Atlas of Genetics and Cytogenetics in Oncology and Haematology


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TWIST1 (twist homolog 1 (Drosophila))

Identity

Other namesACS3
BPES2
BPES3
H-twist
SCS
TWIST
bHLHa38
HGNC (Hugo) TWIST1
LocusID (NCBI) 7291
Location 7p21.1
Location_base_pair Starts at 19155091 and ends at 19157295 bp from pter ( according to hg19-Feb_2009)  [Mapping]

DNA/RNA

Description This gene can be found on Chromosome 7 at location 7p21.2, position 19,121,616-19,123,820 reverse strand.
Transcription The DNA sequence contains 2 exons and the transcript length is 1,669 bp translated to a 202 residues protein.

Protein

Description The 20.9 kDa protein encoded by TWIST1 gene is a highly conserved transcription factor that belongs to the family of basic helix-loop-helix (bHLH) proteins. In vertebrates, it is involved in embryonic development through the regulation of epithelial-mesenchymal transitions (EMT) during neural crest migration, also it regulates mesoderm determination, myogenesis, and morphogenesis (Hebrok et al., 1994; Chen et al., 1995). Additionally, TWIST1 is involved in the negative regulation of cellular determination and in the differentiation of several lineages including myogenesis, osteogenesis (Bialek et al., 2004), and neurogenesis (Soo et al., 2002). Inhibits myogenesis by sequestrating E proteins, avoiding trans-activation by MEF2, and inhibiting DNA-binding by MYOD1 through physical interaction. Also represses expression of proinflammatory cytokines such as TNFA and IL1B (Barnes et al., 2009).
Mutations in this gene have been found in patients with Saethre-Chotzen syndrome (Howard et al., 1997).
TWIST1 has been suggested to be oncogenic, contributing to metastasis through its involvement in EMT regulation (Yang et al., 2004). In addition, TWIST1 is overexpressed in multiple tumor types, and it is usually associated with poor prognosis.
In mammals, there are two Twist-like proteins, TWIST1 and TWIST2 that share high structural homology (Li et al., 1995; Wolf et al., 1991). It is thought that during osteoblast development TWIST2 or Dermo1 may inhibit osteoblast maturation and maintain cells in a preosteoblast phenotype [provided by RefSeq]. Interestingly, TWIST2 has a pro-oncogenic role in human cancer (Ansieau et al., 2008).
Structure
TWIST1 protein contains a helix-loop-helix DNA-binding domain. Efficient DNA binding requires dimerization with another bHLH protein.
 
  (Mod Base provided)
Expression The strongest expression of the mRNA is in placental tissue. In adults, mesoderm-derived tissues express TWIST1 mRNA preferentially.
Localisation Nucleus.
Function Role in embryonic development
The Twist gene was originally identified as being required for mesoderm induction in Drosophila (Thisse et al., 1987; Leptin et al., 1990) which expression is induced by an interleukin-1-like TOLL receptor through nuclear factor kappaB activation (Furlong et al., 2001).
In vertebrates, Twist is predominantly expressed in neural crest cell where is essential for correct patterning of the neural tube (Chen and Behringer, 1995; Soo et al., 2002). However, the nuclear factor kappaB pathway is not involved in mesoderm formation or neural crest development in vertebrates. Instead, BMP-, Wnt-, and fibroblast growth factor-activated pathways are known to modulate vertebrate neural crest development (Meulemans et al., 2004).
During mesoderm formation in Drosophila, Twist induces the expression of the transcription factor Snail to allow invagination and mesoderm differentiation (Leptin and Grunewald, 1990). During neural crest development in vertebrates, expression of Snail and Slug occurs at the neural plate border where Twist is also expressed, and all three transcription factors play critical roles in neural crest formation (Meulemans and Bronner-Fraser, 2004).
Additional evidence supports the key role of Twist in development, since Twist mutation in mice causes failure in cranial neural tube closure, indicating its role in proper migration and differentiation of neural crest and head mesenchymal cells (Chen and Behringer, 1995; Soo et al., 2002).
Role in myogenesis
TWIST1 functionally inhibits muscle development by sequestrating E proteins from forming functional myogenic complexes with the skeletal muscle specific bHLH factor, MyoD. The mechanism of action is through the block of both cis- and trans- MyoD elements, and inhibiting transactivation of Mef2 (Barnes and Firulli, 2009).
Role in EMT
EMT is a process whereby epithelial cell layers lose polarity and cell-cell contacts and undergo a dramatic remodelling of the cytoskeleton. EMT is essential for the morphogenic movements underlying gastrulation and the subsequent formation of various tissues and organs such as the neural crest, heart, musculoskeletal system, craniofacial structures, and peripheral nervous system, and is also implicated in tissue repair in the adult.
TWIST1 induces EMT through repression of E-cadherin (Yang et al., 2004). Cells undergoing EMT acquire expression of mesenchymal components and manifest a migratory phenotype. TWIST1 triggers the acquisition of invasive properties through induction of pro-migratory molecules, such as the cell adhesion protein N-cadherin (Alexander et al., 2006) and RhoC, as consequence of inducing the microRNA molecule miR-10b (Ma et al., 2007).
Role in control of apoptosis
Twist, as a basic helix-loop-helix transcription factor, may activate or suppress diverse downstream targets, including apoptosis genes. Two studies reported that the expression of Twist could inhibit Myc-induced apoptosis in mouse embryo fibroblasts (Maestro et al., 1999) and neuroblastoma cells (Valsesia-Wittmann et al., 2004). This transcriptional control is relevant during EMT, since Twist may need to activate antiapoptotic programs in order to allow epithelial cells to convert to a mesenchymal fate while avoiding cell death due to loss of cell-cell adhesions by epithelial cells.
Role in cancer
TWIST1 has a key role during cancer development and progression in multiple tumour types. There are four main different malignant processes where this transcription factor is involved: EMT (Vernon et al., 2004), resistance to apoptosis by cytotoxic drugs (Wang et al., 2004) and pro-survival signalling (Puisieux et al., 2006) and hypoxia (Yang et al., 2008).

