We are analyzing https://link.springer.com/article/10.1186/s13046-018-0705-7.

Title:
New therapeutic strategies to treat human cancers expressing mutant p53 proteins | Journal of Experimental & Clinical Cancer Research
Description:
The tumor suppressor p53 plays a critical role to preserve DNA fidelity from diverse insults through the regulation of cell-cycle checkpoints, DNA repair, senescence and apoptosis. The TP53 is the most frequently inactivated gene in human cancers. This leads to the production of mutant p53 proteins that loose wild-type p53 tumor suppression functions and concomitantly acquire new oncogenic properties among which deregulated cell proliferation, increased chemoresistance, disruption of tissue architecture, promotion of migration, invasion and metastasis and several other pro-oncogenic activities. Mouse models show that the genetic reconstitution of the wild type p53 tumor suppression functions rescues tumor growth. This strongly supports the notion that either restoring wt-p53 activity or inhibiting mutant p53 oncogenic activity could provide an efficient strategy to treat human cancers. In this review we briefly summarize recent advances in the study of small molecules and compounds that subvert oncogenic activities of mutant p53 protein into wt-p53 tumor suppressor functions. We highlight inhibitors of signaling pathways aberrantly modulated by oncogenic mutant p53 proteins as promising therapeutic strategies. Finally, we consider the clinical applications of compounds targeting mutant p53 and the use of currently available drugs in the treatment of tumors expressing mutant p53 proteins.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Education
Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 7,643,328 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We can't tell how the site generates income.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

pubmed, cancer, article, mutant, google, scholar, cas, cell, cells, central, proteins, mutp, tumor, dna, protein, cancers, activity, breast, patients, wee, human, mutations, expression, inhibition, oncogenic, res, mutation, biol, clinical, repair, checkpoint, brca, genomic, pathway, kinase, growth, carcinoma, nat, role, wildtype, small, tumors, gene, nature, function, apoptosis, inhibitors, pathways, treatment, target,

Topics {✒️}

cond=cancer&term=statin&cntry=&state=&city=&dist= cruciferous-vegetable-derived phenethyl isothiocyanate involves egr-1/egf receptor/erk telomerase template antagonist recurrent high-grade serous hdac6-hsp90 chaperone axis article download pdf silvia di agostino molecularly targeted therapies wild-type p53 proteins wt-p53 expressing cells prima-1met/apr-246 induces apoptosis p53-deficient tumor cells potential long-term survivors preventing wild-type p53 mutant tp53-bearing tumours tumour micro-environment heterogeneity ansamycin-derived highly specific triple-negative breast cancers triple-negative breast cancer breast tumour-bearing mice wild-type p53 expression phase ib/ii study phase 1b/ii study potentiated radiation-induced killing protein complex mutp53r175h/p73 protein complex mutp53r273h/p73 including fda-approved saha pi3k/akt/mtor signaling conformation-specific antip53 antibodies restoring wt-p53 activity p53-targeting compound apr-246 orthotopic murine model wt-p53 transcriptional activity empower tgfbeta-induced metastasis key autophagy-related proteins low-molecular- weight compound pro-proliferative transcriptional activity wild-type tp53 allele block mutantp53-induced inhibition murine cancer models p53r175h mutant-dependent manner p53 dna-binding region molecular targeted therapy mutp53/p63 protein complex adriamycin-induced apoptotic response highly cell-context-dependent tumor suppressor p53 p53 tumor suppressor mouse models show

