Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies

Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Aurora Gazzillo [verfasserIn] Camilla Volponi [verfasserIn] Cristiana Soldani [verfasserIn] Michela Anna Polidoro [verfasserIn] Barbara Franceschini [verfasserIn] Ana Lleo [verfasserIn] Eduardo Bonavita [verfasserIn] Matteo Donadon [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	liver cancer cellular senescence senescence-associated secretory phenotype hepatocellular carcinoma (HCC) cholangiocarcinoma (CCA) colorectal liver mestastases (CLM)

Übergeordnetes Werk:	In: Biomedicines - MDPI AG, 2014, 12(2023), 1, p 26
Übergeordnetes Werk:	volume:12 ; year:2023 ; number:1, p 26

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/biomedicines12010026

Katalog-ID:	DOAJ096197560

Internformat


LEADER	01000naa a22002652 4500
001	DOAJ096197560
003	DE-627
005	20240413143954.0
007	cr uuu---uuuuu
008	240413s2023 xx \|\|\|\|\|o 00\| \|\|eng c
024	7		\|a 10.3390/biomedicines12010026 \|2 doi
035			\|a (DE-627)DOAJ096197560
035			\|a (DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
050		0	\|a QH301-705.5
100	0		\|a Aurora Gazzillo \|e verfasserin \|4 aut
245	1	0	\|a Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies
264		1	\|c 2023
336			\|a Text \|b txt \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
520			\|a Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance.
650		4	\|a liver cancer
650		4	\|a cellular senescence
650		4	\|a senescence-associated secretory phenotype
650		4	\|a hepatocellular carcinoma (HCC)
650		4	\|a cholangiocarcinoma (CCA)
650		4	\|a colorectal liver mestastases (CLM)
653		0	\|a Biology (General)
700	0		\|a Camilla Volponi \|e verfasserin \|4 aut
700	0		\|a Cristiana Soldani \|e verfasserin \|4 aut
700	0		\|a Michela Anna Polidoro \|e verfasserin \|4 aut
700	0		\|a Barbara Franceschini \|e verfasserin \|4 aut
700	0		\|a Ana Lleo \|e verfasserin \|4 aut
700	0		\|a Eduardo Bonavita \|e verfasserin \|4 aut
700	0		\|a Matteo Donadon \|e verfasserin \|4 aut
773	0	8	\|i In \|t Biomedicines \|d MDPI AG, 2014 \|g 12(2023), 1, p 26 \|w (DE-627)750370483 \|w (DE-600)2720867-9 \|x 22279059 \|7 nnns
773	1	8	\|g volume:12 \|g year:2023 \|g number:1, p 26
856	4	0	\|u https://doi.org/10.3390/biomedicines12010026 \|z kostenfrei
856	4	0	\|u https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f \|z kostenfrei
856	4	0	\|u https://www.mdpi.com/2227-9059/12/1/26 \|z kostenfrei
856	4	2	\|u https://doaj.org/toc/2227-9059 \|y Journal toc \|z kostenfrei
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_DOAJ
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_74
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_206
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
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_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 12 \|j 2023 \|e 1, p 26