Mutations

Note Germline mutations in the coding region of TWIST1 gene in humans cause Saethre-Chotzen syndrome (SCS), an autosomal-dominant hereditary disorder characterized by limb abnormalities, facial dysmorphisms, and premature fusion of cranial sutures (Howard et al., 1997). This disease is also known as acrocephalosyndactyly type 3 (ACS3).
A frameshift mutation in TWIST1 that produce defects of this protein is the cause of Robinow-Sorauf syndrome (RSS); also known as craniosynostosis-bifid hallux syndrome. RSS is an autosomal dominant defect characterized by minor skull and limb anomalies which is very similar to Saethre-Chotzen syndrome (Kunz et al., 1999).
Missense mutations in the TWIST1 have been found in a significant number of patients of craniosynostosis type 1 (CRS1). Craniosynostosis consists of premature fusion of one or more cranial sutures, resulting in an abnormal head shape (Seto et al., 2007).

Implicated in

Entity Breast cancer
Oncogenesis In human breast cancer, TWIST1 is overexpressed at protein and mRNA levels (Watanabe et al., 2004; Yang et al., 2004; Martin et al., 2005). This upregulation has been usually associated with malignant features of the tumour: invasive lobular carcinoma, a highly infiltrating tumor type (Yang et al., 2004; Vesuna et al., 2008); the increasing nodal involvement (tumor-node-metastasis status); and the poor prognosis of the patients (Martin et al., 2005). TWIST1 overexpression, as a marker of EMT, has been also associated with the metastasis process. Circulating tumour cells of metastactic breast cancer patients showed an increased in EMT and tumor stem markers, included TWIST1 (Aktas et al., 2009); In addition, micrometastatic cells detected in the bone marrow which have prognostic significance in breast cancer displayed a specific expression of TWIST1 (Watson et al., 2007).
There are a wide number a molecular mechanisms described to explain the oncogenic role of TWIST1 in breast cancer progression. One of the most common is through the inhibition of expression of the epithelial marker E-cadherin (Yang et al., 2004; Vesuna et al., 2008). Recently, it has been reported that the microRNA, miR10b, is transcriptionally regulated by TWIST further leading to the activation of the pro-metastasic gene product RHOC promoting tumor invasion and migration in breast cancer (Ma et al., 2007). TWIST1 prosurvival and proinvasive functions are also mediated by the transcriptional up-regulation of AKT2 (Cheng et al., 2007). Moreover, there is a correlation between Wnt signalling and TWIST1 (Howe et al., 2003), which were included in a poor prognosis gene signature during metastasis to lung (DiMeo et al., 2009). In addition, TWIST1 is able to increased vascular endothelial growth factor (VEGF) synthesis in MCF7 cells inducing angiogenesis and chromosomal instability (Mironchik et al., 2005; Vesuna et al., 2006).
TWIST1 expression is also associated with multidrug resistance since its depletion completely blocked the mesenchymal transformation, partially reversed multidrug resistant and greatly abolished invasion induced by Adriamycin treatment in MCF7 cells (Li et al., 2009). Moreover, TWIST1 specific expression is found in therapy resistant cell populations (Watson et al., 2007; Aktas et al., 2009). Thus, therapy based on interference of TWIST1 might be a successful strategy for chemotherapy resistant breast tumours.
Interestingly, an increase of the grade of methylation at TWIST1 promoter has been shown in breast tumours where this feature was correlated with malignant phenotypes (Fackler et al., 2003; Mehrotra et al., 2004). Despite of these findings are opposite to the oncogene behaviour of TWIST1 gene that had been addressed by other authors, no correlation has been found between TWIST1 promoter methylation and TWIST1 protein or RNA expression (Gort et al., 2008).
  
Entity Rhabdomyosarcomas
Oncogenesis High protein levels of TWIST1 have been observed in 50% of rhabdomyosarcomas. TWIST1 might play multiple roles in the formation of rhabdomyosarcomas, halting terminal differentiation, inhibiting apoptosis, and interfering with the p53 tumor-suppressor pathway (Maestro et al., 1999). Villavicencio and collaborators suggest that TWIST1 could have such oncogenic role at least in part through the activation of GLI1 which is a critical transcription factor of sonic hedgehog signalling able to prevent the exit of the cell cycle and trapping cells in proliferating myoblast pool (Villavicencio et al., 2002).
  
Entity Gastric carcinomas
Oncogenesis TWIST1 mRNA and protein up-regulation is found with different incidences in both Laurén's classification for gastric carcinomas, with an increase of 40-60% in diffuse type and 25% in intestinal type (Rosivatz et al., 2002; Yan-Qi et al., 2007).
Furthermore, TWIST1 expression is correlated with lymph node metastasis, suggesting an association with the neoplastic transformation and subsequent development of gastric cancer (Yan-Qi et al., 2007).
In diffuse type gastric carcinomas overexpression of TWIST1 is significantly associated with the increased of expression of N-cadherin (Rosivatz et al., 2002).
This bHLH transcription factor is able to regulate the expression of several genes involved in the differentiation, adhesion, migration, invasion and proliferation of several gastric cancer cells (Feng et al., 2009). One of the most important pathways altered in this cancer cell lines is the Wnt/Tcf-4 signalling (Luo et al., 2008).
  
Entity Neuroblastomas
Oncogenesis TWIST1 is overexpressed in N-Myc-amplified neuroblastoma tumors and cell lines. This oncogenic cooperation of two key regulators of embryogenesis causes cell transformation and malignant outgrowth. While N-Myc induces cell proliferation, TWIST1 inhibits the ARF/p53 pathway involved in the Myc-dependent apoptotic response (Valsesia-Wittmann et al., 2004).
  
Entity Gliomas
Oncogenesis TWIST1 expression in human gliomas is increased comparing with normal brain at mRNA and protein levels. The mRNA levels are associated with the highest grade gliomas, and increased TWIST1 expression accompanies transition from low to high grade in vivo, suggesting a role in promoting malignant progression in gliomas (Elias et al., 2005).
  