Questions {❓}

Are interactions with p63 and p73 involved in mutant p53 gain of oncogenic function?
Dissecting the pathways that destabilize mutant p53: the proteasome or autophagy?
P73 tumor suppressor protein: a close relative of p53 not only in structure but also in anti-cancer approach?
Gov/ct2/results?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:New therapeutic strategies to treat human cancers expressing mutant p53 proteins
         description:The tumor suppressor p53 plays a critical role to preserve DNA fidelity from diverse insults through the regulation of cell-cycle checkpoints, DNA repair, senescence and apoptosis. The TP53 is the most frequently inactivated gene in human cancers. This leads to the production of mutant p53 proteins that loose wild-type p53 tumor suppression functions and concomitantly acquire new oncogenic properties among which deregulated cell proliferation, increased chemoresistance, disruption of tissue architecture, promotion of migration, invasion and metastasis and several other pro-oncogenic activities. Mouse models show that the genetic reconstitution of the wild type p53 tumor suppression functions rescues tumor growth. This strongly supports the notion that either restoring wt-p53 activity or inhibiting mutant p53 oncogenic activity could provide an efficient strategy to treat human cancers. In this review we briefly summarize recent advances in the study of small molecules and compounds that subvert oncogenic activities of mutant p53 protein into wt-p53 tumor suppressor functions. We highlight inhibitors of signaling pathways aberrantly modulated by oncogenic mutant p53 proteins as promising therapeutic strategies. Finally, we consider the clinical applications of compounds targeting mutant p53 and the use of currently available drugs in the treatment of tumors expressing mutant p53 proteins.
         datePublished:2018-02-15T00:00:00Z
         dateModified:2018-02-15T00:00:00Z
         pageStart:1
         pageEnd:13
         license:http://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/s13046-018-0705-7
         keywords:
            Mutant P53 Protein
            Head And Neck Squamous Cell Carcinoma (HNSCC)
            Triple-negative Breast Cancer (TNBC)
            Mouse Double Minute (MDM2)
            Phenethyl Isothiocyanate (PEITC)
            Cancer Research
            Immunology
            Apoptosis
            Oncology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13046-018-0705-7/MediaObjects/13046_2018_705_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13046-018-0705-7/MediaObjects/13046_2018_705_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13046-018-0705-7/MediaObjects/13046_2018_705_Fig3_HTML.gif
         isPartOf:
            name:Journal of Experimental & Clinical Cancer Research
            issn:
               1756-9966
            volumeNumber:37
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Giovanni Blandino
               affiliation:
                     name:IRCCS Regina Elena National Cancer Institute
                     address:
                        name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Silvia Di Agostino
               url:http://orcid.org/0000-0003-3730-1125
               affiliation:
                     name:IRCCS Regina Elena National Cancer Institute
                     address:
                        name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:New therapeutic strategies to treat human cancers expressing mutant p53 proteins
      description:The tumor suppressor p53 plays a critical role to preserve DNA fidelity from diverse insults through the regulation of cell-cycle checkpoints, DNA repair, senescence and apoptosis. The TP53 is the most frequently inactivated gene in human cancers. This leads to the production of mutant p53 proteins that loose wild-type p53 tumor suppression functions and concomitantly acquire new oncogenic properties among which deregulated cell proliferation, increased chemoresistance, disruption of tissue architecture, promotion of migration, invasion and metastasis and several other pro-oncogenic activities. Mouse models show that the genetic reconstitution of the wild type p53 tumor suppression functions rescues tumor growth. This strongly supports the notion that either restoring wt-p53 activity or inhibiting mutant p53 oncogenic activity could provide an efficient strategy to treat human cancers. In this review we briefly summarize recent advances in the study of small molecules and compounds that subvert oncogenic activities of mutant p53 protein into wt-p53 tumor suppressor functions. We highlight inhibitors of signaling pathways aberrantly modulated by oncogenic mutant p53 proteins as promising therapeutic strategies. Finally, we consider the clinical applications of compounds targeting mutant p53 and the use of currently available drugs in the treatment of tumors expressing mutant p53 proteins.
      datePublished:2018-02-15T00:00:00Z
      dateModified:2018-02-15T00:00:00Z
      pageStart:1
      pageEnd:13
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s13046-018-0705-7
      keywords:
         Mutant P53 Protein
         Head And Neck Squamous Cell Carcinoma (HNSCC)
         Triple-negative Breast Cancer (TNBC)
         Mouse Double Minute (MDM2)
         Phenethyl Isothiocyanate (PEITC)
         Cancer Research
         Immunology
         Apoptosis
         Oncology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13046-018-0705-7/MediaObjects/13046_2018_705_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13046-018-0705-7/MediaObjects/13046_2018_705_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13046-018-0705-7/MediaObjects/13046_2018_705_Fig3_HTML.gif
      isPartOf:
         name:Journal of Experimental & Clinical Cancer Research
         issn:
            1756-9966
         volumeNumber:37
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Giovanni Blandino
            affiliation:
                  name:IRCCS Regina Elena National Cancer Institute
                  address:
                     name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Silvia Di Agostino
            url:http://orcid.org/0000-0003-3730-1125
            affiliation:
                  name:IRCCS Regina Elena National Cancer Institute
                  address:
                     name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Journal of Experimental & Clinical Cancer Research
      issn:
         1756-9966
      volumeNumber:37
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:IRCCS Regina Elena National Cancer Institute
      address:
         name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
         type:PostalAddress
      name:IRCCS Regina Elena National Cancer Institute
      address:
         name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Giovanni Blandino
      affiliation:
            name:IRCCS Regina Elena National Cancer Institute
            address:
               name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
               type:PostalAddress
            type:Organization
      name:Silvia Di Agostino
      url:http://orcid.org/0000-0003-3730-1125
      affiliation:
            name:IRCCS Regina Elena National Cancer Institute
            address:
               name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy
      name:Oncogenomic and Epigenetic Unit, Department of Diagnostic Research and Technological Innovation, IRCCS Regina Elena National Cancer Institute, Rome, Italy

External Links {🔗}(557)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref
Pbgrd

5.76s.

LINK . SPRINGER . COM {}