Indexfelder

author_variant	a g ag c v cv c s cs m a p map b f bf a l al e b eb m d md
matchkey_str	article:22279059:2023----::ellreecneniecnehwyncls
hierarchy_sort_str	2023
callnumber-subject-code	QH
publishDate	2023
allfields	10.3390/biomedicines12010026 doi (DE-627)DOAJ096197560 (DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f DE-627 ger DE-627 rakwb eng QH301-705.5 Aurora Gazzillo verfasserin aut Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance. liver cancer cellular senescence senescence-associated secretory phenotype hepatocellular carcinoma (HCC) cholangiocarcinoma (CCA) colorectal liver mestastases (CLM) Biology (General) Camilla Volponi verfasserin aut Cristiana Soldani verfasserin aut Michela Anna Polidoro verfasserin aut Barbara Franceschini verfasserin aut Ana Lleo verfasserin aut Eduardo Bonavita verfasserin aut Matteo Donadon verfasserin aut In Biomedicines MDPI AG, 2014 12(2023), 1, p 26 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:12 year:2023 number:1, p 26 https://doi.org/10.3390/biomedicines12010026 kostenfrei https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f kostenfrei https://www.mdpi.com/2227-9059/12/1/26 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2023 1, p 26
spelling	10.3390/biomedicines12010026 doi (DE-627)DOAJ096197560 (DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f DE-627 ger DE-627 rakwb eng QH301-705.5 Aurora Gazzillo verfasserin aut Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance. liver cancer cellular senescence senescence-associated secretory phenotype hepatocellular carcinoma (HCC) cholangiocarcinoma (CCA) colorectal liver mestastases (CLM) Biology (General) Camilla Volponi verfasserin aut Cristiana Soldani verfasserin aut Michela Anna Polidoro verfasserin aut Barbara Franceschini verfasserin aut Ana Lleo verfasserin aut Eduardo Bonavita verfasserin aut Matteo Donadon verfasserin aut In Biomedicines MDPI AG, 2014 12(2023), 1, p 26 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:12 year:2023 number:1, p 26 https://doi.org/10.3390/biomedicines12010026 kostenfrei https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f kostenfrei https://www.mdpi.com/2227-9059/12/1/26 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2023 1, p 26
allfields_unstemmed	10.3390/biomedicines12010026 doi (DE-627)DOAJ096197560 (DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f DE-627 ger DE-627 rakwb eng QH301-705.5 Aurora Gazzillo verfasserin aut Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance. liver cancer cellular senescence senescence-associated secretory phenotype hepatocellular carcinoma (HCC) cholangiocarcinoma (CCA) colorectal liver mestastases (CLM) Biology (General) Camilla Volponi verfasserin aut Cristiana Soldani verfasserin aut Michela Anna Polidoro verfasserin aut Barbara Franceschini verfasserin aut Ana Lleo verfasserin aut Eduardo Bonavita verfasserin aut Matteo Donadon verfasserin aut In Biomedicines MDPI AG, 2014 12(2023), 1, p 26 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:12 year:2023 number:1, p 26 https://doi.org/10.3390/biomedicines12010026 kostenfrei https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f kostenfrei https://www.mdpi.com/2227-9059/12/1/26 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2023 1, p 26
allfieldsGer	10.3390/biomedicines12010026 doi (DE-627)DOAJ096197560 (DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f DE-627 ger DE-627 rakwb eng QH301-705.5 Aurora Gazzillo verfasserin aut Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance. liver cancer cellular senescence senescence-associated secretory phenotype hepatocellular carcinoma (HCC) cholangiocarcinoma (CCA) colorectal liver mestastases (CLM) Biology (General) Camilla Volponi verfasserin aut Cristiana Soldani verfasserin aut Michela Anna Polidoro verfasserin aut Barbara Franceschini verfasserin aut Ana Lleo verfasserin aut Eduardo Bonavita verfasserin aut Matteo Donadon verfasserin aut In Biomedicines MDPI AG, 2014 12(2023), 1, p 26 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:12 year:2023 number:1, p 26 https://doi.org/10.3390/biomedicines12010026 kostenfrei https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f kostenfrei https://www.mdpi.com/2227-9059/12/1/26 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2023 1, p 26
allfieldsSound	10.3390/biomedicines12010026 doi (DE-627)DOAJ096197560 (DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f DE-627 ger DE-627 rakwb eng QH301-705.5 Aurora Gazzillo verfasserin aut Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance. liver cancer cellular senescence senescence-associated secretory phenotype hepatocellular carcinoma (HCC) cholangiocarcinoma (CCA) colorectal liver mestastases (CLM) Biology (General) Camilla Volponi verfasserin aut Cristiana Soldani verfasserin aut Michela Anna Polidoro verfasserin aut Barbara Franceschini verfasserin aut Ana Lleo verfasserin aut Eduardo Bonavita verfasserin aut Matteo Donadon verfasserin aut In Biomedicines MDPI AG, 2014 12(2023), 1, p 26 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:12 year:2023 number:1, p 26 https://doi.org/10.3390/biomedicines12010026 kostenfrei https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f kostenfrei https://www.mdpi.com/2227-9059/12/1/26 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2023 1, p 26