Entity Oesophageal squamous cell carcinoma
Oncogenesis Upregulation of TWIST1 has been found in oesophageal squamous cell carcinoma (SCC), and this high level of TWIST1 was significantly associated with a greater risk for developing distant metastasis within 1 year of oesophagectomy (Yuen et al., 2007). TWIST1 has been proposed as a prognostic marker for predicting the development of distant metastasis in oesophageal SCC (Yuen et al., 2007).
The ectopic expression of TWIST1 drives to the suppression of TIMP1, a specific inhibitor of matrix metalloproteinases, promoting tumour invasion the human epithelial-like osteosarcoma cell line Saos-2 (Okamura et al., 2009).
  
Entity Pancreatic cancer
Oncogenesis Decreased or only weak expression of TWIST1 is observed in malignant pancreatic epithelium (Hotz et al., 2007; Cates et al., 2009). However, the different expression levels of TWIST1 in pancreatic juice may be useful to differentiate pancreatic cancer from nonmalignant neoplasms, since Twist expression differed significantly between cancer and intraductal papillary mucinous neoplasm bulk tissues (Ohuchida et al., 2007). Additionally, TWIST1 could be also used as a diagnostic marker in chronic pancreatitis because decreased expression is also seen (Cates et al., 2009).
Despite of the weak expression in pancreatic cancer, it has been demonstrated that TWIST1 is activated after exposure to hypoxia in several pancreatic cancer cell lines, suggesting an important role in the invasive behavior of pancreatic tumors (Hotz et al., 2007). Several signaling molecules have been reported to be able to activate TWIST1 resulting in EMT during tumour progression in this tumour type: Axl receptor tyrosine kinase (Koorstra et al., 2009); MSX2 (Satoh et al., 2008) and VEGFR-1 (Yang et al., 2006).
  
Entity Melanoma
Oncogenesis Increased TWIST1 expression and altered expression of additional transcriptional regulators implicated in embryonic development and epidermal/mesenchymal transition has been reported in melanoma cells lines and tissues. Overexpression of TWIST1 in these tumours is associated with worse outcome suggesting its use in assessing prognosis, staging, and therapy of melanoma patients (Hoek et al., 2004).
The induction of expression of TWIST1 through MFG-E8 secreted protein from tumor microenviroment has been suggested as one of the mechanisms of regulation of this bHLH transcription factor to promote progression of the disease (Jinushi et al., 2008).
  
Entity Prostate cancer
Oncogenesis TWIST1 is highly expressed in the majority of prostate cancer tissues. Its expression levels are positively correlated with high-grade prostatic cancer and metastasis (Kwok et al., 2005; Yuen et al., 2007). Furthermore, TWIST1 is able to specifically promote metastasis to bone regulating the expression of DKK-1 via RUNX2 (Wang et al., 2006). Over-expression of TWIST results in down-regulation of p14 (ARF), which leads to the impairment of DNA damage checkpoint in response to genotoxic stress. This negative effect of TWIST on DNA damage response facilitates uncontrolled cell proliferation with genomic instability and tumorigenesis in non-malignant immortalized human prostate epithelial cell lines (Kwok et al., 2007).
TWIST1 expression has also been associated with chemotherapy and castration resistance prostate tumours through different mechanisms such as the downregulation of Y-box binding protein-1 and androgen receptor signaling respectively (Kwok et al., 2005; Shiota et al., 2009a; 2009b).
  
Entity Hepatocellular carcinoma (HCC)
Oncogenesis TWIST1 mRNA and protein are both increased in HCC as compared to non-cancerous tissues. In addition, patients with high Twist expression have poor prognosis (Lee et al., 2006; Niu et al., 2007). These upregulated levels are associated with invasion and migration as a consequence of EMT induction and also with angiogenesis process (Niu et al., 2007; Matsuo et al., 2009).
  
Entity Epithelial ovarian carcinoma
Oncogenesis Positive TWIST1 expression predicts a poorer overall and progression free survival in patients with epithelial ovarian carcinoma (Kajiyama et al., 2006; Hosono et al., 2007). The role of TWIST1 in tumour progression has been suggested to be associated with EMT and also with chronic paclitaxel-resistance (Kajiyama et al., 2007; Yoshida et al., 2009). There is also a significant incidence of promoter hypermethylation of TWIST1 gene promoter that could be important in early clinical diagnosis and in chemotherapeutic management and treatment of the disease (Dhillon et al., 2004).
  
Entity Endometrial cancer
Oncogenesis TWIST1 is an independent predictor of patient survival in endometrial cancer and is correlated with E-cadherin silencing (Kyo et al., 2006). Furthermore, ionizing irradiation leads to the increased expression of TWIST1 in the HEC1A endometrial carcinoma cell line promoting cell invasion, suggesting a crucial role in the enhanced invasion after irradiation (Tsukamoto et al., 2007).
  
Entity Bladder cancer
Oncogenesis In bladder cancer, TWIST1 overexpression is correlated with advanced-stage, high-grade tumours, metastatic lesions, negative expression of E-cadherin and positive expression of N-cadherin (Zhang et al., 2007). More importantly, TWIST1 high expression levels is associated with smoking status of the patients and with worse clinical outcome (Fondrevelle et al., 2009).
  
Entity Cervical cancer
Oncogenesis Positive TWIST1 expression significantly predicted poorer prognosis in patients with cervical cancer (Shibata et al., 2008). Additionally, the tumour suppressor genes SFRP1 and SFRP2 decrease the invasion abilities of cervical cancer cells through the inhibition of the expression of SLUG, TWIST1 and SNAIL (Chung et al., 2009). However, the promoter methylation status of TWIST1 in combination with RAR-beta and MGMT have also been proposed as markers to distinguish between squamous cell carcinomas and negative squamous intraepithelial lesions from liquid based cytology specimens (Kim et al., 2009).
  
Entity Head and Neck cancer
Oncogenesis TWIST1 malignant effect is dependent on different molecules like HIF-1, Fascin, EBV and AKT (Horikawa et al., 2007; Yang et al., 2008; Chen et al., 2009; Hong et al., 2009). Upregulation of TWIST1 in nasopharyngeal carcinoma cells has been associated with resistance to microtubule disrupting agents, especially taxol (Zhang et al., 2007). TWIST1 increased levels is associated with malignant parameters such as lymph node invasion and distant metastasis, and the poor prognosis of nasopharyngeal carcinoma patients (Song et al., 2006).
  
