### Total Build Time: 219 ms 47.928 KB
CONCEPT_NAME gt=13 ms Completed: 13 ms rowSize= 326 bytes
CONCEPT_SOLR_HIT_STATS gt=0 Completed: 0 ms rowSize= 14 bytes
CONCEPT_DEFINITION gt=0 Completed: 0 ms rowSize= 265 bytes
- Skipping details on:
CONCEPT_SYNONYM gt=NONE 0 Completed: 0 ms rowSize= 0 bytes
- Skipping details on:
CONCEPT_TEXT gt=NONE 0 Completed: 0 ms rowSize= 0 bytes
CONCEPT_SEMANTIC_TYPE gt=3 ms Completed: 3 ms rowSize= 14 bytes
- Skipping details on:
CONCEPT_NAMESPACE gt=NONE 0 Completed: 0 ms rowSize= 0 bytes
CONCEPT_PARENTS gt=0 Completed: 0 ms rowSize= 7 bytes
CONCEPT_CHILDREN gt=0 Completed: 0 ms rowSize= 8 bytes
CONCEPT_ANCESTRAL_ROOTS gt=0 Completed: 0 ms rowSize= 15 bytes
CONCEPT_RELATIONSHIPS gt=61 ms Completed: 61 ms rowSize= 4.100 KB
CONCEPT_GENES gt=127 ms Completed: 127 ms rowSize= 42.032 KB
CONCEPT_XREFS gt=13 ms Completed: 13 ms rowSize= 1.148 KB
CONCEPT_ANCILLARY gt=2 ms Completed: 2 ms rowSize= 14 bytes
human : 132
mouse : 17
|Mouse||GPR132||29933||G protein-coupled receptor 132|
Positron emission tomography imaging analysis of G2A as a negative modifier of lymphoid leukemogenesis initiated by the BCR-ABL oncogene.
|Mouse||BBC3||27113||BCL2 binding component 3|
Like p53 shRNAs, PUMA shRNAs promoted oncogenic transformation of primary murine fibroblasts by the E1A/ras oncogene combination and dramatically accelerated myc-induced lymphomagenesis without disrupting p53-dependent cell-cycle arrest.
|Mouse||IKZF2||22807||IKAROS family zinc finger 2 (Helios)|
Our results suggest a critical role for Helios in the mechanism of leukemogenesis.
|Mouse||PRF1||5551||perforin 1 (pore forming protein)|
Both IFN-gamma and pfp were critical for suppression of lymphomagenesis, however the level of protection afforded by IFN-gamma was strain specific.
Here we show that pfp-deficient mice have a high incidence of malignancy in distinct lymphoid cell lineages (T, B, NKT), indicating a specific requirement for pfp in protection against lymphomagenesis.
|Mouse||PMS2||5395||PMS2 postmeiotic segregation increased 2 (S. cerevisiae)|
Transgenic expression of human MGMT blocks the hypersensitivity of PMS2-deficient mice to low dose MNU thymic lymphomagenesis.
|Mouse||PLSCR1||5359||phospholipid scramblase 1|
OBJECTIVE: We previously cloned a human normal counterpart (MmTRA1b/phospholipid scramblase 1) of the mouse leukemogenesis-associated gene MmTRA1a.
We recently cloned a new leukemogenesis-associated gene MmTRA1a (Mm-1 cell derived transplantability-associated gene 1a, former name _quot_TRA1_quot_) from a mouse leukemogenic and monocytic Mm-P cell cDNA library and also cloned its normal counterpart MmTRA1b (former name _quot_NOR1_quot_) from a normal mouse kidney cDNA library.
This hypothesis has been successfully tested in this article by the observation that deletion of pTalpha in Notch3 transgenic mice abrogates tumor development, indicating a crucial role for pTalpha in T cell leukemogenesis.
Our data suggest that a finely tuned interplay between Notch3 and pre-TCR pathways converges on regulation of NF-kappaB activity, leading to differential NF-kappaB subunit dimerization that regulates distinct gene clusters involved in either cell differentiation or proliferation/leukemogenesis.
Together, these results suggest that the combined expression of Notch3 and pTalpha sustains T cell leukemogenesis and may represent pathognomonic molecular features of human T-ALL.
These results indicate that in addition to Hes1 expression, other Notch1 pathway(s) have a role in thymic lymphomagenesis and suggest the presence of a novel mechanism for oncogenic activation of Notch1 by 5; deletion.
