Targeting PI3K/AKT/mTOR Signaling Pathway in Pancreatic Cancer: From Molecular to Clinical Aspects
Although pancreatic cancer (PC) was considered in the past an orphan cancer type due to its low incidence, it may become in the future one of the leading causes of cancer death. Pancreatic ductal adenocarcinoma (PDAC) is the most frequent type of PC, being a highly aggressive malignancy and having a...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2022-09, Vol.23 (17), p.10132 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 17 |
| container_start_page | 10132 |
| container_title | International journal of molecular sciences |
| container_volume | 23 |
| creator | Stanciu, Silviu Ionita-Radu, Florentina Stefani, Constantin Miricescu, Daniela Stanescu-Spinu, Iulia-Ioana Greabu, Maria Ripszky Totan, Alexandra Jinga, Mariana |
| description | Although pancreatic cancer (PC) was considered in the past an orphan cancer type due to its low incidence, it may become in the future one of the leading causes of cancer death. Pancreatic ductal adenocarcinoma (PDAC) is the most frequent type of PC, being a highly aggressive malignancy and having a 5-year survival rate of less than 10%. Non-modifiable (family history, age, genetic susceptibility) and modifiable (smoking, alcohol, acute and chronic pancreatitis, diabetes mellitus, intestinal microbiota) risk factors are involved in PC pathogenesis. Chronic inflammation induced by various factors plays crucial roles in PC development from initiation to metastasis. In multiple malignant conditions such as PC, cytokines, chemokines, and growth factors activate the class I phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) (PI3K/AKT/mTOR) signaling pathway, which plays key roles in cell growth, survival, proliferation, metabolism, and motility. Currently, mTOR, AKT, and PI3K inhibitors are used in clinical studies. Moreover, PI3K/mTOR dual inhibitors are being tested in vitro and in vivo with promising results for PC patients. The main aim of this review is to present PC incidence, risk factors, tumor microenvironment development, and PI3K/AKT/mTOR dysregulation and inhibitors used in clinical, in vivo, and in vitro studies. |
| doi_str_mv | 10.3390/ijms231710132 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9456549</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2712855951</sourcerecordid><originalsourceid>FETCH-LOGICAL-c411t-933fd3d9059309686af0d007bfb347f5b02aa846e23c949fa79f91f2fb04a0503</originalsourceid><addsrcrecordid>eNpdkctP3DAQxi1UxLNHrshSL72kO34law5Iq1VpESBQuz1bE6-9eJXEi5204r8n5SXg5E-e33yamY-QIwbfhNAwCes2c8EqBkzwLbLHJOcFQFl9eqN3yX7OawAuuNI7ZFeUUFWK6z1SLzCtXB-6Fb05FxeT2cVi0i6uf9HfYdVh8_iP_e0_vKehG2Vnk8M-WDofpUsn9CzFll7FxtmhwUT7SOdjV7DY0FneONvnQ7Ltscnu8_N7QP6cfV_MfxaX1z_O57PLwkrG-kIL4ZdiqUFpAbqcluhhCVDVvhay8qoGjjiVpePCaqk9Vtpr5rmvQSIoEAfk9Ml3M9StW1rX9Qkbs0mhxXRvIgbzvtKFW7OKf42WqlRSjwZfnw1SvBtc7k0bsnVNg52LQza8YnyqlFZsRL98QNdxSOPBHikmJRNMjFTxRNkUc07Ovw7DwPxPz7xLb-SP327wSr_EJR4Az_qUrA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2711441313</pqid></control><display><type>article</type><title>Targeting PI3K/AKT/mTOR Signaling Pathway in Pancreatic Cancer: From Molecular to Clinical Aspects</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>PubMed Central</source><creator>Stanciu, Silviu ; Ionita-Radu, Florentina ; Stefani, Constantin ; Miricescu, Daniela ; Stanescu-Spinu, Iulia-Ioana ; Greabu, Maria ; Ripszky Totan, Alexandra ; Jinga, Mariana</creator><creatorcontrib>Stanciu, Silviu ; Ionita-Radu, Florentina ; Stefani, Constantin ; Miricescu, Daniela ; Stanescu-Spinu, Iulia-Ioana ; Greabu, Maria ; Ripszky Totan, Alexandra ; Jinga, Mariana</creatorcontrib><description>Although pancreatic cancer (PC) was considered in the past an orphan cancer type due to its low incidence, it may become in the future one of the leading causes of cancer death. Pancreatic ductal adenocarcinoma (PDAC) is the most frequent type of PC, being a highly aggressive malignancy and having a 5-year survival rate of less than 10%. Non-modifiable (family history, age, genetic susceptibility) and modifiable (smoking, alcohol, acute and chronic pancreatitis, diabetes