A mathematical model of chromosome recombination-induced drug resistance in cancer therapy
Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which...
Ausführliche Beschreibung
Autor*in: |
Hongli Yang [verfasserIn] Jinzhi Lei [verfasserIn] |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
2019 |
---|
Schlagwörter: |
---|
Übergeordnetes Werk: |
In: Mathematical Biosciences and Engineering - AIMS Press, 2020, 16(2019), 6, Seite 7098-7111 |
---|---|
Übergeordnetes Werk: |
volume:16 ; year:2019 ; number:6 ; pages:7098-7111 |
Links: |
---|
DOI / URN: |
10.3934/mbe.2019356 |
---|
Katalog-ID: |
DOAJ020151985 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | DOAJ020151985 | ||
003 | DE-627 | ||
005 | 20230503145947.0 | ||
007 | cr uuu---uuuuu | ||
008 | 230226s2019 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.3934/mbe.2019356 |2 doi | |
035 | |a (DE-627)DOAJ020151985 | ||
035 | |a (DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
050 | 0 | |a TP248.13-248.65 | |
050 | 0 | |a QA1-939 | |
100 | 0 | |a Hongli Yang |e verfasserin |4 aut | |
245 | 1 | 2 | |a A mathematical model of chromosome recombination-induced drug resistance in cancer therapy |
264 | 1 | |c 2019 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a Computermedien |b c |2 rdamedia | ||
338 | |a Online-Ressource |b cr |2 rdacarrier | ||
520 | |a Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. | ||
650 | 4 | |a delay differential equation | |
650 | 4 | |a genomic disorder | |
650 | 4 | |a non-clonal chromosome aberrations | |
650 | 4 | |a chemotherapy | |
650 | 4 | |a drug resistance | |
653 | 0 | |a Biotechnology | |
653 | 0 | |a Mathematics | |
700 | 0 | |a Jinzhi Lei |e verfasserin |4 aut | |
773 | 0 | 8 | |i In |t Mathematical Biosciences and Engineering |d AIMS Press, 2020 |g 16(2019), 6, Seite 7098-7111 |w (DE-627)522894844 |w (DE-600)2265126-3 |x 15510018 |7 nnns |
773 | 1 | 8 | |g volume:16 |g year:2019 |g number:6 |g pages:7098-7111 |
856 | 4 | 0 | |u https://doi.org/10.3934/mbe.2019356 |z kostenfrei |
856 | 4 | 0 | |u https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9 |z kostenfrei |
856 | 4 | 0 | |u https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML |z kostenfrei |
856 | 4 | 2 | |u https://doaj.org/toc/1551-0018 |y Journal toc |z kostenfrei |
912 | |a GBV_USEFLAG_A | ||
912 | |a SYSFLAG_A | ||
912 | |a GBV_DOAJ | ||
912 | |a SSG-OLC-PHA | ||
912 | |a GBV_ILN_20 | ||
912 | |a GBV_ILN_22 | ||
912 | |a GBV_ILN_23 | ||
912 | |a GBV_ILN_24 | ||
912 | |a GBV_ILN_31 | ||
912 | |a GBV_ILN_39 | ||
912 | |a GBV_ILN_40 | ||
912 | |a GBV_ILN_60 | ||
912 | |a GBV_ILN_62 | ||
912 | |a GBV_ILN_63 | ||
912 | |a GBV_ILN_65 | ||
912 | |a GBV_ILN_69 | ||
912 | |a GBV_ILN_70 | ||
912 | |a GBV_ILN_73 | ||
912 | |a GBV_ILN_95 | ||
912 | |a GBV_ILN_105 | ||
912 | |a GBV_ILN_110 | ||
912 | |a GBV_ILN_151 | ||
912 | |a GBV_ILN_161 | ||
912 | |a GBV_ILN_170 | ||
912 | |a GBV_ILN_213 | ||
912 | |a GBV_ILN_230 | ||
912 | |a GBV_ILN_285 | ||
912 | |a GBV_ILN_293 | ||
912 | |a GBV_ILN_370 | ||
912 | |a GBV_ILN_602 | ||
912 | |a GBV_ILN_2014 | ||
912 | |a GBV_ILN_4012 | ||
912 | |a GBV_ILN_4037 | ||
912 | |a GBV_ILN_4112 | ||
912 | |a GBV_ILN_4125 | ||
912 | |a GBV_ILN_4126 | ||
912 | |a GBV_ILN_4249 | ||
912 | |a GBV_ILN_4305 | ||
912 | |a GBV_ILN_4306 | ||
912 | |a GBV_ILN_4307 | ||
912 | |a GBV_ILN_4313 | ||
912 | |a GBV_ILN_4322 | ||
912 | |a GBV_ILN_4323 | ||
912 | |a GBV_ILN_4324 | ||
912 | |a GBV_ILN_4325 | ||
912 | |a GBV_ILN_4326 | ||
912 | |a GBV_ILN_4335 | ||
912 | |a GBV_ILN_4338 | ||
912 | |a GBV_ILN_4367 | ||
912 | |a GBV_ILN_4700 | ||
951 | |a AR | ||
952 | |d 16 |j 2019 |e 6 |h 7098-7111 |
author_variant |
h y hy j l jl |
---|---|
matchkey_str |
article:15510018:2019----::mteaiamdlfhoooeeobntoidcdrge |
hierarchy_sort_str |
2019 |
callnumber-subject-code |
TP |
publishDate |
2019 |
allfields |
10.3934/mbe.2019356 doi (DE-627)DOAJ020151985 (DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QA1-939 Hongli Yang verfasserin aut A mathematical model of chromosome recombination-induced drug resistance in cancer therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. delay differential equation genomic disorder non-clonal chromosome aberrations chemotherapy drug resistance Biotechnology Mathematics Jinzhi Lei verfasserin aut In Mathematical Biosciences and Engineering AIMS Press, 2020 16(2019), 6, Seite 7098-7111 (DE-627)522894844 (DE-600)2265126-3 15510018 nnns volume:16 year:2019 number:6 pages:7098-7111 https://doi.org/10.3934/mbe.2019356 kostenfrei https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9 kostenfrei https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML kostenfrei https://doaj.org/toc/1551-0018 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2019 6 7098-7111 |
spelling |