Entity Colorectal cancer
Oncogenesis TWIST1 mRNA is upregulated in colorectal cancer patients. High levels of expression is associated with lymph node metastasis suggesting the relevance of TWIST1 in the outcome of the patients (Valdés-Mora et al., 2009). Interestingly, such increased levels are significantly associated with male gender revealing a plausible regulation through sexual hormones (Valdés-Mora et al., 2009).
  
Entity Lung cancer
Oncogenesis Overexpression of TWIST1 is associated with poor survival of non-small cell lung cancer (NSCLC) patients (Hung et al., 2009). Again, TWIST1 is an important player in chemotherapy resistance in A549 cell raising the possibility of TWIST1 depletion as a promising approach to lung cancer therapy (Zhuo et al., 2008). Promoter hypermethylation of this gene has been also proposed as a marker of lung adenocarcinoma (Tsou et al., 2007).
  
Entity Pheochromocytomas
Oncogenesis TWIST1 expression is found in malignant phechromocytomas and correlates with other EMT markers consolidating the relevant role of EMT in the malignant progression of this tumour type (Waldmann et al., 2008).
  

External links

Nomenclature
HGNC (Hugo)TWIST1   12428
Cards
AtlasTWIST1ID44296ch7p21
Entrez_Gene (NCBI)TWIST1  7291  twist family bHLH transcription factor 1
GeneCards (Weizmann)TWIST1
Ensembl (Hinxton)ENSG00000122691 [Gene_View]  chr7:19155091-19157295 [Contig_View]  TWIST1 [Vega]
AceView (NCBI)TWIST1
Genatlas (Paris)TWIST1
WikiGenes7291
SOURCE (Princeton)NM_000474
Genomic and cartography
GoldenPath (UCSC)TWIST1  -  7p21.1   chr7:19155091-19157295 -  7p21   [Description]    (hg19-Feb_2009)
EnsemblTWIST1 - 7p21 [CytoView]
Mapping of homologs : NCBITWIST1 [Mapview]
OMIM101400   123100   180750   601622   
Gene and transcription
Genbank (Entrez)AW173505 BC036704 DQ896770 X99268 Y11177
RefSeq transcript (Entrez)NM_000474
RefSeq genomic (Entrez)AC_000068 AC_000139 NC_000007 NC_018918 NG_008114 NT_007819 NT_079592 NW_001839003 NW_004929329
Consensus coding sequences : CCDS (NCBI)TWIST1
Cluster EST : UnigeneHs.644998 [ NCBI ]
CGAP (NCI)Hs.644998
Alternative Splicing : Fast-db (Paris)GSHG0028033
Alternative Splicing GalleryENSG00000122691
Gene ExpressionTWIST1 [ NCBI-GEO ]     TWIST1 [ SEEK ]   TWIST1 [ MEM ]
Protein : pattern, domain, 3D structure
UniProt/SwissProtQ15672 (Uniprot)
NextProtQ15672  [Medical]
With graphics : InterProQ15672
Splice isoforms : SwissVarQ15672 (Swissvar)
Domaine pattern : Prosite (Expaxy)BHLH (PS50888)   
Domains : Interpro (EBI)bHLH_dom   
Related proteins : CluSTrQ15672
Domain families : Pfam (Sanger)HLH (PF00010)   
Domain families : Pfam (NCBI)pfam00010   
Domain families : Smart (EMBL)HLH (SM00353)  
DMDM Disease mutations7291
Blocks (Seattle)Q15672
Human Protein AtlasENSG00000122691
Peptide AtlasQ15672
HPRD03374
IPIIPI00018907   IPI00893256   IPI01018705   
Protein Interaction databases
DIP (DOE-UCLA)Q15672
IntAct (EBI)Q15672
FunCoupENSG00000122691
BioGRIDTWIST1
InParanoidQ15672
Interologous Interaction database Q15672
IntegromeDBTWIST1
STRING (EMBL)TWIST1
Ontologies - Pathways
Ontology : AmiGOnegative regulation of transcription from RNA polymerase II promoter  sequence-specific DNA binding RNA polymerase II transcription factor activity  ossification  osteoblast differentiation  in utero embryonic development  neuron migration  neural tube closure  aortic valve morphogenesis  mitral valve morphogenesis  endocardial cushion morphogenesis  cardiac neural crest cell migration involved in outflow tract morphogenesis  protein binding  nucleus  transcription from RNA polymerase II promoter  apoptotic process  muscle organ development  transcription factor binding  positive regulation of gene expression  positive regulation of epithelial to mesenchymal transition  negative regulation of phosphatidylinositol 3-kinase cascade  protein domain specific binding  regulation of bone mineralization  positive regulation of fatty acid beta-oxidation  negative regulation of tumor necrosis factor production  positive regulation of tumor necrosis factor production  negative regulation of histone phosphorylation  negative regulation of histone acetylation  embryonic forelimb morphogenesis  embryonic hindlimb morphogenesis  negative regulation of peroxisome proliferator activated receptor signaling pathway  outer ear morphogenesis  embryonic digit morphogenesis  protein homodimerization activity  bHLH transcription factor binding  negative regulation of sequence-specific DNA binding transcription factor activity  negative regulation of DNA damage response, signal transduction by p53 class mediator  negative regulation of osteoblast differentiation  positive regulation of angiogenesis  positive regulation of transcription from RNA polymerase II promoter  positive regulation of transcription from RNA polymerase II promoter  protein heterodimerization activity  negative regulation of skeletal muscle tissue development  embryonic cranial skeleton morphogenesis  cranial suture morphogenesis  embryonic camera-type eye formation  eyelid development in camera-type eye  E-box binding  cellular response to hypoxia  positive regulation of monocyte chemotactic protein-1 production  positive regulation of cell motility  positive regulation of cell motility  negative regulation of oxidative phosphorylation uncoupler activity  positive regulation of transcription regulatory region DNA binding  negative regulation of cellular senescence  positive regulation of interleukin-6 secretion  negative regulation of double-strand break repair  cell proliferation involved in heart valve development  positive regulation of endocardial cushion to mesenchymal transition involved in heart valve formation  
Ontology : EGO-EBInegative regulation of transcription from RNA polymerase II promoter  sequence-specific DNA binding RNA polymerase II transcription factor activity  ossification  osteoblast differentiation  in utero embryonic development  neuron migration  neural tube closure  aortic valve morphogenesis  mitral valve morphogenesis  endocardial cushion morphogenesis  cardiac neural crest cell migration involved in outflow tract morphogenesis  protein binding  nucleus  transcription from RNA polymerase II promoter  apoptotic process  muscle organ development  transcription factor binding  positive regulation of gene expression  positive regulation of epithelial to mesenchymal transition  negative regulation of phosphatidylinositol 3-kinase cascade  protein domain specific binding  regulation of bone mineralization  positive regulation of fatty acid beta-oxidation  negative regulation of tumor necrosis factor production  positive regulation of tumor necrosis factor production  negative regulation of histone phosphorylation  negative regulation of histone acetylation  embryonic forelimb morphogenesis  embryonic hindlimb morphogenesis  negative regulation of peroxisome proliferator activated receptor signaling pathway  outer ear morphogenesis  embryonic digit morphogenesis  protein homodimerization activity  bHLH transcription factor binding  negative regulation of sequence-specific DNA binding transcription factor activity  negative regulation of DNA damage response, signal transduction by p53 class mediator  negative regulation of osteoblast differentiation  positive regulation of angiogenesis  positive regulation of transcription from RNA polymerase II promoter  positive regulation of transcription from RNA polymerase II promoter  protein heterodimerization activity  negative regulation of skeletal muscle tissue development  embryonic cranial skeleton morphogenesis  cranial suture morphogenesis  embryonic camera-type eye formation  eyelid development in camera-type eye  E-box binding  cellular response to hypoxia  positive regulation of monocyte chemotactic protein-1 production  positive regulation of cell motility  positive regulation of cell motility  negative regulation of oxidative phosphorylation uncoupler activity  positive regulation of transcription regulatory region DNA binding  negative regulation of cellular senescence  positive regulation of interleukin-6 secretion  negative regulation of double-strand break repair  cell proliferation involved in heart valve development  positive regulation of endocardial cushion to mesenchymal transition involved in heart valve formation  
Pathways : BIOCARTATumor Suppressor Arf Inhibits Ribosomal Biogenesis [Genes]   
Pathways : KEGGProteoglycans in cancer   
REACTOMETWIST1
Protein Interaction DatabaseTWIST1
Wikipedia pathwaysTWIST1
Gene fusion - rearrangments
Polymorphisms : SNP, mutations, diseases
SNP Single Nucleotide Polymorphism (NCBI)TWIST1
SNP (GeneSNP Utah)TWIST1
SNP : HGBaseTWIST1
Genetic variants : HAPMAPTWIST1
1000_GenomesTWIST1 
ICGC programENSG00000122691 
Somatic Mutations in Cancer : COSMICTWIST1 
CONAN: Copy Number AnalysisTWIST1 
Mutations and Diseases : HGMDTWIST1
OMIM101400    123100    180750    601622   
GENETestsTWIST1
Disease Genetic AssociationTWIST1
Huge Navigator TWIST1 [HugePedia]  TWIST1 [HugeCancerGEM]
Genomic VariantsTWIST1  TWIST1 [DGVbeta]
Exome VariantTWIST1
dbVarTWIST1
ClinVarTWIST1
snp3D : Map Gene to Disease7291
General knowledge
Homologs : HomoloGeneTWIST1
Homology/Alignments : Family Browser (UCSC)TWIST1
Phylogenetic Trees/Animal Genes : TreeFamTWIST1
Chemical/Protein Interactions : CTD7291
Chemical/Pharm GKB GenePA37088
Clinical trialTWIST1
Cancer Resource (Charite)ENSG00000122691
Other databases
Probes
Litterature
PubMed250 Pubmed reference(s) in Entrez
CoreMineTWIST1
iHOPTWIST1