mellitus, intestinal microbiota) risk factors are involved in PC pathogenesis. Chronic inflammation induced by various factors plays crucial roles in PC development from initiation to metastasis. In multiple malignant conditions such as PC, cytokines, chemokines, and growth factors activate the class I phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) (PI3K/AKT/mTOR) signaling pathway, which plays key roles in cell growth, survival, proliferation, metabolism, and motility. Currently, mTOR, AKT, and PI3K inhibitors are used in clinical studies. Moreover, PI3K/mTOR dual inhibitors are being tested in vitro and in vivo with promising results for PC patients. The main aim of this review is to present PC incidence, risk factors, tumor microenvironment development, and PI3K/AKT/mTOR dysregulation and inhibitors used in clinical, in vivo, and in vitro studies.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms231710132</identifier><identifier>PMID: 36077529</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>1-Phosphatidylinositol 3-kinase ; Adenocarcinoma ; Age ; AKT protein ; Alcohol ; Cell Proliferation ; Chemokines ; Clinical aspects ; Cytokines ; Diabetes ; Diabetes mellitus ; Diet ; Family medical history ; Genetic disorders ; Growth factors ; Humans ; In vivo methods and tests ; Intestinal microflora ; Malignancy ; Medical prognosis ; Metastases ; Microbiota ; Mortality ; Mutation ; Neuroendocrine tumors ; Pancreatic cancer ; Pancreatic Neoplasms ; Pancreatic Neoplasms - metabolism ; Pancreatitis ; Phosphatidylinositol 3-Kinase - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rapamycin ; Review ; Risk analysis ; Risk factors ; Signal transduction ; Signal Transduction - physiology ; Smoking ; Survival ; TOR protein ; TOR Serine-Threonine Kinases - metabolism ; Tumor Microenvironment ; Tumors ; Vitamin deficiency</subject><ispartof>International journal of molecular sciences, 2022-09, Vol.23 (17), p.10132</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c411t-933fd3d9059309686af0d007bfb347f5b02aa846e23c949fa79f91f2fb04a0503</citedby><cites>FETCH-LOGICAL-c411t-933fd3d9059309686af0d007bfb347f5b02aa846e23c949fa79f91f2fb04a0503</cites><orcidid>0000-0001-9829-5035 ; 0000-0002-4345-282X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9456549/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9456549/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36077529$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stanciu, Silviu</creatorcontrib><creatorcontrib>Ionita-Radu, Florentina</creatorcontrib><creatorcontrib>Stefani, Constantin</creatorcontrib><creatorcontrib>Miricescu, Daniela</creatorcontrib><creatorcontrib>Stanescu-Spinu, Iulia-Ioana</creatorcontrib><creatorcontrib>Greabu, Maria</creatorcontrib><creatorcontrib>Ripszky Totan, Alexandra</creatorcontrib><creatorcontrib>Jinga, Mariana</creatorcontrib><title>Targeting PI3K/AKT/mTOR Signaling Pathway in Pancreatic Cancer: From Molecular to Clinical Aspects</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Although pancreatic cancer (PC) was considered in the past an orphan cancer type due to its low incidence, it may become in the future one of the leading causes of cancer death. Pancreatic ductal adenocarcinoma (PDAC) is the most frequent type of PC, being a highly aggressive malignancy and having a 5-year survival rate of less than 10%. Non-modifiable (family history, age, genetic susceptibility) and modifiable (smoking, alcohol, acute and chronic pancreatitis, diabetes mellitus, intestinal microbiota) risk factors are involved in PC pathogenesis. Chronic inflammation induced by various factors plays crucial roles in PC development from initiation to metastasis. In multiple malignant conditions such as PC, cytokines, chemokines, and growth factors activate the class I phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) (PI3K/AKT/mTOR) signaling pathway, which plays key roles in cell growth, survival, proliferation, metabolism, and motility. Currently, mTOR, AKT, and PI3K inhibitors are used in clinical studies. Moreover, PI3K/mTOR dual inhibitors are being tested in vitro and in vivo with promising results for PC patients. The main aim of this review is to present PC incidence, risk factors, tumor microenvironment development, and PI3K/AKT/mTOR dysregulation and inhibitors used in clinical, in vivo, and in vitro studies.