10.3934/mbe.2019356 doi (DE-627)DOAJ020151985 (DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QA1-939 Hongli Yang verfasserin aut A mathematical model of chromosome recombination-induced drug resistance in cancer therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. delay differential equation genomic disorder non-clonal chromosome aberrations chemotherapy drug resistance Biotechnology Mathematics Jinzhi Lei verfasserin aut In Mathematical Biosciences and Engineering AIMS Press, 2020 16(2019), 6, Seite 7098-7111 (DE-627)522894844 (DE-600)2265126-3 15510018 nnns volume:16 year:2019 number:6 pages:7098-7111 https://doi.org/10.3934/mbe.2019356 kostenfrei https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9 kostenfrei https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML kostenfrei https://doaj.org/toc/1551-0018 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2019 6 7098-7111 |
allfields_unstemmed |
10.3934/mbe.2019356 doi (DE-627)DOAJ020151985 (DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QA1-939 Hongli Yang verfasserin aut A mathematical model of chromosome recombination-induced drug resistance in cancer therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. delay differential equation genomic disorder non-clonal chromosome aberrations chemotherapy drug resistance Biotechnology Mathematics Jinzhi Lei verfasserin aut In Mathematical Biosciences and Engineering AIMS Press, 2020 16(2019), 6, Seite 7098-7111 (DE-627)522894844 (DE-600)2265126-3 15510018 nnns volume:16 year:2019 number:6 pages:7098-7111 https://doi.org/10.3934/mbe.2019356 kostenfrei https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9 kostenfrei https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML kostenfrei https://doaj.org/toc/1551-0018 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2019 6 7098-7111 |
allfieldsGer |
10.3934/mbe.2019356 doi (DE-627)DOAJ020151985 (DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QA1-939 Hongli Yang verfasserin aut A mathematical model of chromosome recombination-induced drug resistance in cancer therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. delay differential equation genomic disorder non-clonal chromosome aberrations chemotherapy drug resistance Biotechnology Mathematics Jinzhi Lei verfasserin aut In Mathematical Biosciences and Engineering AIMS Press, 2020 16(2019), 6, Seite 7098-7111 (DE-627)522894844 (DE-600)2265126-3 15510018 nnns volume:16 year:2019 number:6 pages:7098-7111 https://doi.org/10.3934/mbe.2019356 kostenfrei https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9 kostenfrei https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML kostenfrei https://doaj.org/toc/1551-0018 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2019 6 7098-7111 |
allfieldsSound |
10.3934/mbe.2019356 doi (DE-627)DOAJ020151985 (DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QA1-939 Hongli Yang verfasserin aut A mathematical model of chromosome recombination-induced drug resistance in cancer therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. delay differential equation genomic disorder non-clonal chromosome aberrations chemotherapy drug resistance Biotechnology Mathematics Jinzhi Lei verfasserin aut In Mathematical Biosciences and Engineering AIMS Press, 2020 16(2019), 6, Seite 7098-7111 (DE-627)522894844 (DE-600)2265126-3 15510018 nnns volume:16 year:2019 number:6 pages:7098-7111 https://doi.org/10.3934/mbe.2019356 kostenfrei https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9 kostenfrei https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML kostenfrei https://doaj.org/toc/1551-0018 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2019 6 7098-7111 |
language |
English |
source |
In Mathematical Biosciences and Engineering 16(2019), 6, Seite 7098-7111 volume:16 year:2019 number:6 pages:7098-7111 |
sourceStr |
In Mathematical Biosciences and Engineering 16(2019), 6, Seite 7098-7111 volume:16 year:2019 number:6 pages:7098-7111 |
format_phy_str_mv |
Article |
institution |
findex.gbv.de |
topic_facet |
delay differential equation genomic disorder non-clonal chromosome aberrations chemotherapy drug resistance Biotechnology Mathematics |
isfreeaccess_bool |
true |
container_title |
Mathematical Biosciences and Engineering |
authorswithroles_txt_mv |
Hongli Yang @@aut@@ Jinzhi Lei @@aut@@ |
publishDateDaySort_date |
2019-01-01T00:00:00Z |
hierarchy_top_id |
522894844 |
id |
DOAJ020151985 |
language_de |