Bibliography

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Cell shape changes during gastrulation in Drosophila.
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PMID 10465122
 
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Patterns of gene expression during Drosophila mesoderm development.
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Science. 2001 Aug 31;293(5535):1629-33. Epub 2001 Aug 2.
PMID 11486054
 
Differential expression of the epithelial-mesenchymal transition regulators snail, SIP1, and twist in gastric cancer.
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PMID 12414534
 
Twist function is required for the morphogenesis of the cephalic neural tube and the differentiation of the cranial neural crest cells in the mouse embryo.
Soo K, O'Rourke MP, Khoo PL, Steiner KA, Wong N, Behringer RR, Tam PP.
Dev Biol. 2002 Jul 15;247(2):251-70.
PMID 12086465
 
Cooperative E-box regulation of human GLI1 by TWIST and USF.
Villavicencio EH, Yoon JW, Frank DJ, Fuchtbauer EM, Walterhouse DO, Iannaccone PM.
Genesis. 2002 Apr;32(4):247-58.
PMID 11948912
 
DNA methylation of RASSF1A, HIN-1, RAR-beta, Cyclin D2 and Twist in in situ and invasive lobular breast carcinoma.
Fackler MJ, McVeigh M, Evron E, Garrett E, Mehrotra J, Polyak K, Sukumar S, Argani P.
Int J Cancer. 2003 Dec 20;107(6):970-5.
PMID 14601057
 
Twist is up-regulated in response to Wnt1 and inhibits mouse mammary cell differentiation.
Howe LR, Watanabe O, Leonard J, Brown AM.
Cancer Res. 2003 Apr 15;63(8):1906-13.
PMID 12702582
 
A twist code determines the onset of osteoblast differentiation.
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Dev Cell. 2004 Mar;6(3):423-35.
PMID 15030764
 
