INT92141

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Context Info
Confidence 0.57
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 53
Total Number 53
Disease Relevance 44.23
Pain Relevance 2.48

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
arm 2
pancreatic duct 2
Mouse 1
GALT 1
melanocyte 1
CDKN2A (Homo sapiens)
Pain Link Frequency Relevance Heat
Dismenorea 6 100.00 Very High Very High Very High
Chronic pancreatitis 32 92.04 High High
endometriosis 5 91.72 High High
melanocortin 1 receptor 319 87.72 High High
ischemia 11 84.52 Quite High
palliative 9 76.76 Quite High
Opioid 3 75.00 Quite High
cINOD 187 74.64 Quite High
Pain 34 69.36 Quite High
Inflammation 45 61.88 Quite High
Disease Link Frequency Relevance Heat
Cancer 2010 100.00 Very High Very High Very High
Acute Renal Failure 51 100.00 Very High Very High Very High
Dysmenorrhea 6 100.00 Very High Very High Very High
Apoptosis 337 99.92 Very High Very High Very High
Skin Cancer 243 99.84 Very High Very High Very High
Pressure Volume 2 Under Development 9 99.36 Very High Very High Very High
Pancreatic Cancer 285 99.28 Very High Very High Very High
Rhabdomyolysis 202 99.28 Very High Very High Very High
Chromosome Aberrations 50 99.20 Very High Very High Very High
Disease 288 99.08 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
P16 protein is a known inhibitor of cyclin-dependent kinase 4 (CDK4) that binds to CDK4 in the G1 phase of the cell cycle to down-regulate its activity.
Negative_regulation (inhibitor) of CDK4
1) Confidence 0.57 Published 2007 Journal Environ Health Perspect Section Body Doc Link PMC1852665 Disease Relevance 0.39 Pain Relevance 0
This change over time is also reported in the literature as loss of p16 in some cases of MMMTs when they recurred [2].
Negative_regulation (loss) of p16
2) Confidence 0.53 Published 2010 Journal World J Surg Oncol Section Body Doc Link PMC2913917 Disease Relevance 1.01 Pain Relevance 0
Many of these defects are similar to those seen in the earliest lesions of breast malignancy, and Crawford and coworkers have already described this variant HMEC population to contain cells with hypermethylated INK4a promoter sequences, which leads to loss of p16INK4A protein and allows increased cell cycling through cyclin D1.
Negative_regulation (loss) of p16INK4A associated with malignant neoplastic disease
3) Confidence 0.48 Published 2005 Journal Breast Cancer Res Section Body Doc Link PMC1064113 Disease Relevance 0.39 Pain Relevance 0
Both CDKN2A and CDKN2B losses have been well documented in UC, with a CDKN2A deletion often associated with worsened outcomes [24,25].
Negative_regulation (losses) of CDKN2A associated with carcinoma
4) Confidence 0.44 Published 2010 Journal BMC Med Genomics Section Body Doc Link PMC3022544 Disease Relevance 0.27 Pain Relevance 0
We have observed hypermethylation to be a major mechanism of p16 inactivation.
Negative_regulation (inactivation) of p16
5) Confidence 0.43 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1185532 Disease Relevance 0.14 Pain Relevance 0
Inactivation of p16 gene occurs through intragenic mutation, homozygous deletion and methylation associated transcriptional silencing.
Negative_regulation (Inactivation) of p16
6) Confidence 0.43 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1185532 Disease Relevance 0.68 Pain Relevance 0
For pancreatic carcinoma, this disruption is caused exclusively by inactivation of p16INK4a gene and, only rarely, the Rb gene [24,25].
Negative_regulation (inactivation) of p16INK4a associated with pancreatic cancer
7) Confidence 0.43 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1185532 Disease Relevance 0.63 Pain Relevance 0
These genetic alterations correlated well with p16 protein expression as complete loss of p16 protein was found in 18 of 25 tumors (72%).