More than 50% of radiation-induced thymic lymphomas exhibited Notch1 rearrangements, suggesting that Notch1 acts as a major oncogene in radiation-induced lymphomagenesis.
Notch1-dependent lymphomagenesis is assisted by but does not essentially require pre-TCR signaling.
To elucidate the effect of Notch1 abnormalities in radiation-induced lymphomagenesis, we determined the structure of the Notch1 gene and examined the frequency and the sites of Notch1 rearrangements in radiation-induced mouse thymic lymphomas.
|Mouse||MYH11||4629||myosin, heavy chain 11, smooth muscle|
Exposing mice transplanted with CBFbeta-SMMHC-transduced cells to a mutagen, ethylnitrosourea, markedly accelerated leukemogenesis compared to expressing CBFbeta-SMMHC with loss of p16p19, indicating the need for multiple _quot_hits_quot_ for transformation.
|Mouse||LMO2||4005||LIM domain only 2 (rhombotin-like 1)|
Transgenic mice with enforced expression of LMO2 in their thymocytes develop T cell leukemias thus demonstrating the role of LMO2 in leukemogenesis.
|Mouse||ID2||3398||inhibitor of DNA binding 2, dominant negative helix-loop-helix protein|
Id2 is dispensable for myc-induced lymphomagenesis.
In mouse models of leukemia produced by Hoxa9, Meis1 accelerates leukemogenesis.
|Mouse||TLX1||3195||T-cell leukemia homeobox 1|
Dysregulated expression of mitotic regulators is associated with B-cell lymphomagenesis in HOX11-transgenic mice.
Loss of Ubr1 promotes aneuploidy and accelerates B-cell lymphomagenesis in TLX1/HOX11-transgenic mice.
|Mouse||CDX4||1046||caudal type homeobox 4|
Cdx4 regulates Hox gene expression in the adult murine hematopoietic system and dysregulates Hox genes that are implicated in leukemogenesis.
|Mouse||CDKN2C||1031||cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4)|
Our recent study showed that the absence of the CDK inhibitor p18(INK4C) (p18) enhances self-renewal of normal hematopoietic stem cell (HSC) in vivo, whereas previous studies by others showed an increased incidence of leukemogenesis in older p18-null mice.
|Mouse||BMI1||648||BMI1 polycomb ring finger oncogene|
Click here to display 11 evidence detail records.
|Mouse||APAF1||317||apoptotic peptidase activating factor 1|
Apaf-1 and caspase-9 do not act as tumor suppressors in myc-induced lymphomagenesis or mouse embryo fibroblast transformation.
Thus, Apaf-1 and caspase-9 do not suppress c-myc-induced lymphomagenesis and embryo fibroblast transformation.
CDKN1A/p21 appears to be an essential target of miR-17-92 during B-cell lymphomagenesis, which suggests the miR-17-92 polycistron has distinct targets in different B-cell lymphoma subtypes
|Human||FOXD4L4||349334||forkhead box D4-like 4|
Based upon these studies, our results suggest that FOXD4a and FOXD4b may play a role in leukemogenesis.
role for IL-14alpha (Txln gene product)in the development of both autoimmunity and lymphomagenesis
|Human||PTCRA||171558||pre T-cell antigen receptor alpha|
Combined expression of pTalpha and Notch3 in T cell leukemia identifies the requirement of preTCR for leukemogenesis
|Human||LHX4||89884||LIM homeobox 4|
The aberrant expression of the LHX4 gene by the t(1;14)(q25;q32) has very recently been reported in a case of ALL, thus, representing a rare, but recurrent genetic abnormality of possible importance in leukemogenesis.
The Lhx4 gene is deregulated in the leukemic cells and Lhx4 protein may play an important role, possibly as an activator, in leukemogenesis.
|Human||DOT1L||84444||DOT1-like histone H3K79 methyltransferase|
mistargeting of hDOT1L to Hoxa9 plays an important role in MLL-AF10-mediated leukemogenesis
|Human||PRDM16||63976||PR domain containing 16|
It is suggested that PRDM16 and MDS1/EVI1 share a common molecular mechanism for the leukemogenesis of RUNX1-associated leukemia.
Aberrant gene expression associated with DNA hypomethylation is implicated in leukemogenesis of adult T-cell leukemia
|Human||BACH2||60468||BTB and CNC homology 1, basic leucine zipper transcription factor 2|
Because BACH2 is a putative tumor suppressor gene, loss of its expression through EBV integration might contribute to lymphomagenesis.
loss of BACH2 expression through Epstein-Barr virus integration might contribute to lymphomagenesis