibitor PP2 and the MEK inhibitor PD98059. On the other hand, calcium flux activation in AtT-20 cells resulted in increased CD44 cleavage, with reduction of the interaction between calmodulin and ADAM10. The induction of enhanced CD44 cleavage by calcium flux activation was inhibited by knockdown of Adam10. In addition, Adam10 knockdown repressed AtT-20 cell migration, which was reversed by CD44EXT (CD44 ectodomain cleavage). Collectively, these data indicated that ADAM10 facilitated cell migration through modulation of CD44 and L1 cleavage.