Dinutuximab beta-targeted therapy kills beta-cell tumors of the pancreas
Purpose Dinutuximab beta is a monoclonal antibody used only in glioblastoma. Streptozotocin is an agent that is particularly toxic to pancreatic beta cells. Dinutuximab beta causes cytotoxicity through natural killer cells and neutrophils and shows effects. In this study, cytotoxicity was induced by...
Gespeichert in:
Veröffentlicht in: | Holistic Integrative Oncology 2023-02, Vol.2 (1), p.3, Article 3 |
---|---|
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 | 1 |
container_start_page | 3 |
container_title | Holistic Integrative Oncology |
container_volume | 2 |
creator | Karatug Kacar, Ayse Adıguzel, Zelal |
description | Purpose
Dinutuximab beta is a monoclonal antibody used only in glioblastoma. Streptozotocin is an agent that is particularly toxic to pancreatic beta cells. Dinutuximab beta causes cytotoxicity through natural killer cells and neutrophils and shows effects. In this study, cytotoxicity was induced by streptozotocin without natural killer cells and neutrophils. Gaining the ability to show the effect of Dinutuximab beta without a natural killer was the first aim of this study. This will be especially important in cases where the immune system is deficient, such as cancer. The second aim of the study was to investigate the effects of Dinutuximab beta on cell viability and cell death in insulinoma under the conditions created.
Methods
The effect of Dinutuximab beta in the presence of natural killer cells in vivo was created by the application of Streptozotocin to Beta-cell tumors of the pancreas in vitro. The cell viability was determined with WST-1 assay. Reactive oxygen species were measured by using dichlorofluorescein diacetate as a spectrophotometer. The cells were marked with DAPI to indicate apoptotic markers (nuclear condensation and fragmentation) with the confocal microscope.
GLUT2
(Glucose transporter 2),
IR
(Insulin receptor),
INS1
, and
INS2
expression levels were analyzed with q-RT-PCR.
Results
The cell cytotoxicity was induced by Streptozotocin. The cells proliferated with the administration of Dinutuximab beta alone. The result of Dinutuximab beta administered following Streptozotocin administration resulted in more cell death, increased ROS levels,
GLUT2, Ins1,
and
Ins2
mRNA expression levels, and decreased
IR
mRNA expression levels. Furthermore, the cells predominantly died via apoptosis showing cytoplasmic condensation and DNA fragmentation.
Conclusions
The lethal effect of Dinutuximab beta without a natural killer was provided by Streptozotocin in Beta cell tumors of the pancreas. |
doi_str_mv | 10.1007/s44178-023-00026-z |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2778817768</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2778817768</sourcerecordid><originalsourceid>FETCH-LOGICAL-c208z-b1dd37469eb0af5a6a2f4153dae9ef7815f3f20f002f3d5d8d1b2cf02ee3ccbd3</originalsourceid><addsrcrecordid>eNp9kMtOwzAQRS0EElXpD7CKxNrgRxI7S1QeRarEBtaWY49LS5oE25Fovx6HIMGK1Yw0596ZuQhdUnJNCRE3Ic-pkJgwjgkhrMTHEzRjglOcF6w6_dOfo0UIuxGShWB5OUOru207xOFzu9d1VkPUOGq_gQg2i2_gdX_I3rdNE6aZgabJ4rDvfMg6NxJZr1vjQYcLdOZ0E2DxU-fo9eH-ZbnC6-fHp-XtGhtG5BHX1Fou8rKCmmhX6FIzl9OCWw0VOCFp4bhjxKUTHbeFlZbWzDjCALgxteVzdDX59r77GCBEtesG36aVigkhJRWilIliE2V8F4IHp3qfXvQHRYkaQ1NTaCqFpr5DU8ck4pMoJLjdgP-1_kf1BVoecNc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2778817768</pqid></control><display><type>article</type><title>Dinutuximab beta-targeted therapy kills beta-cell tumors of the pancreas</title><source>DOAJ Directory of Open Access Journals</source><source>Springer Nature OA Free Journals</source><creator>Karatug Kacar, Ayse ; Adıguzel, Zelal</creator><creatorcontrib>Karatug Kacar, Ayse ; Adıguzel, Zelal</creatorcontrib><description>Purpose
Dinutuximab beta is a monoclonal antibody used only in glioblastoma. Streptozotocin is an agent that is particularly toxic to pancreatic beta cells. Dinutuximab beta causes cytotoxicity through natural killer cells and neutrophils and shows effects. In this study, cytotoxicity was induced by streptozotocin without natural killer cells and neutrophils. Gaining the ability to show the effect of Dinutuximab beta without a natural killer was the first aim of this study. This will be especially important in cases where the immune system is deficient, such as cancer. The second aim of the study was to investigate the effects of Dinutuximab beta on cell viability and cell death in insulinoma under the conditions created.
