Matrix metalloproteinase-9, a potential biological marker in invasive pituitary adenomas

Gong, Jianbin; Zhao, Yunge; Abdel-Fattah, Rana; Amos, Samson; Xiao, Aizhen; Lopes, M. Beatriz S.; Hussaini, Isa M.; Laws, Edward R.

doi:10.1007/s11102-007-0066-2

Cited by 63 publications

(39 citation statements)

References 45 publications

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“…PTTG and MMP9 were also up-regulated in the invasive tumors, as measured by qRT-PCR (data not shown), in keeping with previous findings (Turner et al 2000, Trouillas et al 2003, Filippella et al 2006, Gong et al 2008, Hussaini et al 2007, Wierinckx et al 2007. At the protein level, PTTG staining was stronger in invasive tissues and displayed a good correlation with that of MYO5A.…”

Section: Igfbp5supporting

confidence: 90%

“…The role of PTTG (Zhang et al 1999, Salehi et al 2008 and the N-terminally truncated isoform of fibroblast growth factor receptor 4 (FGFR4) (ptd-FGFR4; Qian et al 2004) has been suggested. Overexpression of polysialylated neural cell adhesion molecule has been related to pituitary adenoma invasion (Trouillas et al 2003), and overexpression of matrix metalloproteases (MMPs), and particularly MMP-9, has been detected in various types of invasive adenoma (Turner et al 2000, Gong et al 2008, Hussaini et al 2007. Bone morphogenic protein, a factor involved in gonadotroph tumor development, might also play a role along with retinoic acid-inducible neural-specific protein 3 (Shorts-Cary et al 2007).…”

Section: Introductionmentioning

confidence: 99%

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Differential gene expression profiles of invasive and non-invasive non-functioning pituitary adenomas based on microarray analysis

Galland¹,

Lacroix²,

Saulnier³

et al. 2010

Endocrine-Related Cancer

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Non-functioning pituitary adenomas (NFPAs) may be locally invasive. Markers of invasiveness are needed to guide patient management and particularly the use of adjuvant radiotherapy. To examine whether invasive NFPAs display a specific gene expression profile relative to non-invasive tumors, we selected 40 NFPAs (38 of the gonadotroph type) and classified them as invasive (nZ22) or non-invasive (nZ18) on the basis of magnetic resonance imaging and surgical findings. We then performed pangenomic analysis with the 44k Agilent human whole genome expression oligonucleotide microarray in order to identify genes with differential expression between invasive and non-invasive NFPAs. Candidate genes were then tested in qRT-PCR. Prediction class analysis showed that the expression of 346 genes differed between invasive and non-invasive NFPAs (P!0.001), of which 233 genes were up-regulated and 113 genes were down-regulated in invasive tumors. On the basis of Ingenuity networks and the degree of up-or down-regulation in invasive versus non-invasive tumors, 35 genes were selected for expression quantification by qRT-PCR. Overexpression of only four genes was confirmed, namely IGFBP5 (PZ0.02), MYO5A (PZ0.04), FLT3 (PZ0.01), and NFE2L1 (PZ0.02). At the protein level, only myosin 5A (MYO5A) immunostaining was stronger in invasive than in non-invasive NFPAs. Molecular signature allows to differentiate 'grossly' invasive from non-invasive NFPAs. The product of one of these genes, MYO5A, may be a useful marker of tumor invasiveness.

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Section: Igfbp5supporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Differential gene expression profiles of invasive and non-invasive non-functioning pituitary adenomas based on microarray analysis

Galland¹,

Lacroix²,

Saulnier³

et al. 2010

Endocrine-Related Cancer

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“…6 Alternatively, the biology of GH-secreting adenomas may enable them to more easily invade surrounding dural and/or bony structures, perhaps due to differential expression of proteins involved with degradation, such as matrix metalloproteinases. 5,7,15 Consistent with this reasoning is that GH-secreting adenomas with a more aggressive inherent tumor biology that met the WHO criteria for atypical adenomas demonstrated especially peculiar patterns of isolated extension through the sellar floor and into the clivus, comprising 5 of the 13 GH-secreting adenomas with such growth. However, nonfunctional adenomas are typically larger tumors at the time of diagnosis and tend to grow through the diaphragmatic aperture and into the suprasellar cistern without primarily invading bony structures or the cavernous sinus, until they become larger tumors.…”

Section: Discussionmentioning

confidence: 84%

Patterns of extrasellar extension in growth hormone–secreting and nonfunctional pituitary macroadenomas

Zada¹,

Lin²,

Laws³

2010

FOC

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Object Growth patterns of pituitary adenomas have been observed to vary by histopathological subtype. The authors aimed to analyze variations in the patterns of extrasellar extension of nonfunctional macroadenomas (NFMAs) and growth hormone (GH)–secreting macroadenomas. Methods A retrospective review was conducted of data obtained in 75 patients who underwent transsphenoidal operations for histologically confirmed NFMAs (50 patients) and GH-secreting macroadenomas (25 patients) at the Brigham and Women's Hospital over an 18-month period. Patients with microadenomas and prior operations were excluded from the analysis. Preoperative MR images were reviewed to assess patterns of extrasellar extension in the varying tumor subtypes. Results The mean maximal tumor diameter in NFMAs and GH-secreting macroadenomas was 26 and 16 mm, respectively (p < 0.0001). Extension of the NFMAs occurred into the following regions: infrasellar, 23 patients (46%); suprasellar, 41 patients (82%); and cavernous sinus, 20 patients (40%). Extension of GH-macroadenomas occurred into the following regions: infrasellar, 18 patients (72%); suprasellar, 4 patients (16%); and cavernous sinus, 4 patients (16%). Compared with GH-adenomas, NFMAs were more likely to develop suprasellar extension (82% vs 16%, p < 0.0001), cavernous sinus extension (40% vs 16%, p = 0.04), and isolated suprasellar extension (30% vs 4%, p = 0.0145). GH-macroadenomas had higher overall rates of infrasellar extension (72% vs 46%, p < 0.05), and isolated infrasellar extension (52% vs 6%, p < 0.0001). Of the 13 GH-macroadenomas with isolated infrasellar extension, 5 (42%) met WHO criteria for atypical adenomas. Conclusions Substantial differences in extrasellar growth patterns were observed among varying histological subtypes of pituitary macroadenomas. Despite smaller tumor diameters, GH-macroadenomas demonstrated a proclivity for infrasellar extension, whereas NFMAs exhibited preferential extension into the suprasellar region.

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“…Many researches have illustrated that MMP2 (Liu et al 2005) and MMP9 (Gong et al 2008) play important roles in pituitary tumor invasion. Both MMP2 and MMP9 are type IV collagenases, which can break down basement membrane, in particular, cleaving type IV collagen (Kawamoto et al 1996).…”

Section: Discussionmentioning

confidence: 99%

ADAM10 promotes pituitary adenoma cell migration by regulating cleavage of CD44 and L1

Pan¹,

Han²,

Wang³

et al. 2012

Journal of Molecular Endocrinology

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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 highgrade 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.

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Matrix metalloproteinase-9, a potential biological marker in invasive pituitary adenomas

Cited by 63 publications

References 45 publications

Differential gene expression profiles of invasive and non-invasive non-functioning pituitary adenomas based on microarray analysis

Differential gene expression profiles of invasive and non-invasive non-functioning pituitary adenomas based on microarray analysis

Patterns of extrasellar extension in growth hormone–secreting and nonfunctional pituitary macroadenomas

ADAM10 promotes pituitary adenoma cell migration by regulating cleavage of CD44 and L1

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