INT199072

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Context Info
Confidence 0.58
First Reported 2006
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 12
Disease Relevance 9.64
Pain Relevance 0.07

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

intracellular (Vav1)
Anatomy Link Frequency
T-cell 3
B-cell 1
thymus 1
microglia 1
Vav1 (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 16 80.16 Quite High
agonist 1 56.24 Quite High
Pain 11 12.32 Low Low
Inflammation 10 5.00 Very Low Very Low Very Low
cINOD 6 5.00 Very Low Very Low Very Low
Inflammatory response 5 5.00 Very Low Very Low Very Low
Inflammatory stimuli 2 5.00 Very Low Very Low Very Low
chemokine 2 5.00 Very Low Very Low Very Low
Central nervous system 1 5.00 Very Low Very Low Very Low
Nerve growth factor 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Lymphatic System Cancer 484 99.76 Very High Very High Very High
Cancer 716 98.96 Very High Very High Very High
Autoimmune Disease 22 98.64 Very High Very High Very High
Leukemia 231 98.60 Very High Very High Very High
Precursor Cell Lymphoblastic Leukemia-lymphoma 66 98.40 Very High Very High Very High
Aging 23 96.88 Very High Very High Very High
Lymphopenia 22 96.64 Very High Very High Very High
Chronic Lymphoid Leukemia 44 95.28 Very High Very High Very High
Disease 135 94.60 High High
Metastasis 11 81.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The combined inactivation of the Rasgrf2 and Vav1 loci did not aggravate the thymocyte developmental/selection defects or the T–cell lymphopenia induced by the single Vav1 gene deficiency (Figure 3).
Negative_regulation (inactivation) of Vav1 in T-cell associated with lymphopenia
1) Confidence 0.58 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 0.31 Pain Relevance 0
They also suggest that the inactivation of Vav1 function may represent an inadequate strategy to treat T–cell lymphomas, especially those associated with low levels of Rasgrf2 gene expression.



Negative_regulation (inactivation) of Vav1 in T-cell associated with lymphatic system cancer
2) Confidence 0.43 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2788417 Disease Relevance 0.74 Pain Relevance 0
Unexpectedly, our studies revealed that the inactivation of the Vav1 proto–oncogene favors the formation of lymphoblastic lymphoma–like tumors in aging mice.
Negative_regulation (inactivation) of Vav1 associated with aging, cancer and precursor cell lymphoblastic leukemia-lymphoma
3) Confidence 0.43 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2788417 Disease Relevance 0.66 Pain Relevance 0
In the case of the VAV1 mRNA, we found a significant downmodulation in a small subgroup of samples derived from patients affected by diffuse large B–cell lymphoma (Figure 6A, Table 2), chronic lymphocytic leukemia (Table 2), and acute myeloid leukemia (Table 2).
Negative_regulation (downmodulation) of VAV1 in B-cell associated with chronic lymphoid leukemia, leukemia and lymphatic system cancer
4) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 1.31 Pain Relevance 0
Thus, the loss of the Vav1 proto–oncogene increases preferentially the frequency of “thymus–localized” lymphomas in one–year–old animals and, to a much lower extent, the percentage of “widespread” tumors.
Negative_regulation (loss) of Vav1 in thymus associated with lymphatic system cancer and cancer
5) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 0.90 Pain Relevance 0
Unexpectedly, we found that the loss of Vav1 and Rasgrf2 genes cooperated synergistically in the development of very aggressive T–cell lymphomas in mice.
Negative_regulation (loss) of Vav1 in T-cell associated with lymphatic system cancer
6) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 0.47 Pain Relevance 0.04
However, when combined with the inactivation of the Vav1 gene, the Rasgrf2 gene deficiency promotes a two–fold increase in the development of “widespread” lymphomas, shorter latency periods for the development of the disease, and enhanced mortality/sickness rates.
Negative_regulation (inactivation) of Vav1 associated with lymphatic system cancer and disease
7) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 0.80 Pain Relevance 0
These results indicated that the Vav1 proto–oncogene deficiency in mice leads in the long–term to leukemia/lymphoma and that the loss of the Rasgrf2 gene further accentuates the progression of that disease.


Negative_regulation (deficiency) of Vav1 associated with leukemia, lymphatic system cancer and disease
8) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 1.25 Pain Relevance 0
Thus, it has been always assumed that the inactivation of the function of Vav and Rho/Rac family proteins could be of interest to treat cancer cells.
Negative_regulation (inactivation) of Vav associated with cancer
9) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 1.06 Pain Relevance 0
However, our present data puts a note of caution on those possible avenues, since they indicate that the blockage of Vav family–dependent signaling could be highly counterproductive in the case of lymphoblastic lymphoma patients with reduced levels of RASGRF2 gene expression in tumor cells.
Negative_regulation (blockage) of Vav associated with cancer and precursor cell lymphoblastic leukemia-lymphoma
10) Confidence 0.42 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 1.04 Pain Relevance 0
The Vav1 and Rasgrf2 gene deficiencies seem to contribute differently to these two lymphoma stages.
Negative_regulation (deficiencies) of Vav1 associated with lymphatic system cancer
11) Confidence 0.19 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2788417 Disease Relevance 0.84 Pain Relevance 0
Importantly, genetic deletion of Vav from primary microglia resulted in severe attenuation of ROS production following fA?
Negative_regulation (deletion) of Vav in microglia
12) Confidence 0.16 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1637099 Disease Relevance 0.28 Pain Relevance 0.03

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