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Adenocarcinoma</subject><subject>Age</subject><subject>AKT protein</subject><subject>Alcohol</subject><subject>Cell Proliferation</subject><subject>Chemokines</subject><subject>Clinical aspects</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diet</subject><subject>Family medical history</subject><subject>Genetic disorders</subject><subject>Growth factors</subject><subject>Humans</subject><subject>In vivo methods and tests</subject><subject>Intestinal microflora</subject><subject>Malignancy</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Microbiota</subject><subject>Mortality</subject><subject>Mutation</subject><subject>Neuroendocrine tumors</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatitis</subject><subject>Phosphatidylinositol 3-Kinase - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rapamycin</subject><subject>Review</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>Smoking</subject><subject>Survival</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Tumor Microenvironment</subject><subject>Tumors</subject><subject>Vitamin deficiency</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkctP3DAQxi1UxLNHrshSL72kO34law5Iq1VpESBQuz1bE6-9eJXEi5204r8n5SXg5E-e33yamY-QIwbfhNAwCes2c8EqBkzwLbLHJOcFQFl9eqN3yX7OawAuuNI7ZFeUUFWK6z1SLzCtXB-6Fb05FxeT2cVi0i6uf9HfYdVh8_iP_e0_vKehG2Vnk8M-WDofpUsn9CzFll7FxtmhwUT7SOdjV7DY0FneONvnQ7Ltscnu8_N7QP6cfV_MfxaX1z_O57PLwkrG-kIL4ZdiqUFpAbqcluhhCVDVvhay8qoGjjiVpePCaqk9Vtpr5rmvQSIoEAfk9Ml3M9StW1rX9Qkbs0mhxXRvIgbzvtKFW7OKf42WqlRSjwZfnw1SvBtc7k0bsnVNg52LQza8YnyqlFZsRL98QNdxSOPBHikmJRNMjFTxRNkUc07Ovw7DwPxPz7xLb-SP327wSr_EJR4Az_qUrA</recordid><startdate>20220904</startdate><enddate>20220904</enddate><creator>Stanciu, Silviu</creator><creator>Ionita-Radu, Florentina</creator><creator>Stefani, Constantin</creator><creator>Miricescu, Daniela</creator><creator>Stanescu-Spinu, Iulia-Ioana</creator><creator>Greabu, Maria</creator><creator>Ripszky Totan, Alexandra</creator><creator>Jinga, Mariana</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9829-5035</orcidid><orcidid>https://orcid.org/0000-0002-4345-282X</orcidid></search><sort><creationdate>20220904</creationdate><title>Targeting PI3K/AKT/mTOR Signaling Pathway in Pancreatic Cancer: From Molecular to Clinical Aspects</title><author>Stanciu, Silviu ; Ionita-Radu, Florentina ; Stefani, Constantin ; Miricescu, Daniela ; Stanescu-Spinu, Iulia-Ioana ; Greabu, Maria ; Ripszky Totan, Alexandra ; Jinga, Mariana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-933fd3d9059309686af0d007bfb347f5b02aa846e23c949fa79f91f2fb04a0503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Adenocarcinoma</topic><topic>Age</topic><topic>AKT protein</topic><topic>Alcohol</topic><topic>Cell Proliferation</topic><topic>Chemokines</topic><topic>Clinical aspects</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diet</topic><topic>Family medical history</topic><topic>Genetic disorders</topic><topic>Growth factors</topic><topic>Humans</topic><topic>In vivo methods and tests</topic><topic>Intestinal microflora</topic><topic>Malignancy</topic><topic>Medical prognosis</topic><topic>Metastases</topic><topic>Microbiota</topic><topic>Mortality</topic><topic>Mutation</topic><topic>Neuroendocrine tumors</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatitis</topic><topic>Phosphatidylinositol 3-Kinase - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rapamycin</topic><topic>Review</topic><topic>Risk analysis</topic><topic>Risk factors</topic><topic>Signal transduction</topic><topic>Signal Transduction - physiology</topic><topic>Smoking</topic><topic>Survival</topic><topic>TOR protein</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Tumor Microenvironment</topic><topic>Tumors</topic><topic>Vitamin deficiency</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stanciu, Silviu</creatorcontrib><creatorcontrib>Ionita-Radu, Florentina</creatorcontrib><creatorcontrib>Stefani, Constantin</creatorcontrib><creatorcontrib>Miricescu, Daniela</creatorcontrib><creatorcontrib>Stanescu-Spinu, Iulia-Ioana</creatorcontrib><creatorcontrib>Greabu, Maria</creatorcontrib><creatorcontrib>Ripszky