The contribution of genetic and epigenetic changes in granulosa cell tumors of ovarian origin.
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Oncogene. 2004 Jan 15;23(2):474-82.
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Cell. 2004 Jun 25;117(7):927-39.
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TWIST is expressed in human gliomas and promotes invasion.
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Cancer Res. 2005 Jun 15;65(12):5153-62.
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Ann Surg Oncol. 2005 Jun;12(6):488-96. Epub 2005 Apr 19.
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Twist overexpression induces in vivo angiogenesis and correlates with chromosomal instability in breast cancer.
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Cancer Res. 2006 Apr 1;66(7):3365-9.
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Twist expression predicts poor clinical outcome of patients with clear cell carcinoma of the ovary.
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Oncology. 2006;71(5-6):394-401. Epub 2007 Aug 9.
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High Twist expression is involved in infiltrative endometrial cancer and affects patient survival.
Kyo S, Sakaguchi J, Ohno S, Mizumoto Y, Maida Y, Hashimoto M, Nakamura M, Takakura M, Nakajima M, Masutomi K, Inoue M.
Hum Pathol. 2006 Apr;37(4):431-8.
PMID 16564917
 
Twist overexpression correlates with hepatocellular carcinoma metastasis through induction of epithelial-mesenchymal transition.
Lee TK, Poon RT, Yuen AP, Ling MT, Kwok WK, Wang XH, Wong YC, Guan XY, Man K, Chau KL, Fan ST.
Clin Cancer Res. 2006 Sep 15;12(18):5369-76.
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A twist for survival and cancer progression.
Puisieux A, Valsesia-Wittmann S, Ansieau S.
Br J Cancer. 2006 Jan 16;94(1):13-7.
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The clinical significance of twist expression in nasopharyngeal carcinoma.
Song LB, Liao WT, Mai HQ, Zhang HZ, Zhang L, Li MZ, Hou JH, Fu LW, Huang WL, Zeng YX, Zeng MS.
Cancer Lett. 2006 Oct 28;242(2):258-65. Epub 2006 Jan 18.
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Twist overexpression promotes chromosomal instability in the breast cancer cell line MCF-7.
Vesuna F, Winnard P Jr, Glackin C, Raman V.
Cancer Genet Cytogenet. 2006 Jun;167(2):189-91.
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Identification of a unique set of genes altered during cell-cell contact in an in vitro model of prostate cancer bone metastasis.
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Int J Mol Med. 2006 May;17(5):849-56.
PMID 16596270
 
Vascular endothelial growth factor receptor-1 activation mediates epithelial to mesenchymal transition in human pancreatic carcinoma cells.
Yang AD, Camp ER, Fan F, Shen L, Gray MJ, Liu W, Somcio R, Bauer TW, Wu Y, Hicklin DJ, Ellis LM.
Cancer Res. 2006 Jan 1;66(1):46-51.
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Twist transcriptionally up-regulates AKT2 in breast cancer cells leading to increased migration, invasion, and resistance to paclitaxel.
Cheng GZ, Chan J, Wang Q, Zhang W, Sun CD, Wang LH.
Cancer Res. 2007 Mar 1;67(5):1979-87.
PMID 17332325
 
Twist and epithelial-mesenchymal transition are induced by the EBV oncoprotein latent membrane protein 1 and are associated with metastatic nasopharyngeal carcinoma.
Horikawa T, Yang J, Kondo S, Yoshizaki T, Joab I, Furukawa M, Pagano JS.
Cancer Res. 2007 Mar 1;67(5):1970-8.
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Expression of Twist increases the risk for recurrence and for poor survival in epithelial ovarian carcinoma patients.
Hosono S, Kajiyama H, Terauchi M, Shibata K, Ino K, Nawa A, Kikkawa F.
Br J Cancer. 2007 Jan 29;96(2):314-20. Epub 2007 Jan 9.
PMID 17211477
 
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Clin Cancer Res. 2007 Aug 15;13(16):4769-76.
PMID 17699854
 
Chemoresistance to paclitaxel induces epithelial-mesenchymal transition and enhances metastatic potential for epithelial ovarian carcinoma cells.
Kajiyama H, Shibata K, Terauchi M, Yamashita M, Ino K, Nawa A, Kikkawa F.
Int J Oncol. 2007 Aug;31(2):277-83.
PMID 17611683
 
Role of p14ARF in TWIST-mediated senescence in prostate epithelial cells.
Kwok WK, Ling MT, Yuen HF, Wong YC, Wang X.
Carcinogenesis. 2007 Dec;28(12):2467-75. Epub 2007 Aug 8.
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Ma L, Teruya-Feldstein J, Weinberg RA.
Nature. 2007 Oct 11;449(7163):682-8. Epub 2007 Sep 26.
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Up-regulation of Twist induces angiogenesis and correlates with metastasis in hepatocellular carcinoma.
Niu RF, Zhang L, Xi GM, Wei XY, Yang Y, Shi YR, Hao XS.
J Exp Clin Cancer Res. 2007 Sep;26(3):385-94.
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Twist, a novel oncogene, is upregulated in pancreatic cancer: clinical implication of Twist expression in pancreatic juice.
Ohuchida K, Mizumoto K, Ohhashi S, Yamaguchi H, Konomi H, Nagai E, Yamaguchi K, Tsuneyoshi M, Tanaka M.
Int J Cancer. 2007 Apr 15;120(8):1634-40.
PMID 17236203
 
Isolated sagittal and coronal craniosynostosis associated with TWIST box mutations.
Seto ML, Hing AV, Chang J, Hu M, Kapp-Simon KA, Patel PK, Burton BK, Kane AA, Smyth MD, Hopper R, Ellenbogen RG, Stevenson K, Speltz ML, Cunningham ML.
Am J Med Genet A. 2007 Apr 1;143(7):678-86.
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Identification of a panel of sensitive and specific DNA methylation markers for lung adenocarcinoma.
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Mol Cancer. 2007 Oct 29;6:70.
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Irradiation-induced epithelial-mesenchymal transition (EMT) related to invasive potential in endometrial carcinoma cells.
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Gynecol Oncol. 2007 Dec;107(3):500-4. Epub 2007 Oct 1.
PMID 17905419
 
Isolation and molecular profiling of bone marrow micrometastases identifies TWIST1 as a marker of early tumor relapse in breast cancer patients.
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Clin Cancer Res. 2007 Sep 1;13(17):5001-9.
PMID 17785550
 