Methods
The effect of Dinutuximab beta in the presence of natural killer cells in vivo was created by the application of Streptozotocin to Beta-cell tumors of the pancreas in vitro. The cell viability was determined with WST-1 assay. Reactive oxygen species were measured by using dichlorofluorescein diacetate as a spectrophotometer. The cells were marked with DAPI to indicate apoptotic markers (nuclear condensation and fragmentation) with the confocal microscope.
GLUT2
(Glucose transporter 2),
IR
(Insulin receptor),
INS1
, and
INS2
expression levels were analyzed with q-RT-PCR.
Results
The cell cytotoxicity was induced by Streptozotocin. The cells proliferated with the administration of Dinutuximab beta alone. The result of Dinutuximab beta administered following Streptozotocin administration resulted in more cell death, increased ROS levels,
GLUT2, Ins1,
and
Ins2
mRNA expression levels, and decreased
IR
mRNA expression levels. Furthermore, the cells predominantly died via apoptosis showing cytoplasmic condensation and DNA fragmentation.
Conclusions
The lethal effect of Dinutuximab beta without a natural killer was provided by Streptozotocin in Beta cell tumors of the pancreas.</description><identifier>ISSN: 2731-4529</identifier><identifier>EISSN: 2731-4529</identifier><identifier>DOI: 10.1007/s44178-023-00026-z</identifier><language>eng</language><publisher>Singapore: Springer Nature Singapore</publisher><subject>Apoptosis ; Cell death ; Cytotoxicity ; Drug dosages ; Glucose ; Immunotherapy ; Insulin ; Medicine ; Medicine & Public Health ; Monoclonal antibodies ; Neuroblastoma ; Neuroendocrine tumors ; Neutrophils ; Oncology ; Original Research ; Pancreatic cancer ; Pediatrics ; Reactive oxygen species ; Targeted cancer therapy ; Tumors ; Variance analysis</subject><ispartof>Holistic Integrative Oncology, 2023-02, Vol.2 (1), p.3, Article 3</ispartof><rights>The Author(s) 2023</rights><rights>The Author(s) 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c208z-b1dd37469eb0af5a6a2f4153dae9ef7815f3f20f002f3d5d8d1b2cf02ee3ccbd3</citedby><cites>FETCH-LOGICAL-c208z-b1dd37469eb0af5a6a2f4153dae9ef7815f3f20f002f3d5d8d1b2cf02ee3ccbd3</cites><orcidid>0000-0002-0769-2906 ; 0000-0001-6032-470X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s44178-023-00026-z$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://doi.org/10.1007/s44178-023-00026-z$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,864,27924,27925,41120,42189,51576</link.rule.ids></links><search><creatorcontrib>Karatug Kacar, Ayse</creatorcontrib><creatorcontrib>Adıguzel, Zelal</creatorcontrib><title>Dinutuximab beta-targeted therapy kills beta-cell tumors of the pancreas</title><title>Holistic Integrative Oncology</title><addtitle>Holist Integ Oncol</addtitle><description>Purpose
Dinutuximab beta is a monoclonal antibody used only in glioblastoma. Streptozotocin is an agent that is particularly toxic to pancreatic beta cells. Dinutuximab beta causes cytotoxicity through natural killer cells and neutrophils and shows effects. In this study, cytotoxicity was induced by streptozotocin without natural killer cells and neutrophils. Gaining the ability to show the effect of Dinutuximab beta without a natural killer was the first aim of this study. This will be especially important in cases where the immune system is deficient, such as cancer. The second aim of the study was to investigate the effects of Dinutuximab beta on cell viability and cell death in insulinoma under the conditions created.