englisch |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ020151985</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230503145947.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2019 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3934/mbe.2019356</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ020151985</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">TP248.13-248.65</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QA1-939</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Hongli Yang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="2"><subfield code="a">A mathematical model of chromosome recombination-induced drug resistance in cancer therapy</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">delay differential equation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">genomic disorder</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">non-clonal chromosome aberrations</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">chemotherapy</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">drug resistance</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biotechnology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Mathematics</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jinzhi Lei</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Mathematical Biosciences and Engineering</subfield><subfield code="d">AIMS Press, 2020</subfield><subfield code="g">16(2019), 6, Seite 7098-7111</subfield><subfield code="w">(DE-627)522894844</subfield><subfield code="w">(DE-600)2265126-3</subfield><subfield code="x">15510018</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:16</subfield><subfield code="g">year:2019</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:7098-7111</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3934/mbe.2019356</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1551-0018</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_370</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4326</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4335</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">16</subfield><subfield code="j">2019</subfield><subfield code="e">6</subfield><subfield code="h">7098-7111</subfield></datafield></record></collection>
|
callnumber-first |
T - Technology |
author |
Hongli Yang |
spellingShingle |
Hongli Yang misc TP248.13-248.65 misc QA1-939 misc delay differential equation misc genomic disorder misc non-clonal chromosome aberrations misc chemotherapy misc drug resistance misc Biotechnology misc Mathematics A mathematical model of chromosome recombination-induced drug resistance in cancer therapy |
authorStr |
Hongli Yang |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)522894844 |
format |
electronic Article |
delete_txt_mv |
keep |
author_role |
aut aut |
collection |
DOAJ |
remote_str |
true |
callnumber-label |
TP248 |
illustrated |
Not Illustrated |
issn |
15510018 |
topic_title |
TP248.13-248.65 QA1-939 A mathematical model of chromosome recombination-induced drug resistance in cancer therapy delay differential equation genomic disorder non-clonal chromosome aberrations chemotherapy drug resistance |
topic |
misc TP248.13-248.65 misc QA1-939 misc delay differential equation misc genomic disorder misc non-clonal chromosome aberrations misc chemotherapy misc drug resistance misc Biotechnology misc Mathematics |
topic_unstemmed |
misc TP248.13-248.65 misc QA1-939 misc delay differential equation misc genomic disorder misc non-clonal chromosome aberrations misc chemotherapy misc drug resistance misc Biotechnology misc Mathematics |
topic_browse |
misc TP248.13-248.65 misc QA1-939 misc delay differential equation misc genomic disorder misc non-clonal chromosome aberrations misc chemotherapy misc drug resistance misc Biotechnology misc Mathematics |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
cr |
hierarchy_parent_title |
Mathematical Biosciences and Engineering |
hierarchy_parent_id |
522894844 |
hierarchy_top_title |
Mathematical Biosciences and Engineering |
isfreeaccess_txt |
true |
familylinks_str_mv |
(DE-627)522894844 (DE-600)2265126-3 |
title |
A mathematical model of chromosome recombination-induced drug resistance in cancer therapy |
ctrlnum |
(DE-627)DOAJ020151985 (DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9 |
title_full |
A mathematical model of chromosome recombination-induced drug resistance in cancer therapy |
author_sort |
Hongli Yang |
journal |
Mathematical Biosciences and Engineering |
journalStr |
Mathematical Biosciences and Engineering |
callnumber-first-code |
T |
lang_code |
eng |
isOA_bool |
true |
recordtype |
marc |
publishDateSort |
2019 |
contenttype_str_mv |
txt |
container_start_page |
7098 |
author_browse |
Hongli Yang Jinzhi Lei |
container_volume |
16 |
class |
TP248.13-248.65 QA1-939 |
format_se |
Elektronische Aufsätze |
author-letter |
Hongli Yang |
doi_str_mv |
10.3934/mbe.2019356 |
author2-role |
verfasserin |
title_sort |
mathematical model of chromosome recombination-induced drug resistance in cancer therapy |
callnumber |
TP248.13-248.65 |
title_auth |
