INT308400

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Context Info
Confidence 0.40
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.87
Pain Relevance 0

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

nucleoplasm (CDKN2A) DNA binding (CDKN2A) protein complex (CDKN2A)
cytoplasm (CDKN2A) cytosol (CDKN2A) nucleolus (CDKN2A)
Anatomy Link Frequency
melanocyte 2
CDKN2A (Homo sapiens)
Pain Link Frequency Relevance Heat
melanocortin 1 receptor 2 5.00 Very Low Very Low Very Low
addiction 1 5.00 Very Low Very Low Very Low
cytokine 1 5.00 Very Low Very Low Very Low
withdrawal 1 5.00 Very Low Very Low Very Low
Inflammation 1 5.00 Very Low Very Low Very Low
Versed 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Skin Cancer 140 100.00 Very High Very High Very High
Melanoma 27 98.36 Very High Very High Very High
Aging 4 97.88 Very High Very High Very High
Cancer 40 86.76 High High
Retinoblastoma 3 70.08 Quite High
Sunburn 3 50.00 Quite Low
Gastrointestinal Stromal Tumor 1 14.12 Low Low
Chronic Myeloid Leukemia 1 12.68 Low Low
Apoptosis 33 5.00 Very Low Very Low Very Low
Death 17 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Ha et al., recently used a mouse model to demonstrate that p14ARF but not p53, suppressed early melanomagenesis and operated independent of p53 to induce melanocyte senescence.[57] This added benefit of p14ARF loss may help explain why CDKN2A, as opposed to p53, is preferentially abrogated in melanoma.[4] CDKN2A expression changes were identified in the vast majority of melanomas through mutation, deletion or promoter hypermethylation of CDKN2A gene.[2] CDKN2A harbors mutations in melanoma at dipyrimidine sites but many of these genetic alterations are not UVB signature mutations.[13] An ongoing trial is aimed to identify gene mutations in patients with melanoma and in families with a history of hereditary melanoma and monitors for CDKN2A mutations.[58] Restoring function of a lost or defective gene in cancer has generally proven to be more difficult than blocking a hyperfunctional gene; thus it is not surprising that most efforts in targeted melanoma therapy have focused on suppression of oncogene signaling rather than TSG restoration.
Negative_regulation (abrogated) of Regulation (changes) of CDKN2A in melanocyte associated with aging, cancer, melanoma and skin cancer
1) Confidence 0.40 Published 2010 Journal Journal of Carcinogenesis Section Body Doc Link PMC2862505 Disease Relevance 0.87 Pain Relevance 0

General Comments

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