Wnt and Kras signaling-dark siblings in lung cancer

Pacheco-Pinedo, Eugenia C.; Morrisey, Edward E.

doi:10.18632/oncotarget.305

Cited by 31 publications

(26 citation statements)

References 30 publications

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“…This supports again a joint role with mutant KRAS status as the latter is linked with higher circumference as well. An interesting study (50) in lung cancer concludes that combinational activation of KRAS and wnt/β-catenin pathway leads to a significant increase on the lung tumour formation and, therefore, worse prognosis effect.…”

Section: Discussionmentioning

confidence: 99%

KRAS Mutant Status, p16 and β-catenin Expression May Predict Local Recurrence in Patients Who Underwent Transanal Endoscopic Microsurgery (TEMS) for Stage I Rectal Cancer

Sideris

Moorhead

Díaz‐Cano

et al. 2016

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Abstract. Background The method of local excision, that has recently, gained wider acceptance, in early rectal cancer, is transanal endoscopic microsurgery (TEMS). TEMS generally offers advantages in operative access and oncological clearance over transanal resection (TAR), but recently a number of similar logic techniques with various rectal ports for endoscopic excision of rectal tumours has been invented. Those methods are collectively named transanal minimal-invasive surgery (TAMIS) and for oncological purposes they share the same features of local excision as TEMS (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14).TEMS is a minimally invasive technique that was introduced by Buess in the early 1980's (2). Through the new rectoscope with 3D binocular optic and the endoscopic instruments, it offers better access to proximal lesions with lower margin positivity and fragmentation and magnification of the operative field (2, 15). TEMS is a safe procedure that offers low complication rates and peri-operative morbidity (10.7%) (4). There have been multiple studies to suggest that TEMS is the operation of choice for rectal adenomas (1), retrorectal and submucosal rectal lesions (5). Furthermore, TEMS offers the advantage of not damaging the anorectal function (7).TEMS is indicated as a curative treatment for malignant neoplasms that are histologically confirmed as pT1 sm1 carcinomas, whereas T1 sm2-3 and T2 lesions are still under question (8). A number of studies have shown that TEMS can have comparable results with radical surgery (1,8,12,16) for rectal cancer.There has been concern about oncologic outcomes following TEMS (17). Some studies support that there is potentially a higher risk of local recurrence rate with TEMS (8,10,18). Efforts have been made to classify risk with morphological and histological criteria with better patients' selection (1, 6-9); however, the risk stratification remains 5315

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Section: Discussionmentioning

confidence: 99%

KRAS Mutant Status, p16 and β-catenin Expression May Predict Local Recurrence in Patients Who Underwent Transanal Endoscopic Microsurgery (TEMS) for Stage I Rectal Cancer

Sideris

Moorhead

Díaz‐Cano

et al. 2016

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“…Although there is documented evidence that miRNAs influence lung biology 19,20 and cancer, [21][22][23] to date how the miRNA network is intertwined with the pulmonary transcriptional program responsible for lung development and malignancy remains poorly defined. 24 To fill this void, we set out to uncover the miRNAs that directly regulate TTF-1. Initially, we used the in silico tool, TargetScan, 25 to select candidate miRNAs predicted to bind to TTF-1 3'UTR.…”

Section: Introductionmentioning

confidence: 99%

MiR-365 regulates lung cancer and developmental gene thyroid transcription factor 1

Rice

Salzberg

et al. 2012

Cell Cycle

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“…Subsequently, stabilized β-catenin enters the nucleus, binds to the TCF/LEF-1 transcription factor and activates the transcription of target genes involved in cell proliferation, 27 migration and invasion. The Wnt/β-catenin signaling pathway has been shown not only to promote tumor formation and progression in multiple cancers, 28,29 including colorectal cancer, 7,30,31 lung cancer 32 and endometrial cancer, 33,34 but also to regulate drug resistance. 35 Since α-catenin directly binds to β-catenin, it is tempting to hypothesize that α-catenin modulates β-catenin signaling.…”

Section: α-Catenin Signaling In Cancermentioning

confidence: 99%

α-catenin

Sun

Zhang

2014

Cell Cycle

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ExtrA ViEws 2334Cell Cycle Volume 13 issue 15 PErsPECtiVE D ownregulation or loss of α-catenin occurs in multiple human cancer types. The traditional view of α-catenin is that it is one of the core components of the E-cadherin-catenin complex and is required for maintaining the integrity of the intercellular adherens junction, a cell junction whose cytoplasmic face is linked to the actin cytoskeleton. Therefore, loss of α-catenin can result in loss of cell-cell adhesion, a common characteristic of cancer cells. There is an emerging recognition; however, that α-catenin also regulates multiple signaling pathways independent of adherens junctions. For instance, α-catenin functions as a tumor suppressor in E-cadherin-negative basal like breast cancer cells by inhibiting NF-κB signaling. In this perspective, we discuss the role and mechanisms of α-catenin in regulating several signaling pathways in cancer.

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Wnt and Kras signaling-dark siblings in lung cancer

Cited by 31 publications

References 30 publications

KRAS Mutant Status, p16 and β-catenin Expression May Predict Local Recurrence in Patients Who Underwent Transanal Endoscopic Microsurgery (TEMS) for Stage I Rectal Cancer

KRAS Mutant Status, p16 and β-catenin Expression May Predict Local Recurrence in Patients Who Underwent Transanal Endoscopic Microsurgery (TEMS) for Stage I Rectal Cancer

MiR-365 regulates lung cancer and developmental gene thyroid transcription factor 1

α-catenin

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