LRIG1 Was Down-Regulated in Medullary Thyroid Cancer but No Significant Effect of LRIG1 Was Found in RET2B Transgenic Mice and Human Differentiated Thyroid Cancer Abstract #1587

Introduction: There are four main types of thyroid cancer, papillary (PTC), follicular (FTC), medullary (MTC), and anaplastic. In both PTC and MTC, genomic rearrangements and point mutations in the proto-oncogene RET are common. RET encodes a receptor tyrosine kinase that is negatively regulated by leucine-rich repeats and immunoglobulin-like domains-1 (LRIG1). LRIG1 gene status and mRNA and protein expression correlate with patient survival in different types of cancer.
Aim(s): The possible effect of LRIG1 expression in thyroid cancer was investigated in a mouse model and two different clinical cohorts.
Materials and methods: A transgenic mouse strain which ectopically expresses the human RET2B oncogene was crossed with Lrig1 knock-out mice. In the RET2B-positive offspring, calcitonin levels were measured and the thyroid glands were investigated by histology.
Conference: 14th Annual ENETS conference 2017 (2017)
Category: Biomarkers
Presenting Author: Associate profes David Lindquist
Keywords: LRIG1, RET, MTC

To read results and conclusion, please login ...

Further abstracts you may be interested in

#2749 Impact of Next-Generation Sequencing Analyses on Treatment Management of Patients with Advanced Neuroendocrine Neoplasms
Introduction: Molecular genomic analyses are widely used in oncology but experience in advanced neuroendocrine neoplasms (NENs) is still limited.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Biomarkers
Presenting Author: Alejandro Garcia-Alvarez
Keywords: NGS, BRAF, RET
#3074 Medullary Thyroid Carcinoma and DIPNECH: An Unexpected Association
Introduction: Medullary thyroid carcinoma (MTC) is a neuroendocrine tumour of the C-cells of thyroid gland. Diffuse idiopathic pulmonary neuroendocrine cells hyperplasia (DIPNECH) is a rare condition, thought to be primarily a neuroendocrine proliferative process which can develop into carcinoid tumours.
Conference: 17th Annual ENETS Conference 2020 (2020)
Category: Case reports
Presenting Author: Joana Lima Ferreira
#48 Preliminary report of the use of everolimus in a patient with progressive medullary thyroid carcinoma
Introduction: Medullary thyroid carcinoma (MTC) accounts for about 5-10% of all thyroid cancers, and while disease localized to the thyroid can be cured by surgery, there is no effective treatment for disseminated MTC. Constitutive activation of the RET proto-oncogene is implicated in familial and a proportion of sporadic cases, and up-regulates the AKT/PI3-kinase/mTOR signal transduction pathway. Recent studies have shown that the inhibitor of mTOR, everolimus (RAD001, Novartis, Basel), can inhibit the proliferation of the TT cell line and human MTC tumor cells in vitro. Clinically, everolimus has been shown to attenuate the progression of some gastrointestinal neuroendocrine tumors, but its clinical use in MTC has not yet been evaluated.
Conference: 7th Annual ENETS Conference (2010)
Category: Clinical
Presenting Author: Dr Maralyn R Druce
#276 Mammalian Target of Rapamycin Pathway Activation is Associated with RET Mutation Status in Medullary Thyroid Carcinoma
Introduction: The genetic pathways involved in medullary thyroid carcinoma (MTC), except for RET mutations, are largely unknown, as well as the detailed expression mapping of intracellular signalling transducers.
Conference: 8th Annual ENETS Conference (2011)
Category: Basic
Presenting Author: MD Marco Volante
#631 Genotype – Phenotype Correlations and Timing of Prophylactic Thyroidectomy in Patients with Familial Medullary Thyroid Carcinoma
Introduction: Recommendations on the timing of prophylactic thyroidectomy (PTTE) in patients with familial medullary carcinoma (FMTC) are based on classification of RET mutations into four risk levels (ATA 2009).
Conference: 10th Annual ENETS Conference 2013 (2013)
Category: Non digestive NETs (bronchial, MTC, pheochromocytoma)
Presenting Author: prof. MD, PhD Jan Podoba