Gene Summary

Gene:ECT2L; epithelial cell transforming 2 like
Aliases: LFDH, FBXO49, C6orf91, ARHGEF32, dJ509I19.2, dJ509I19.3, dJ509I19.5
Databases:HGNC, Ensembl, GeneCard, Gene
Protein:epithelial cell-transforming sequence 2 oncogene-like
Source:NCBIAccessed: 31 August, 2019


What does this gene/protein do?
ECT2L is implicated in:
- intracellular
- regulation of Rho protein signal transduction
- Rho guanyl-nucleotide exchange factor activity
Data from Gene Ontology via CGAP

Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 01 September 2019 using data from PubMed using criteria.

Literature Analysis

Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic.

  • T-Lymphocytes
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
  • Mutation
  • Molecular Sequence Data
  • Stem Cells
  • Age of Onset
  • Translocation
  • DNA Sequence Analysis
  • Chromosome 6
  • Janus Kinases
  • DNA Copy Number Variations
  • Genomics
  • RAS Genes
  • Hematopoiesis
  • Histones
  • Acute Myeloid Leukaemia
  • Genome, Human
  • Receptors, Interleukin-7
  • Childhood Cancer
  • Signal Transduction
  • Genetic Predisposition
Tag cloud generated 31 August, 2019 using data from PubMed, MeSH and CancerIndex

Specific Cancers (2)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

Latest Publications: ECT2L (cancer-related)

Zhang J, Ding L, Holmfeldt L, et al.
The genetic basis of early T-cell precursor acute lymphoblastic leukaemia.
Nature. 2012; 481(7380):157-63 [PubMed] Free Access to Full Article Related Publications
Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole-genome sequencing of 12 ETP ALL cases and assessed the frequency of the identified somatic mutations in 94 T-cell acute lymphoblastic leukaemia cases. ETP ALL was characterized by activating mutations in genes regulating cytokine receptor and RAS signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF), inactivating lesions disrupting haematopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1 and EP300) and histone-modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of recurrent mutation including DNM2, ECT2L and RELN. The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haematopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL.

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Cite this page: Cotterill SJ. ECT2L, Cancer Genetics Web: Accessed:

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This page in Cancer Genetics Web by Simon Cotterill is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
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