Expression and significance of TWIST basic helix-loop-helix protein over-expression in gastric cancer.
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Pathology. 2007 Oct;39(5):470-5.
PMID 17886095
 
Upregulation of Twist in oesophageal squamous cell carcinoma is associated with neoplastic transformation and distant metastasis.
Yuen HF, Chan YP, Wong ML, Kwok WK, Chan KK, Lee PY, Srivastava G, Law SY, Wong YC, Wang X, Chan KW.
J Clin Pathol. 2007 May;60(5):510-4. Epub 2006 Jul 5.
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Significance of TWIST and E-cadherin expression in the metastatic progression of prostatic cancer.
Yuen HF, Chua CW, Chan YP, Wong YC, Wang X, Chan KW.
Histopathology. 2007 Apr;50(5):648-58.
PMID 17394502
 
Anti-apoptotic role of TWIST and its association with Akt pathway in mediating taxol resistance in nasopharyngeal carcinoma cells.
Zhang X, Wang Q, Ling MT, Wong YC, Leung SC, Wang X.
Int J Cancer. 2007 May 1;120(9):1891-8.
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Significance of TWIST expression and its association with E-cadherin in bladder cancer.
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Hum Pathol. 2007 Apr;38(4):598-606. Epub 2007 Jan 29.
PMID 17258791
 
Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence.
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Cancer Cell. 2008 Jul 8;14(1):79-89.
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Methylation of the TWIST1 promoter, TWIST1 mRNA levels, and immunohistochemical expression of TWIST1 in breast cancer.
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Cancer Epidemiol Biomarkers Prev. 2008 Dec;17(12):3325-30.
PMID 19064546
 
Milk fat globule EGF-8 promotes melanoma progression through coordinated Akt and twist signaling in the tumor microenvironment.
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Cancer Res. 2008 Nov 1;68(21):8889-98.
PMID 18974133
 
Effect and mechanism of the Twist gene on invasion and metastasis of gastric carcinoma cells.
Luo GQ, Li JH, Wen JF, Zhou YH, Hu YB, Zhou JH.
World J Gastroenterol. 2008 Apr 28;14(16):2487-93.
PMID 18442194
 
Up-regulation of MSX2 enhances the malignant phenotype and is associated with twist 1 expression in human pancreatic cancer cells.
Satoh K, Hamada S, Kimura K, Kanno A, Hirota M, Umino J, Fujibuchi W, Masamune A, Tanaka N, Miura K, Egawa S, Motoi F, Unno M, Vonderhaar BK, Shimosegawa T.
Am J Pathol. 2008 Apr;172(4):926-39. Epub 2008 Mar 18.
PMID 18349132
 
Twist expression in patients with cervical cancer is associated with poor disease outcome.
Shibata K, Kajiyama H, Ino K, Terauchi M, Yamamoto E, Nawa A, Nomura S, Kikkawa F.
Ann Oncol. 2008 Jan;19(1):81-5. Epub 2007 Oct 8.
PMID 17925286
 
Twist is a transcriptional repressor of E-cadherin gene expression in breast cancer.
Vesuna F, van Diest P, Chen JH, Raman V.
Biochem Biophys Res Commun. 2008 Mar 7;367(2):235-41. Epub 2007 Dec 4.
PMID 18062917
 
Expression of the zinc-finger transcription factor Snail in adrenocortical carcinoma is associated with decreased survival.
Waldmann J, Feldmann G, Slater EP, Langer P, Buchholz M, Ramaswamy A, Saeger W, Rothmund M, Fendrich V.
Br J Cancer. 2008 Dec 2;99(11):1900-7. Epub 2008 Nov 18.
PMID 19018264
 
TWIST activation by hypoxia inducible factor-1 (HIF-1): implications in metastasis and development.
Yang MH, Wu KJ.
Cell Cycle. 2008 Jul 15;7(14):2090-6. Epub 2008 May 21.
PMID 18635960
 
Direct regulation of TWIST by HIF-1alpha promotes metastasis.
Yang MH, Wu MZ, Chiou SH, Chen PM, Chang SY, Liu CJ, Teng SC, Wu KJ.
Nat Cell Biol. 2008 Mar;10(3):295-305. Epub 2008 Feb 24.
PMID 18297062
 
Short interfering RNA directed against TWIST, a novel zinc finger transcription factor, increases A549 cell sensitivity to cisplatin via MAPK/mitochondrial pathway.
Zhuo WL, Wang Y, Zhuo XL, Zhang YS, Chen ZT.
Biochem Biophys Res Commun. 2008 May 16;369(4):1098-102. Epub 2008 Mar 10.
PMID 18331824
 
Stem cell and epithelial-mesenchymal transition markers are frequently overexpressed in circulating tumor cells of metastatic breast cancer patients.
Aktas B, Tewes M, Fehm T, Hauch S, Kimmig R, Kasimir-Bauer S.
Breast Cancer Res. 2009;11(4):R46. Epub 2009 Jul 9.
PMID 19589136
 
A twist of insight - the role of Twist-family bHLH factors in development.
Barnes RM, Firulli AB.
Int J Dev Biol. 2009;53(7):909-24.
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Epithelial-mesenchymal transition markers in pancreatic ductal adenocarcinoma.
Cates JM, Byrd RH, Fohn LE, Tatsas AD, Washington MK, Black CC.
Pancreas. 2009 Jan;38(1):e1-6.
PMID 18766116
 
Effects of small interfering RNAs targeting Fascin on gene expression in oral cancer cells.
Chen SF, Lin CY, Chang YC, Li JW, Fu E, Chang FN, Lin YL, Nieh S.
J Oral Pathol Med. 2009 Oct;38(9):722-30. Epub 2009 Apr 15.
PMID 19473443
 
SFRP1 and SFRP2 suppress the transformation and invasion abilities of cervical cancer cells through Wnt signal pathway.
Chung MT, Lai HC, Sytwu HK, Yan MD, Shih YL, Chang CC, Yu MH, Liu HS, Chu DW, Lin YW.
Gynecol Oncol. 2009 Mar;112(3):646-53. Epub 2008 Dec 18.
PMID 19095296
 
