Epithelial–mesenchymal transition and clinicopathological correlation in craniopharyngioma

Qi, Songtao; Zhou, Jie; Zhang, Chao; Chotai, Silky; Xing, Yan

doi:10.1111/j.1365-2559.2012.04297.x

Cited by 27 publications

(20 citation statements)

References 36 publications

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“…The presence of squamous metaplasia makes the distinction between a papillary craniopharyngioma and an RCC difficult. 18,27,31,33,35,40,52 In the present study, 4 of the 11 recurrent cases demonstrated a tumor-like appearance of the cyst on preoperative MRI; however, the histopathology revealed RCCs with squamous metaplasia (Fig. 4D).…”

Section: Squamous Metaplasiamentioning

confidence: 76%

Characteristics of Rathke's cleft cyst based on cyst location with a primary focus on recurrence after resection

Chotai¹,

Liu²,

Qi³

2015

JNS

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Rathke's cleft cysts (RCCs) are nonneoplastic epithelial lesions of the sellar and suprasellar region. They are typically asymptomatic with a slow growth rate. An asymptomatic RCC is most often diagnosed at autopsy with a reported incidence of 5%-33%. 5,[47][48][49] Quite often some RCCs grow over time and can become sufficiently large to cause a compressive effect on surrounding structures, resulting in neurological and endocrine abnormalities. 7,28,37,42 Sixteen patients (18%) had an entirely intrasellar RCC, 21 (24%) had a purely suprasellar cyst, and 50 (58%) had an intrasuprasellar RCC. The mean cyst volume was 2.4 ± 0.9 cm 3 (range 0.36-4.9 cm 3 ). Headache was the most frequent initial symptom (76%) followed by visual disturbance (45%). The transsphenoidal approach was performed for all intrasellar RCCs (16 cysts) and 33 of 50 intrasuprasellar RCCs. The transcranial route was used for all suprasellar cysts (21 cysts) and 17 of 50 intrasuprasellar RCCs. Squamous metaplasia was present in 27 (31%) of 87 RCCs. The occurrence of squamous metaplasia was associated with cyst location (p = 0.027), T1 signal intensity (p = 0.004) and ring enhancement on Gd-enhanced MRI (p = 0.017), and cyst volume (p = 0.045). A suprasellar location (p = 0.048, OR 3.89, 95% CI 1.010-15.020), ring enhancement on Gd-enhanced MRI (p = 0.028, OR 3.922, 95% CI 1.158-13.288), hypointensity on T1-weighted MRI (p = 0.002, OR 6.86, 95% CI 1.972-23.909), and cyst volume (p = 0.01, OR 0.367, 95% CI 0.170-0.789) were independent predictors of squamous metaplasia. The mean time to reaccumulation (11 [12.6%] of 87 cases) and recurrence (7 [8%] of 87 cases) was 14 ± 6 months. Recurrence-free survival was 84.5% at a mean of 98.2 ± 4.6 months after treatment. A suprasellar cyst location (p = 0.007, OR 7.7, 95% CI 1.75-34.54), the occurrence of squamous metaplasia (p = 0.007, OR 19.3,, and isointensity on T2-weighted MRI (p = 0.041, OR 10.29, 95% CI 1.094-96.872) were the independent predictors of RCC recurrence. coNclusioNs A suprasellar cyst location, the occurrence of squamous metaplasia, and isointensity on T2-weighted MRI were independent predictors of RCC recurrence. The extent of resection and type of surgical approach used were not associated with recurrence. A tailored extent of resection based on cyst location and predictive factors is recommended.

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Section: Squamous Metaplasiamentioning

confidence: 76%

Characteristics of Rathke's cleft cyst based on cyst location with a primary focus on recurrence after resection

Chotai¹,

Liu²,

Qi³

2015

JNS

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“…Our previous research revealed that EMT may serve a role in the pathogenesis and development of CP, particularly ACP (7). However, the role of IL-6, particularly in association with EMT, in ACP progression is unclear.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-6 induces an epithelial-mesenchymal transition phenotype in human adamantinomatous craniopharyngioma cells and promotes tumor cell migration

Zhou

Zhang

Pan

et al. 2017

Molecular Medicine Reports

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Total resection of adamantinomatous craniopharyngioma (ACP) is complex and often leads to postoperative recurrence. This is due to the tendency of the tumor to invade the surrounding brain tissue and the generation of a local inflammatory state between the tumor cells and parenchyma. While there is evidence to suggest that interleukin-6 (IL-6) induces craniopharyngioma (CP)-associated inflammation, particularly in ACP, the role of IL-6 in the progression of ACP remains unclear. The results of the present study demonstrated that CP inflammation was associated with pathological classification, extent of surgery, degree of calcification and postoperative hypothalamic status scale. Cytokine antibody arrays were conducted to measure the expression of IL-6 and other inflammatory factors in tumor tissues in response to various levels of inflammatory exposure. IL-6, IL-6 receptor (IL-6R) and glycoprotein 130 expression was detected by immunohistochemistry. In addition, an ELISA was performed to quantify the levels of soluble IL-6R (sIL-6R) in the cystic fluid and supernatants of ACP cells and tumor-associated fibroblasts. These measurements demonstrated that ACP cells produce IL-6 and its associated proteins. In addition, the results revealed that while the viability of ACP cells was not affected, the migration of ACP cells was promoted by IL-6 treatment in a concentration-dependent manner. Conversely, treatment with an IL-6-blocking monoclonal antibody significantly decreased the migration of ACP cells. In addition, IL-6 treatment increased the expression of vimentin and decreased the expression of E-cadherin in a dose-dependent manner. The findings of the present study demonstrate that IL-6 may promote migration in vitro via the classic- and trans-signaling pathways by inducing epithelial-mesenchymal transition in ACP cell cultures.

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“…22 Other factors suggested to have roles in the invasion of ACP include matrix metalloproteinases, E-cadherin, vimentin, and claudin-1. 42,49 However, so far no studies have assessed the relevance of these pathways and their inhibition in in vivo models of human ACP.…”

Section: Molecular Biology Of B-cateninaccumulating Cell Clustersmentioning

confidence: 99%

Molecular pathology of adamantinomatous craniopharyngioma: review and opportunities for practice

Apps¹,

Martinez-Barbera²

2016

FOC

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Since the first identification of CTNNB1 mutations in adamantinomatous craniopharyngioma (ACP), much has been learned about the molecular pathways and processes that are disrupted in ACP pathogenesis. To date this understanding has not translated into tangible patient benefit. The recent development of novel techniques and a range of preclinical models now provides an opportunity to begin to support treatment decisions and develop new therapeutics based on molecular pathology. In this review the authors summarize many of the key findings and pathways implicated in ACP pathogenesis and discuss the challenges that need to be tackled to translate these basic science findings for the benefit of patients.

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Epithelial–mesenchymal transition and clinicopathological correlation in craniopharyngioma

Abstract: Our study demonstrates, for the first time, the potential prognostic implications of vimentin, E-cadherin and β-catenin expression in craniopharyngiomas. EMT may represent a crucial mechanism in the progression of craniopharyngiomas.

Cited by 27 publications

References 36 publications

Characteristics of Rathke's cleft cyst based on cyst location with a primary focus on recurrence after resection

Characteristics of Rathke's cleft cyst based on cyst location with a primary focus on recurrence after resection

Interleukin-6 induces an epithelial-mesenchymal transition phenotype in human adamantinomatous craniopharyngioma cells and promotes tumor cell migration

Molecular pathology of adamantinomatous craniopharyngioma: review and opportunities for practice

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