A vicious partnership between AKT and PHLDA3 to facilitate neuroendocrine tumors.

Existing Reviews

Please note, new claims can take a short while to show up.

No claims yet.

Annotation Summary

Term Occurence Count Dictionary
everolimus 6 endocrinologydiseasesdrugs
neuroendocrine tumor 9 endocrinologydiseases
carcinoid 1 endocrinologydiseases

Graph of close proximity drug and disease terms (within 200 characters).

Note: If this graph is empty, then there are no terms that meet the proximity constraint.

Review

Having read the paper, please pick a pair of statements from the paper to indicate that a drug and disease are related.

Select Drug Character Offset Drug Term Instance
everolimus 611 molecular mechanisms underlying the development of PanNET. It has been shown that the mTOR inhibitor everolimus can improve the progression‐free survival of PanNET patients, suggesting that inhibition of the PI3K‐Akt‐mTOR
everolimus 2672 poor prognosis compared to other NET cancers, with a 5‐year survival rate of 27–43%.1, 2 The drug everolimus , which targets the mammalian target of rapamycin (mTOR), has been shown to improve the progression‐free
everolimus 3038 regulator that activates cell proliferation, growth and anti‐apoptosis pathways. The efficacy of everolimus against PanNET strongly indicates that PanNET cells proliferate in a manner that involves the mTOR cascade.We
everolimus 11443 RADIANT‐3, a double‐blind phase 3 study, PanNET patients were randomly assigned to treatment with oral everolimus or a matching placebo.3 Progression‐free survival was significantly prolonged in patients receiving
everolimus 11556 a matching placebo.3 Progression‐free survival was significantly prolonged in patients receiving everolimus (11.0 months) compared to patients receiving placebo (4.6 months), representing a 65% reduction in the
everolimus 11727 months), representing a 65% reduction in the estimated risk of progression or death.3 The efficacy of everolimus against PanNET strongly indicates that PanNET cell proliferation depends on the PI3K‐Akt‐mTOR cascade.In
Select Disease Character Offset Disease Term Instance
carcinoid 13680 loss at the PTPN7 locus in 12 out of 29 large‐cell neuroendocrine carcinoma (LCNEC), 8 out of 13 carcinoid samples, and 1 out of 8 small cell lung carcinomas (21 out of 50 lung NET in all). However, copy number
neuroendocrine tumor 80 Title: Cancer ScienceA vicious partnership between AKT and PHLDA3 to facilitate neuroendocrine tumor sAlternative Title: Takikawa and OhkiMasahiro TakikawaRieko Ohki1Division of Rare Cancer ResearchNational
neuroendocrine tumor 329 InstituteTokyoJapanPublication date (epub): 5/2017Publication date (ppub): 6/2017AbstractPancreatic neuroendocrine tumor s (PanNET) are rare cancers that generally have a poor prognosis. Accurate diagnosis and proper treatment
neuroendocrine tumor 1131 suppression of PHLDA3 transcription. Such alterations in the PHLDA3 gene were also frequently found in lung neuroendocrine tumor s (NET), suggesting the possibility that various types of NET have in common the functional loss of the
neuroendocrine tumor 3548 specimens.5 In this paper, we will review the significance and molecular modes of action of PHLDA3 and Akt in neuroendocrine tumor s.PI3K‐Akt‐mTOR CascadePhosphatidylinositols (PI) are pivotal factors that control the PI3K (phosphoinositide
neuroendocrine tumor 14144 3d). These observations are consistent with our hypothesis that aberrant cell proliferation of lung neuroendocrine tumor /carcinoma depends on Akt hyper‐activation resulting from PHLDA3 inactivation. This indicates that
neuroendocrine tumor 14722 of p53 in tumor suppression.Figure 3PHLDA3 locus is lost and PHLDA3 expression is downregulated in neuroendocrine tumor s (NET). (a) Chromosomal locations of the PHLDA3 gene and microsatellite markers used in the study. D1S306
neuroendocrine tumor 17413 development of PanNET. Taken together, these data indicate that PHLDA3 is a tumor suppressor gene in neuroendocrine tumor s.In addition to our study showing importance of PHLDA3 in the suppression of NET, Brady et al. have
neuroendocrine tumor 22407 facilitates apoptosis in vivo.ConclusionIn this paper we have reviewed the importance of PHLDA3 and Akt in neuroendocrine tumor s. Akt is an oncogene that facilitates cell proliferation and cell growth, and suppresses apoptosis.
neuroendocrine tumor 23559 these pathways suppress PanNET tumorigenesis independently.Figure 5PHLDA3 is a tumor suppressor gene of neuroendocrine tumor s (NET). PHLDA3 suppresses proliferation of various types of neuroendocrine cells, such as lung, pancreas,

You must be authorized to submit a review.