Methods
The effect of Dinutuximab beta in the presence of natural killer cells in vivo was created by the application of Streptozotocin to Beta-cell tumors of the pancreas in vitro. The cell viability was determined with WST-1 assay. Reactive oxygen species were measured by using dichlorofluorescein diacetate as a spectrophotometer. The cells were marked with DAPI to indicate apoptotic markers (nuclear condensation and fragmentation) with the confocal microscope.
GLUT2
(Glucose transporter 2),
IR
(Insulin receptor),
INS1
, and
INS2
expression levels were analyzed with q-RT-PCR.
Results
The cell cytotoxicity was induced by Streptozotocin. The cells proliferated with the administration of Dinutuximab beta alone. The result of Dinutuximab beta administered following Streptozotocin administration resulted in more cell death, increased ROS levels,
GLUT2, Ins1,
and
Ins2
mRNA expression levels, and decreased
IR
mRNA expression levels. Furthermore, the cells predominantly died via apoptosis showing cytoplasmic condensation and DNA fragmentation.
Conclusions
The lethal effect of Dinutuximab beta without a natural killer was provided by Streptozotocin in Beta cell tumors of the pancreas.</description><subject>Apoptosis</subject><subject>Cell death</subject><subject>Cytotoxicity</subject><subject>Drug dosages</subject><subject>Glucose</subject><subject>Immunotherapy</subject><subject>Insulin</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Monoclonal antibodies</subject><subject>Neuroblastoma</subject><subject>Neuroendocrine tumors</subject><subject>Neutrophils</subject><subject>Oncology</subject><subject>Original Research</subject><subject>Pancreatic cancer</subject><subject>Pediatrics</subject><subject>Reactive oxygen species</subject><subject>Targeted cancer therapy</subject><subject>Tumors</subject><subject>Variance analysis</subject><issn>2731-4529</issn><issn>2731-4529</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp9kMtOwzAQRS0EElXpD7CKxNrgRxI7S1QeRarEBtaWY49LS5oE25Fovx6HIMGK1Yw0596ZuQhdUnJNCRE3Ic-pkJgwjgkhrMTHEzRjglOcF6w6_dOfo0UIuxGShWB5OUOru207xOFzu9d1VkPUOGq_gQg2i2_gdX_I3rdNE6aZgabJ4rDvfMg6NxJZr1vjQYcLdOZ0E2DxU-fo9eH-ZbnC6-fHp-XtGhtG5BHX1Fou8rKCmmhX6FIzl9OCWw0VOCFp4bhjxKUTHbeFlZbWzDjCALgxteVzdDX59r77GCBEtesG36aVigkhJRWilIliE2V8F4IHp3qfXvQHRYkaQ1NTaCqFpr5DU8ck4pMoJLjdgP-1_kf1BVoecNc</recordid><startdate>20230222</startdate><enddate>20230222</enddate><creator>Karatug Kacar, Ayse</creator><creator>Adıguzel, Zelal</creator><general>Springer Nature Singapore</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0002-0769-2906</orcidid><orcidid>https://orcid.org/0000-0001-6032-470X</orcidid></search><sort><creationdate>20230222</creationdate><title>Dinutuximab beta-targeted therapy kills beta-cell tumors of the pancreas</title><author>Karatug Kacar, Ayse ; Adıguzel, Zelal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c208z-b1dd37469eb0af5a6a2f4153dae9ef7815f3f20f002f3d5d8d1b2cf02ee3ccbd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>Cell death</topic><topic>Cytotoxicity</topic><topic>Drug dosages</topic><topic>Glucose</topic><topic>Immunotherapy</topic><topic>Insulin</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Monoclonal antibodies</topic><topic>Neuroblastoma</topic><topic>Neuroendocrine tumors</topic><topic>Neutrophils</topic><topic>Oncology</topic><topic>Original Research</topic><topic>Pancreatic cancer</topic><topic>Pediatrics</topic><topic>Reactive oxygen species</topic><topic>Targeted cancer therapy</topic><topic>Tumors</topic><topic>Variance analysis</topic><toplevel>online_resources</toplevel><creatorcontrib>Karatug Kacar, Ayse</creatorcontrib><creatorcontrib>Adıguzel, Zelal</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</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>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content (ProQuest)</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><jtitle>Holistic Integrative Oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Karatug Kacar, Ayse</au><au>Adıguzel, Zelal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dinutuximab beta-targeted therapy kills beta-cell tumors of the pancreas</atitle><jtitle>Holistic Integrative Oncology</jtitle><stitle>Holist Integ Oncol</stitle><date>2023-02-22</date><risdate>2023</risdate><volume>2</volume><issue>1</issue><spage>3</spage><pages>3-</pages><artnum>3</artnum><issn>2731-4529</issn><eissn>2731-4529</eissn><abstract>Purpose
