Expression of E-cadherin, Slug and NCAM and its relationship to tumor invasiveness in patients with acromegaly

Mendes, Graziella Alebrant; Haag, Taiana; Trott, Geraldine; Rech, Carolina Garcia Soares Leães; Ferreira, Nelson Pires; Oliveira, Miriam C.; Kohek, Maria Beatriz da Fonte; Pereira-Lima, Júlia Fernanda Semmelmann

doi:10.1590/1414-431x20176808

Cited by 10 publications

(12 citation statements)

References 39 publications

(57 reference statements)

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“…Elston et al [15] assessed 10 GH producing adenomas, of whom 4 had strong to moderate immunohistochemical expression for ECAD, 2 had weak expression for it and 4 had none. They also identified positivity in 96.7% of the acromegalic patients [17]. Other authors reported lower ECAD expression on the cytoplasmic membrane of GH producing adenomas with prominent fibrous bodies than on other pituitary adenoma subtypes.…”

Section: Resultsmentioning

confidence: 87%

“…There are few studies about ECAD gene expression in pituitary adenomas. The research conducted by Elston et al [15] showed ECAD expression in 29 out of 30 assessed pituitary adenomas, whereas Mendes et al [17] found it in 50% of their sample. According to research that have assessed the methylation of CDH1, up to 37% of pituitary adenomas have hypermethylation.…”

Section: Resultsmentioning

confidence: 92%

“…The role of ECAD in pituitary adenoma invasiveness is not yet fully known, it remains inconclusive see Table 1. Four studies about the functioning and nonfunctioning pituitary adenomas did not find correlation between ECAD gene or immunohistochemical expression and tumor invasiveness [11][12][13][14][15][16][17]. In the study conducted by Elston et al [15], only ECAD nuclear expression was related to tumor invasiveness.…”

Section: Resultsmentioning

confidence: 99%

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Pituitary Adenoma Pathogenesis: The Presence Of E-Cadherin and Its Influence on Tumor Invasiveness

Mendes¹

2019

BJSTR

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E-cadherin (ECAD) loss on cell surface is related to invasiveness, metastases and bad prognosis in several malignant tumors of epithelial origin. Pituitary adenomas are common and benign tumors; however, they can become aggressive and invade other tissues. The herein assessed research describe ECAD positivity in most pituitary adenomas, but the relation between ECAD and tumor invasiveness led to different results. Further research is needed in order to better understand the ECAD impact on tumor development.

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Section: Resultsmentioning

confidence: 87%

Section: Resultsmentioning

confidence: 92%

Section: Resultsmentioning

confidence: 99%

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Pituitary Adenoma Pathogenesis: The Presence Of E-Cadherin and Its Influence on Tumor Invasiveness

Mendes¹

2019

BJSTR

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“…Similarly, E-cadherin among other adhesion molecules was related to invasiveness and proliferative status of prolactinomas ( 20 , 21 ). Other classical EMT markers, such as N-cadherin, SNAI1 , SNAI2 and TWIST ( 21 , 22 ) or β-catenin ( 23 ) have also been associated with a worse clinical course in pituitary tumors, especially indicating an invasive phenotype, although there is some controversy regarding this subject in acromegaly ( 21 , 24 ).…”

Section: Epithelial–mesenchymal Transition In Pituitary Tumorsmentioning

confidence: 99%

Epithelial–Mesenchymal Transition in the Resistance to Somatostatin Receptor Ligands in Acromegaly

et al. 2021

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Epithelial-mesenchymal transition (EMT) is a dynamic process by which epithelial cells loss their phenotype and acquire mesenchymal traits, including increased migratory and invasive capacities. EMT is involved in physiological processes, such as embryogenesis and wound healing, and in pathological processes such as cancer, playing a pivotal role in tumor progression and metastasis. Pituitary tumors, although typically benign, can be locally invasive. Different studies have shown the association of EMT with increased tumor size and invasion in pituitary tumors, and in particular with a poor response to Somatostatin Receptor Ligands (SRLs) treatment in GH-producing pituitary tumors, the main cause of acromegaly. This review will summarize the current knowledge regarding EMT and SRLs resistance in acromegaly and, based on this relation, will suggest new biomarkers and possible therapies to SRLs resistant tumors.

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“…28 Increased NCAM was associated with PitNET invasion, particularly its polysialylated form, which was not detected in the normal pituitary. 13,29 However, other studies have reported no association between NCAM expression and pituitary tumour invasiveness, 27,30 and so the role of NCAM in the pathophysiology and aggressiveness of pituitary tumours remains to be elucidated. Moreover, the influence of the TME on NCAM has not previously been studied in PitNETs.…”

Section: Introductionmentioning

confidence: 99%

The expression of neural cell adhesion molecule and the microenvironment of pituitary neuroendocrine tumours

Marques

Barry

Carlsen³

et al. 2021

J Neuroendocrinology

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The neural cell adhesion molecule (NCAM) has previously been studied in pituitary neuroendocrine tumours (PitNETs), but its role in tumour biology and aggressiveness remains controversial, and its relationship with the tumour microenvironment remains unknown. We aimed to characterise NCAM expression in PitNETs, to correlate this with clinico-pathological features, and to assess the role of various microenvironment components on NCAM expression. NCAM and immune cells were investigated by immunohistochemistry in 16 human non-functioning-PitNETs (NF-PitNETs) and eight somatotrophinomas, including macrophages (CD68, CD163, HLA-DR), cytotoxic (CD8) and T helper (CD4) lymphocytes, regulatory T cells (FOXP3), B cells (CD20), and neutrophils (neutrophil elastase). Five normal pituitaries were included for comparison. The cytokine secretome from these PitNETs and from PitNETderived tumour-associated fibroblasts (TAFs) were assessed on culture supernatants using a multiplex immunoassay panel. There were no significant NCAM expression differences between PitNETs and normal pituitary, and no difference between types of pituitary tumours (NF-PitNETs vs. somatotrophinomas). There was no association between NCAM expression and different clinico-pathological features, including cavernous sinus invasion and Ki-67, nor with serum hormone levels. NCAM immunoreactivity correlated negatively with PitNET-derived CXCL10 (rho = −0.417; p = .042) and CX3CL1 (rho = −0.423; p = .040) levels. NCAM immunoreactivity was negatively correlated with TAF-derived fibroblast growth factor (FGF)-2 (rho = −0.632; p = .009), but not with other TAF-derived cytokines. Within the PitNET cohort, there were no correlations between NCAM immunoreactivity and immune infiltrates or ratios, although, within NF-PitNETs, NCAM expression was higher in tumours with more FOXP3+ cells. NCAM expression does not differ between PitNETs and normal pituitary, and does not appear to relate to tumour invasiveness or proliferation.However, our data suggest a possible role for cytokines in the modulation of NCAM expression in PitNETs, particularly CXCL10, CX3CL1 and FGF-2, but not for immune cell infiltrates.

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Expression of E-cadherin, Slug and NCAM and its relationship to tumor invasiveness in patients with acromegaly

Cited by 10 publications

References 39 publications

Pituitary Adenoma Pathogenesis: The Presence Of E-Cadherin and Its Influence on Tumor Invasiveness

Pituitary Adenoma Pathogenesis: The Presence Of E-Cadherin and Its Influence on Tumor Invasiveness

Epithelial–Mesenchymal Transition in the Resistance to Somatostatin Receptor Ligands in Acromegaly

The expression of neural cell adhesion molecule and the microenvironment of pituitary neuroendocrine tumours

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