Totan, Alexandra</creatorcontrib><creatorcontrib>Jinga, Mariana</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stanciu, Silviu</au><au>Ionita-Radu, Florentina</au><au>Stefani, Constantin</au><au>Miricescu, Daniela</au><au>Stanescu-Spinu, Iulia-Ioana</au><au>Greabu, Maria</au><au>Ripszky Totan, Alexandra</au><au>Jinga, Mariana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting PI3K/AKT/mTOR Signaling Pathway in Pancreatic Cancer: From Molecular to Clinical Aspects</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-09-04</date><risdate>2022</risdate><volume>23</volume><issue>17</issue><spage>10132</spage><pages>10132-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Although pancreatic cancer (PC) was considered in the past an orphan cancer type due to its low incidence, it may become in the future one of the leading causes of cancer death. Pancreatic ductal adenocarcinoma (PDAC) is the most frequent type of PC, being a highly aggressive malignancy and having a 5-year survival rate of less than 10%. Non-modifiable (family history, age, genetic susceptibility) and modifiable (smoking, alcohol, acute and chronic pancreatitis, diabetes mellitus, intestinal microbiota) risk factors are involved in PC pathogenesis. Chronic inflammation induced by various factors plays crucial roles in PC development from initiation to metastasis. In multiple malignant conditions such as PC, cytokines, chemokines, and growth factors activate the class I phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) (PI3K/AKT/mTOR) signaling pathway, which plays key roles in cell growth, survival, proliferation, metabolism, and motility. Currently, mTOR, AKT, and PI3K inhibitors are used in clinical studies. Moreover, PI3K/mTOR dual inhibitors are being tested in vitro and in vivo with promising results for PC patients. The main aim of this review is to present PC incidence, risk factors, tumor microenvironment development, and PI3K/AKT/mTOR dysregulation and inhibitors used in clinical, in vivo, and in vitro studies.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36077529</pmid><doi>10.3390/ijms231710132</doi><orcidid>https://orcid.org/0000-0001-9829-5035</orcidid><orcidid>https://orcid.org/0000-0002-4345-282X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2022-09, Vol.23 (17), p.10132 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9456549 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; MDPI - Multidisciplinary Digital Publishing Institute; PubMed Central |
| subjects | 1-Phosphatidylinositol 3-kinase Adenocarcinoma Age AKT protein Alcohol Cell Proliferation Chemokines Clinical aspects Cytokines Diabetes Diabetes mellitus Diet Family medical history Genetic disorders Growth factors Humans In vivo methods and tests Intestinal microflora Malignancy Medical prognosis Metastases Microbiota Mortality Mutation Neuroendocrine tumors Pancreatic cancer Pancreatic Neoplasms Pancreatic Neoplasms - metabolism Pancreatitis Phosphatidylinositol 3-Kinase - metabolism Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rapamycin Review Risk analysis Risk factors Signal transduction Signal Transduction - physiology Smoking Survival TOR protein TOR Serine-Threonine Kinases - metabolism Tumor Microenvironment Tumors Vitamin deficiency |
| title | Targeting PI3K/AKT/mTOR Signaling Pathway in Pancreatic Cancer: From Molecular to Clinical Aspects |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-15T18%3A07%3A58IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Targeting%20PI3K/AKT/mTOR%20Signaling%20Pathway%20in%20Pancreatic%20Cancer:%20From%20Molecular%20to%20Clinical%20Aspects&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Stanciu,%20Silviu&rft.date=2022-09-04&rft.volume=23&rft.issue=17&rft.spage=10132&rft.pages=10132-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms231710132&rft_dat=%3Cproquest_pubme%3E2712855951%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2711441313&rft_id=info:pmid/36077529&rfr_iscdi=true |