Negative_regulation (loss) of p16 associated with cancer
8) Confidence 0.43 Published 2005 Journal BMC Gastroenterol Section Abstract Doc Link PMC1185532 Disease Relevance 0.58 Pain Relevance 0
In cancers, functional loss of p16INK4a occurs as a consequence of somatic mutations, homozygous and heterozygous deletions [6,7].
Negative_regulation (loss) of p16INK4a associated with cancer
9) Confidence 0.43 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1185532 Disease Relevance 1.05 Pain Relevance 0
In the present study, all known mechanisms of p16 inactivation were analysed and we found evidence of p16 inactivation in a high proportion (80%) of the pancreatic tumors examined.
Negative_regulation (inactivation) of p16 associated with pancreatic cancer
10) Confidence 0.43 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1185532 Disease Relevance 0.71 Pain Relevance 0
In the present study, all known mechanisms of p16 inactivation were analysed and we found evidence of p16 inactivation in a high proportion (80%) of the pancreatic tumors examined.
Negative_regulation (inactivation) of p16 associated with pancreatic cancer
11) Confidence 0.43 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1185532 Disease Relevance 0.71 Pain Relevance 0
LOH could also be selected as the “second hit” for inactivating TP53 and CDKN2A.
Negative_regulation (inactivating) of CDKN2A
12) Confidence 0.43 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1808095 Disease Relevance 0.91 Pain Relevance 0
We simultaneously measured DNA content abnormalities (tetraploidy and aneuploidy), inactivation of TP53 (mutation and LOH), and inactivation of CDKN2A (mutation, methylation, and LOH), all of which have been shown to be mechanistically related to neoplastic progression in BE [28,29,34,80–82].
Negative_regulation (inactivation) of CDKN2A associated with aneuploidy, tetraploidy and congenital anomalies
13) Confidence 0.43 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1808095 Disease Relevance 1.15 Pain Relevance 0
Hence, in these three cases there was presumably a homozygous deletion of the p16 gene.


Negative_regulation (deletion) of p16
14) Confidence 0.43 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1185532 Disease Relevance 0.25 Pain Relevance 0
Further investigation of the TYR and CDKN2A/MTAP loci in families segregating CDKN2A mutations will allow assessment of whether common variants of these genes also modify penetrance of CDKN2A deleterious mutations.
Negative_regulation (segregating) of CDKN2A
15) Confidence 0.42 Published 2010 Journal JNCI Journal of the National Cancer Institute Section Body Doc Link PMC2957428 Disease Relevance 0.80 Pain Relevance 0.36
The most common genetic aberrations in pancreatic duct cell carcinogenesis involve the activation of KRAS oncogene and inactivation of tumor suppressor genes p16/CDKN2, p53 and SMAD4/DPC4 [3].
Negative_regulation (inactivation) of p16 in pancreatic duct associated with cancer
16) Confidence 0.42 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2270852 Disease Relevance 0.95 Pain Relevance 0
Inactivation of the CDKN2A/ARF locus on the short arm of chromosome 9 commonly occurs 18,19.
Negative_regulation (Inactivation) of CDKN2A in arm
17) Confidence 0.42 Published 2008 Journal Current Oncology Section Body Doc Link PMC2365488 Disease Relevance 1.12 Pain Relevance 0
Inactivation of the CDKN2A/ARF locus on the short arm of chromosome 9 commonly occurs 18,19.
Negative_regulation (Inactivation) of ARF in arm
18) Confidence 0.42 Published 2008 Journal Current Oncology Section Body Doc Link PMC2365488 Disease Relevance 1.12 Pain Relevance 0
The most common genetic aberrations in pancreatic duct cell carcinogenesis involve the activation of KRAS oncogene and inactivation of tumor suppressor genes p16/CDKN2, p53 and SMAD4/DPC4 [3].
Negative_regulation (inactivation) of CDKN2 in pancreatic duct associated with cancer
19) Confidence 0.42 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2270852 Disease Relevance 0.95 Pain Relevance 0
The cell content of E2F1 and Cyclin A, two proteins that promote cell cycle progression, were suppressed in both U251-MG and U87-MG human glioblastoma cell lines, whereas the level of p16(INK4A), a cell cycle inhibitor was upregulated.
Negative_regulation (level) of INK4A
20) Confidence 0.42 Published 2008 Journal Acta Oncol Section Body Doc Link 17934890 Disease Relevance 0 Pain Relevance 0

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