Dinutuximab beta is a monoclonal antibody used only in glioblastoma. Streptozotocin is an agent that is particularly toxic to pancreatic beta cells. Dinutuximab beta causes cytotoxicity through natural killer cells and neutrophils and shows effects. In this study, cytotoxicity was induced by streptozotocin without natural killer cells and neutrophils. Gaining the ability to show the effect of Dinutuximab beta without a natural killer was the first aim of this study. This will be especially important in cases where the immune system is deficient, such as cancer. The second aim of the study was to investigate the effects of Dinutuximab beta on cell viability and cell death in insulinoma under the conditions created.
Methods
The effect of Dinutuximab beta in the presence of natural killer cells in vivo was created by the application of Streptozotocin to Beta-cell tumors of the pancreas in vitro. The cell viability was determined with WST-1 assay. Reactive oxygen species were measured by using dichlorofluorescein diacetate as a spectrophotometer. The cells were marked with DAPI to indicate apoptotic markers (nuclear condensation and fragmentation) with the confocal microscope.
GLUT2
(Glucose transporter 2),
IR
(Insulin receptor),
INS1
, and
INS2
expression levels were analyzed with q-RT-PCR.
Results
The cell cytotoxicity was induced by Streptozotocin. The cells proliferated with the administration of Dinutuximab beta alone. The result of Dinutuximab beta administered following Streptozotocin administration resulted in more cell death, increased ROS levels,
GLUT2, Ins1,
and
Ins2
mRNA expression levels, and decreased
IR
mRNA expression levels. Furthermore, the cells predominantly died via apoptosis showing cytoplasmic condensation and DNA fragmentation.
Conclusions
The lethal effect of Dinutuximab beta without a natural killer was provided by Streptozotocin in Beta cell tumors of the pancreas.</abstract><cop>Singapore</cop><pub>Springer Nature Singapore</pub><doi>10.1007/s44178-023-00026-z</doi><orcidid>https://orcid.org/0000-0002-0769-2906</orcidid><orcidid>https://orcid.org/0000-0001-6032-470X</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 2731-4529 |
ispartof | Holistic Integrative Oncology, 2023-02, Vol.2 (1), p.3, Article 3 |
issn | 2731-4529 2731-4529 |
language | eng |
recordid | cdi_proquest_journals_2778817768 |
source | DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals |
subjects | Apoptosis Cell death Cytotoxicity Drug dosages Glucose Immunotherapy Insulin Medicine Medicine & Public Health Monoclonal antibodies Neuroblastoma Neuroendocrine tumors Neutrophils Oncology Original Research Pancreatic cancer Pediatrics Reactive oxygen species Targeted cancer therapy Tumors Variance analysis |
title | Dinutuximab beta-targeted therapy kills beta-cell tumors of the pancreas |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T09%3A26%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Dinutuximab%20beta-targeted%20therapy%20kills%20beta-cell%20tumors%20of%20the%20pancreas&rft.jtitle=Holistic%20Integrative%20Oncology&rft.au=Karatug%20Kacar,%20Ayse&rft.date=2023-02-22&rft.volume=2&rft.issue=1&rft.spage=3&rft.pages=3-&rft.artnum=3&rft.issn=2731-4529&rft.eissn=2731-4529&rft_id=info:doi/10.1007/s44178-023-00026-z&rft_dat=%3Cproquest_cross%3E2778817768%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2778817768&rft_id=info:pmid/&rfr_iscdi=true |