Ureteropelvic junction obstruction caused by metastatic cholangiocarcinoma

Pickersgill, Nicholas A.; Wright, Alec J.; Figenshau, Robert S.

doi:10.1590/s1677-5538.ibju.2019.0053

Cited by 7 publications

(5 citation statements)

References 10 publications

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“…Cholangiocarcinoma (CCA), the second most common type of primary liver cancer, is a type of cancer that pathologically arises from the dysregulation of bile duct epithelial cells [1]. CCA-related morbidity has been significantly increasing, as confirmed by a large surveillance, epidemiology and end results database review reporting a 128% net increase in the last 40 years [2].…”

Section: Introductionmentioning

confidence: 99%

LINC00630 promotes cholangiocarcinoma cell proliferation, migration and invasion by mediating the miR-199a/FGF7 axis

Zhong¹,

Caixin²,

He³

et al. 2022

J. Cancer

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Cholangiocarcinoma (CCA) is a type of cancer with a relatively low morbidity, but poor prognosis. Aberrant long non-coding RNA (lncRNA) expression has been observed in the pathological development of CCA. In the present study, lncRNA long intergenic non-protein coding RNA 630 (LINC00630) was found to be significantly upregulated in CCA tissues and cultured cells. LINC00630 expression was positively associated with histological differentiation, TNM stage and lymph node invasion. Short hairpin RNA (sh)-LINC00630 transfection could effectively decrease CCA cell proliferation, migration and invasion. Further investigations found that LINC00630 could interact with microRNA (miR)-199a, which specifically targeted fibroblast growth factor 7 (FGF7) for degradation. FGF7 overexpression restored the sh-LINC00630 transfection-induced decrease in CCA cell proliferation, migration and invasion. In conclusion, LINC00630 significantly promoted CCA cell proliferation, migration and invasion by upregulating FGF7 through miR-199a sponging.

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Section: Introductionmentioning

confidence: 99%

LINC00630 promotes cholangiocarcinoma cell proliferation, migration and invasion by mediating the miR-199a/FGF7 axis

Zhong¹,

Caixin²,

He³

et al. 2022

J. Cancer

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“…Pelviureteric junction (PUJ) obstruction is a common urological disorder with an incidence of 1 in 1000 to 1500 live births; however, the incidence is not well-defined in adults. [1][2][3] Congenital causes are common, and PUJ obstruction (PUJO) accounts for 5% of antenatal hydronephrosis cases. [2] However, patients may present at any stage of life, and the most common primary symptom is flank pain, although PUJO may also be detected incidentally.…”

Section: Introductionmentioning

confidence: 99%

Pelviureteric junction obstruction in adults: A systematic review of the literature

O’Sullivan

Anderson

2022

Curr Urol

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BackgroundPelviureteric junction obstruction (PUJO) is a common urological disorder that can present at any stage of life. The underlying etiology in children has been well studied; however, a gap exists in the literature for the adult population. Herein, we performed a systematic review of the literature to evaluate the current evidence on the underlying etiologies of adult patients presenting with PUJO.Materials and methodsFour electronic databases were searched for relevant studies assessing the underlying etiologies of pelviureteric junction obstruction in adults. Studies were assessed for eligibility based on predefined inclusion and exclusion criteria, and a critical appraisal of methodological quality and risk of bias was performed. Finally, qualitative and quantitative data analyses were performed.ResultsTwelve studies comprising a total of 513 patients with radiologically confirmed PUJO met the inclusion criteria and were included in our analysis. The most common finding was crossing vessels, which were observed in 50.5% of patients, followed by intrinsic ureteral stenosis (27.1%), adhesions (15.3%), and high insertion of the ureter (10.1%).ConclusionsThe underlying etiologies of PUJO in adults remain unclear. This study indicated that obstruction secondary to crossing vessels is the most common cause of obstruction in adults and occurs more frequently than in the pediatric population.

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“…Cholangiocarcinoma (CCA) is the uncontrollable transformation of biliary duct cells derived from intrahepatic and extrahepatic bile ducts (Blechacz 2017 ; Pickersgill et al 2019 ). In recent years, the frequency of cholangiocarcinoma has increased gradually (Siegel et al 2018 ).…”

Section: Introductionmentioning

confidence: 99%

SP1 induced long non-coding RNA AGAP2-AS1 promotes cholangiocarcinoma proliferation via silencing of CDKN1A

Wang

et al. 2021

Mol Med

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Background LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration. Methods We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1. Results AGAP2-AS1 was significantly upregulated in CCA tumor tissues. SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA. Conclusions We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.

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Ureteropelvic junction obstruction caused by metastatic cholangiocarcinoma

Cited by 7 publications

References 10 publications

LINC00630 promotes cholangiocarcinoma cell proliferation, migration and invasion by mediating the miR-199a/FGF7 axis

LINC00630 promotes cholangiocarcinoma cell proliferation, migration and invasion by mediating the miR-199a/FGF7 axis

Pelviureteric junction obstruction in adults: A systematic review of the literature

SP1 induced long non-coding RNA AGAP2-AS1 promotes cholangiocarcinoma proliferation via silencing of CDKN1A

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