A mathematical model of chromosome recombination-induced drug resistance in cancer therapy |
abstract |
Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. |
abstractGer |
Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. |
abstract_unstemmed |
Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy. |
collection_details |
GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 |
container_issue |
6 |
title_short |
A mathematical model of chromosome recombination-induced drug resistance in cancer therapy |
url |
https://doi.org/10.3934/mbe.2019356 https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9 https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML https://doaj.org/toc/1551-0018 |
remote_bool |
true |
author2 |
Jinzhi Lei |
author2Str |
Jinzhi Lei |
ppnlink |
522894844 |
callnumber-subject |
TP - Chemical Technology |
mediatype_str_mv |
c |
isOA_txt |
true |
hochschulschrift_bool |
false |
doi_str |
10.3934/mbe.2019356 |
callnumber-a |
TP248.13-248.65 |
up_date |
2024-07-04T02:16:38.315Z |
_version_ |
1803613003650695168 |
fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ020151985</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230503145947.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2019 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3934/mbe.2019356</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ020151985</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ40b87c8cf2114adea0b851a921e922e9</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">TP248.13-248.65</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QA1-939</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Hongli Yang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="2"><subfield code="a">A mathematical model of chromosome recombination-induced drug resistance in cancer therapy</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Cytotoxic chemotherapeutics are common treatment methods of many cancers, and patients are often dosed at maximum tolerated dose (MTD), which is trying to eliminate cancer cells as much as possible. However, highly doses chemotherapy may induce unexpected gene mutations or DNA recombinations, which in turn result in unpredictable outcomes and drug resistance. In this study, we focus on the occurrence of DNA recombinations, and present a mathematical model for the influence of genomic disorder due to chemotherapy, and investigate how it may lead to drug resistance. We show that there is an optimal dose so that the tumor cells number is minimum at the steady state, which suggests the existence of an optimal dose of chemotherapy below the MTD. Model simulations show that when the dose is either low or high, the tumor cancer cells number may maintain a higher level steady state, or even sustained oscillations when the dose is too high, which are clinically inappropriate. Our results provide a theoretical study on the dose control of chemotherapy in cancer therapy.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">delay differential equation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">genomic disorder</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">non-clonal chromosome aberrations</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">chemotherapy</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">drug resistance</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biotechnology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Mathematics</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jinzhi Lei</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Mathematical Biosciences and Engineering</subfield><subfield code="d">AIMS Press, 2020</subfield><subfield code="g">16(2019), 6, Seite 7098-7111</subfield><subfield code="w">(DE-627)522894844</subfield><subfield code="w">(DE-600)2265126-3</subfield><subfield code="x">15510018</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:16</subfield><subfield code="g">year:2019</subfield><subfield code="g">number:6</subfield><subfield code="g">pages:7098-7111</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3934/mbe.2019356</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/40b87c8cf2114adea0b851a921e922e9</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.aimspress.com/article/10.3934/mbe.2019356?viewType=HTML</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/1551-0018</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_370</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4326</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4335</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">16</subfield><subfield code="j">2019</subfield><subfield code="e">6</subfield><subfield code="h">7098-7111</subfield></datafield></record></collection>
|
score |
7.4003096 |