Ways to improve tumor uptake and penetration of drugs into solid tumors (Record no. 74976)

MARC details
000 -LEADER
fixed length control field 04485naaaa2200385uu 4500
001 - CONTROL NUMBER
control field https://directory.doabooks.org/handle/20.500.12854/62540
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20220220080608.0
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 978-2-88919-350-9
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9782889193509
024 7# - OTHER STANDARD IDENTIFIER
Standard number or code 10.3389/978-2-88919-350-9
Terms of availability doi
041 0# - LANGUAGE CODE
Language code of text/sound track or separate title English
042 ## - AUTHENTICATION CODE
Authentication code dc
100 1# - MAIN ENTRY--PERSONAL NAME
Personal name Ronald Berenson
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245 10 - TITLE STATEMENT
Title Ways to improve tumor uptake and penetration of drugs into solid tumors
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Name of publisher, distributor, etc. Frontiers Media SA
Date of publication, distribution, etc. 2014
300 ## - PHYSICAL DESCRIPTION
Extent 1 electronic resource (129 p.)
506 0# - RESTRICTIONS ON ACCESS NOTE
Terms governing access Open Access
Source of term star
Standardized terminology for access restriction Unrestricted online access
520 ## - SUMMARY, ETC.
Summary, etc. The main scope of this topic is to give an update on pharmacologic and non-pharmacologic approaches to enhance uptake and penetration of cancer drugs into tumors. Inadequate accumulation of drugs in tumors has emerged over the last decade as one of the main problems underlying therapeutic failure and drug resistance in the treatment of cancer. Insufficient drug uptake and penetration is causally related to the abnormal tumor architecture. Thus, poor vascularization, increased resistance to blood flow and impaired blood supply represent a first obstacle to the delivery of antitumor drugs to tumor tissue. Decreased or even inverted transvascular pressure gradients compromise convective delivery of drugs. Eventually, an abnormal extracellular matrix offers increased frictional resistance to tumor drug penetration. Abnormal tumor architecture also changes the biology of tumor cells, which contributes to drug resistance through several different mechanisms. The variability in vessel location and structure can make many areas of the tumor hypoxic, which causes the tumor cells to become quiescent and thereby resistant to many antitumor drugs. In addition, the abnormally long distance of part of the tumor cell population from blood vessels provides a challenge to delivering cancer drugs to these cells. We have recently proposed additional mechanisms of tumor drug resistance, which are also related to abnormal tumor architecture. First, increased interstitial fluid pressure can by itself induce drug resistance through the induction of resistance-promoting paracrine factors. Second, the interaction of drug molecules with vessel- proximal tumor cell layers may also induce the release of these factors, which can spread throughout the cancer, and induce drug resistance in tumor cells distant from blood vessels. As can be seen, abnormal tumor architecture, inadequate drug accumulation and tumor drug resistance are tightly linked phenomena, suggesting the need to normalize the tumor architecture, including blood vessels, and/or increase the accumulation of cancer drugs in tumors in order to increase therapeutic effects. Indeed, several classes of drugs (that we refer to as promoter drugs) have been described, that promote tumor uptake and penetration of antitumor drugs, including those that are vasoactive, modify the barrier function of tumor vessels, debulk tumor cells, and overcome intercellular and stromal barriers. In addition, also non-pharmacologic approaches have been described that enhance tumor accumulation of effector drugs (e.g. convection-enhanced delivery, hyperthermia, etc.). Some drugs that have already received regulatory approval (e.g. the anti-VEGF antibody bevacizumab) exert antitumor effects at least in part through normalization of the tumor vasculature and enhancement of the accumulation of effector drugs. Other drugs, acting through different mechanisms of action, are now in clinical development (e.g. NGR-TNF in phase II/III studies) and others are about to enter clinical investigation (e.g. JO-1).
540 ## - TERMS GOVERNING USE AND REPRODUCTION NOTE
Terms governing use and reproduction Creative Commons
Use and reproduction rights https://creativecommons.org/licenses/by/4.0/
Source of term cc
-- https://creativecommons.org/licenses/by/4.0/
546 ## - LANGUAGE NOTE
Language note English
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term Resistance
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Uncontrolled term microenvironment
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Uncontrolled term Administration
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Uncontrolled term targeting
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Uncontrolled term Penetration
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Uncontrolled term Drug delivery
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Uncontrolled term Permeability
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Uncontrolled term Junctions
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Uncontrolled term Cancer
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Uncontrolled term Integrins
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Angelo Corti
Relationship auth
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Fabrizio Marcucci
Relationship auth
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="http://journal.frontiersin.org/researchtopic/1094/ways-to-improve-tumor-uptake-and-penetration-of-drugs-into-solid-tumors">http://journal.frontiersin.org/researchtopic/1094/ways-to-improve-tumor-uptake-and-penetration-of-drugs-into-solid-tumors</a>
Access status 0
Public note DOAB: download the publication
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="https://directory.doabooks.org/handle/20.500.12854/62540">https://directory.doabooks.org/handle/20.500.12854/62540</a>
Access status 0
Public note DOAB: description of the publication

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