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Loss of Lkb1 provokes highly invasive endometrial adenocarcinomas
Cristina M. Contreras
, Sushma Gurumurthy
, J. Marshall Haynie
, Lane J. Shirley
, Esra A. Akbay
, Shana N. Wingo
, John O. Schorge
, Russell R. Broaddus
, Kwok Kin Wong
, Nabeel Bardeesy
, Diego H. Castrillon
Pediatrics
Research output
:
Contribution to journal
›
Article
›
peer-review
97
Scopus citations
Overview
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Biochemistry, Genetics and Molecular Biology
Allele
100%
Cell Polarity
100%
Phosphotransferase
50%
Kinase
50%
Adenosine Monophosphate
50%
Downregulation
50%
Tumor Suppressor Gene
50%
Autosomal Dominant Inheritance
50%
Gastrointestinal Tract
50%
Cell Loss
50%
Endometrium
50%
Malignant Transformation
50%
Medicine and Dentistry
Cancer
100%
Endometrium Carcinoma
100%
Allele
50%
Cell Polarity
50%
Neoplasm
25%
Downregulation
25%
Kinase Signaling
25%
Gastrointestinal Tract
25%
Polyp
25%
Malignant Transformation
25%
Endometrium
25%
Adenosine Phosphate
25%
Tumor Suppressor Gene
25%
Autosomal Dominant Inheritance
25%
Uterine Cancer
25%
Female Reproductive Tract
25%
Peutz Jeghers Syndrome
25%
Tumor
25%
Keyphrases
Endometrial Adenocarcinoma
100%
Liver Kinase B1 (LKB1)
100%
Endometrial Cancer
23%
Invasive Phenotype
15%
Cell Polarity
15%
Epithelial Malignancies
7%
Cancer Progression
7%
Tumor
7%
Adenoviral
7%
Autosomal Dominant
7%
Tumor Suppressor Gene
7%
Malignant Transformation
7%
Gastrointestinal Tract
7%
Hamartomatous Polyp
7%
Cell Loss
7%
Female Mice
7%
Endometrium
7%
Well-differentiated
7%
Heterozygote
7%
Tumor Stage
7%
Tumor Grade
7%
Human Endometrial Cancer
7%
Kinase Signaling
7%
Female Reproductive Tract
7%
Peutz-Jeghers Syndrome
7%
AMP-dependent Kinase
7%
Conditional Allele
7%
Uterine Lumen
7%