INT184803

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Context Info
Confidence 0.37
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 5
Total Number 6
Disease Relevance 6.13
Pain Relevance 0.32

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

cytosol (TSC1) embryo development (TSC1) protein complex (TSC1)
cytoplasm (TSC1)
Anatomy Link Frequency
skin 1
kidney 1
TSC1 (Homo sapiens)
Pain Link Frequency Relevance Heat
transdermal 3 97.56 Very High Very High Very High
imagery 16 93.16 High High
cva 6 61.40 Quite High
Intractable pain 6 58.24 Quite High
Inflammation 1 39.52 Quite Low
pain flank 4 5.00 Very Low Very Low Very Low
cerebral cortex 3 5.00 Very Low Very Low Very Low
adenocard 3 5.00 Very Low Very Low Very Low
Angina 3 5.00 Very Low Very Low Very Low
cINOD 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cancer 187 100.00 Very High Very High Very High
Disease 69 100.00 Very High Very High Very High
Lymphangioleiomyomatosis 35 100.00 Very High Very High Very High
Convulsion 33 100.00 Very High Very High Very High
Intellectual Impairment 21 100.00 Very High Very High Very High
Nasal Tumor 11 100.00 Very High Very High Very High
Skin Diseases 3 100.00 Very High Very High Very High
Myeloid Leukemia 69 98.64 Very High Very High Very High
Autosomal Dominant Polycystic Kidney 3 96.94 Very High Very High Very High
Tuberous Sclerosis 43 94.18 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Major genes for TSC and autosomal dominant polycystic kidney disease (PKD), TSC2 and PKD1, respectively, lie adjacent to each other at chromosome 16p3.3, suggesting a role for PKD1 in the etiology of renal cystic disease in TSC.
Localization (disease) of TSC in kidney associated with autosomal dominant polycystic kidney and disease
1) Confidence 0.37 Published 2008 Journal Current Genomics Section Body Doc Link PMC2691673 Disease Relevance 0.65 Pain Relevance 0
The TSC2 R1772C, T993M, S132C, F143L and A196T substitutions are rare polymorphisms that do not inhibit TSC1–TSC2 function, and do not cause TSC.
Neg (not) Localization (cause) of TSC
2) Confidence 0.37 Published 2008 Journal Current Genomics Section Body Doc Link PMC2691673 Disease Relevance 0.16 Pain Relevance 0
Rauktys et al. [123] have also shown that topical administration of rapamycin is an effective treatment for TSC-related tumours in a mouse model demonstrating that transdermal delivery of rapamycin is feasible and topical rapamycin should be further investigated as a novel treatment approach for TSC skin disease such as facial angiofibromas.
Localization (disease) of TSC in skin associated with transdermal, nasal tumor, skin diseases and cancer
3) Confidence 0.37 Published 2008 Journal Current Genomics Section Body Doc Link PMC2691673 Disease Relevance 1.13 Pain Relevance 0.05
TSC was suspected in patients with facial angiofibromas, mental retardation, seizure, or pulmonary lymphangiomyomatosis, and were categorized as definite when positive for TSC1 and TSC2 loss of heterozygosity.


Localization (categorized) of TSC associated with convulsion, intellectual impairment, nasal tumor and lymphangioleiomyomatosis
4) Confidence 0.09 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2908871 Disease Relevance 1.49 Pain Relevance 0.27
Renal AMLs occupy 1-3% of renal tumors and occur in 2 clinical spectrums: sporadic and those associated with TSC.8 TSC is an autosomal disease entity with various characteristics such as mental retardation, adenoma sebaceum, seizure, renal manifestations, and loss of heterozygosity of TSC1 and TSC2 genes.4,9 Although AML is uncommon among the general population, previous studies has shown that 20% of patients with TSC are known to develop AML while on the other hand, more than 50% of AMLs are associated with TSC.7 In this rare setting, tumors tend to be larger, develop earlier in life, and are more often multiple or bilateral.3
Localization (multiple) of TSC associated with myeloid leukemia, convulsion, intellectual impairment, cancer, tuberous sclerosis, renal cancer and disease
5) Confidence 0.09 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2908871 Disease Relevance 1.21 Pain Relevance 0
Based on the stimulation of AA release by known cancer chemopreventative agents, I have proposed that AA release by cells is associated with cancer chemoprevention [23-27], possibly, but not necessarily, by activating a secreted tumor suppressor phospholipase A2 (PLA2) [28,29].
Localization (secreted) of tumor suppressor associated with cancer
6) Confidence 0.01 Published 2005 Journal BMC Pharmacol Section Body Doc Link PMC1180457 Disease Relevance 1.48 Pain Relevance 0

General Comments

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