A novel lung metastasis signature links Wnt signaling with cancer cell self-renewal and epithelial-mesenchymal transition in basal-like breast cancer.
DiMeo TA, Anderson K, Phadke P, Fan C, Perou CM, Naber S, Kuperwasser C.
Cancer Res. 2009 Jul 1;69(13):5364-73. Epub 2009 Jun 23.
PMID 19549913
 
Gene expression profiling in TWIST-depleted gastric cancer cells.
Feng MY, Wang K, Shi QT, Yu XW, Geng JS.
Anat Rec (Hoboken). 2009 Feb;292(2):262-70.
PMID 19051271
 
The expression of Twist has an impact on survival in human bladder cancer and is influenced by the smoking status.
Fondrevelle ME, Kantelip B, Reiter RE, Chopin DK, Thiery JP, Monnien F, Bittard H, Wallerand H.
Urol Oncol. 2009 May-Jun;27(3):268-76. Epub 2008 Apr 28.
PMID 18440840
 
Inhibition of Akt activity induces the mesenchymal-to-epithelial reverting transition with restoring E-cadherin expression in KB and KOSCC-25B oral squamous cell carcinoma cells.
Hong KO, Kim JH, Hong JS, Yoon HJ, Lee JI, Hong SP, Hong SD.
J Exp Clin Cancer Res. 2009 Feb 26;28:28.
PMID 19243631
 
Prognostic significance of hypoxia-inducible factor-1 alpha, TWIST1 and Snail expression in resectable non-small cell lung cancer.
Hung JJ, Yang MH, Hsu HS, Hsu WH, Wu KJ.
Thorax. 2009 Sep 23. [Epub ahead of print]
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Assessment of DNA methylation for the detection of cervical neoplasia in liquid-based cytology specimens.
Kim JH, Choi YD, Lee JS, Lee JH, Nam JH, Choi C.
Gynecol Oncol. 2009 Oct 14. [Epub ahead of print]
PMID 19836067
 
The Axl receptor tyrosine kinase confers an adverse prognostic influence in pancreatic cancer and represents a new therapeutic target.
Koorstra JB, Karikari CA, Feldmann G, Bisht S, Rojas PL, Offerhaus GJ, Alvarez H, Maitra A.
Cancer Biol Ther. 2009 Apr;8(7):618-26. Epub 2009 Apr 22.
PMID 19252414
 
Twist1-mediated adriamycin-induced epithelial-mesenchymal transition relates to multidrug resistance and invasive potential in breast cancer cells.
Li QQ, Xu JD, Wang WJ, Cao XX, Chen Q, Tang F, Chen ZQ, Liu XP, Xu ZD.
Clin Cancer Res. 2009 Apr 15;15(8):2657-65. Epub 2009 Mar 31.
PMID 19336515
 
Twist expression promotes migration and invasion in hepatocellular carcinoma.
Matsuo N, Shiraha H, Fujikawa T, Takaoka N, Ueda N, Tanaka S, Nishina S, Nakanishi Y, Uemura M, Takaki A, Nakamura S, Kobayashi Y, Nouso K, Yagi T, Yamamoto K.
BMC Cancer. 2009 Jul 18;9:240.
PMID 19615090
 
Negative regulation of TIMP1 is mediated by transcription factor TWIST1.
Okamura H, Yoshida K, Haneji T.
Int J Oncol. 2009 Jul;35(1):181-6.
PMID 19513566
 
Programmed cell death protein 4 down-regulates Y-box binding protein-1 expression via a direct interaction with Twist1 to suppress cancer cell growth.
Shiota M, Izumi H, Tanimoto A, Takahashi M, Miyamoto N, Kashiwagi E, Kidani A, Hirano G, Masubuchi D, Fukunaka Y, Yasuniwa Y, Naito S, Nishizawa S, Sasaguri Y, Kohno K.
Cancer Res. 2009a Apr 1;69(7):3148-56. Epub 2009 Mar 24.
PMID 19318582
 
Castration resistance of prostate cancer cells caused by castration-induced oxidative stress through Twist1 and androgen receptor overexpression.
Shiota M, Yokomizo A, Tada Y, Inokuchi J, Kashiwagi E, Masubuchi D, Eto M, Uchiumi T, Naito S.
Oncogene. 2009b Oct 5. [Epub ahead of print]
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TWIST1 overexpression is associated with nodal invasion and male sex in primary colorectal cancer.
Valdes-Mora F, Gomez del Pulgar T, Bandres E, Cejas P, Ramirez de Molina A, Perez-Palacios R, Gallego-Ortega D, Garcia-Cabezas MA, Casado E, Larrauri J, Nistal M, Gonzalez-Baron M, Garcia-Foncillas J, Lacal JC.
Ann Surg Oncol. 2009 Jan;16(1):78-87. Epub 2008 Nov 11.
PMID 19002529
 
Changes in the expression of E-cadherin repressors, Snail, Slug, SIP1, and Twist, in the development and progression of ovarian carcinoma: the important role of Snail in ovarian tumorigenesis and progression.
Yoshida J, Horiuchi A, Kikuchi N, Hayashi A, Osada R, Ohira S, Shiozawa T, Konishi I.
Med Mol Morphol. 2009 Jun;42(2):82-91. Epub 2009 Jun 18.
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Contributor(s)

Written11-2009Fátima Valdés-Mora, Teresa Gómez del Pulgar, Juan Carlos Lacal
Garvan Institute of Medical Research, Sydney 2010, New South Wales, Australia (FVM); Centro Nacional de Biotecnologia, C/ Darwin, 3. Campus Cantoblanco, 28049 Madrid, Spain (TGdP, JCL)

Citation

This paper should be referenced as such :
Valdés-Mora F, Gómez del Pulgar T, Lacal JC . TWIST1 (twist homolog 1 (Drosophila)). Atlas Genet Cytogenet Oncol Haematol. November 2009 .
URL : http://AtlasGeneticsOncology.org/Genes/TWIST1ID44296ch7p21.html

The various updated versions of this paper are referenced and archived by INIST as such :
http://documents.irevues.inist.fr/bitstream/2042/44846/1/11-2009-TWIST1ID44296ch7p21.pdf   [ Bibliographic record ]

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