language	English
source	In Biomedicines 12(2023), 1, p 26 volume:12 year:2023 number:1, p 26
sourceStr	In Biomedicines 12(2023), 1, p 26 volume:12 year:2023 number:1, p 26
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	liver cancer cellular senescence senescence-associated secretory phenotype hepatocellular carcinoma (HCC) cholangiocarcinoma (CCA) colorectal liver mestastases (CLM) Biology (General)
isfreeaccess_bool	true
container_title	Biomedicines
authorswithroles_txt_mv	Aurora Gazzillo @@aut@@ Camilla Volponi @@aut@@ Cristiana Soldani @@aut@@ Michela Anna Polidoro @@aut@@ Barbara Franceschini @@aut@@ Ana Lleo @@aut@@ Eduardo Bonavita @@aut@@ Matteo Donadon @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	750370483
id	DOAJ096197560
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">DOAJ096197560</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240413143954.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240413s2023 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3390/biomedicines12010026</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ096197560</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f</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">QH301-705.5</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Aurora Gazzillo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2023</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">Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">liver cancer</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">cellular senescence</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">senescence-associated secretory phenotype</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">hepatocellular carcinoma (HCC)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">cholangiocarcinoma (CCA)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">colorectal liver mestastases (CLM)</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biology (General)</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Camilla Volponi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Cristiana Soldani</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Michela Anna Polidoro</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Barbara Franceschini</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ana Lleo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Eduardo Bonavita</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Matteo Donadon</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">Biomedicines</subfield><subfield code="d">MDPI AG, 2014</subfield><subfield code="g">12(2023), 1, p 26</subfield><subfield code="w">(DE-627)750370483</subfield><subfield code="w">(DE-600)2720867-9</subfield><subfield code="x">22279059</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:12</subfield><subfield code="g">year:2023</subfield><subfield code="g">number:1, p 26</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3390/biomedicines12010026</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.mdpi.com/2227-9059/12/1/26</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2227-9059</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">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_74</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_206</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_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_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">12</subfield><subfield code="j">2023</subfield><subfield code="e">1, p 26</subfield></datafield></record></collection>
callnumber-first	Q - Science
author	Aurora Gazzillo
spellingShingle	Aurora Gazzillo misc QH301-705.5 misc liver cancer misc cellular senescence misc senescence-associated secretory phenotype misc hepatocellular carcinoma (HCC) misc cholangiocarcinoma (CCA) misc colorectal liver mestastases (CLM) misc Biology (General) Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies
authorStr	Aurora Gazzillo
ppnlink_with_tag_str_mv	@@773@@(DE-627)750370483
format	electronic Article
delete_txt_mv	keep
author_role	aut aut aut aut aut aut aut aut
collection	DOAJ
remote_str	true
callnumber-label	QH301-705
illustrated	Not Illustrated
issn	22279059
topic_title	QH301-705.5 Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies liver cancer cellular senescence senescence-associated secretory phenotype hepatocellular carcinoma (HCC) cholangiocarcinoma (CCA) colorectal liver mestastases (CLM)
topic	misc QH301-705.5 misc liver cancer misc cellular senescence misc senescence-associated secretory phenotype misc hepatocellular carcinoma (HCC) misc cholangiocarcinoma (CCA) misc colorectal liver mestastases (CLM) misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc liver cancer misc cellular senescence misc senescence-associated secretory phenotype misc hepatocellular carcinoma (HCC) misc cholangiocarcinoma (CCA) misc colorectal liver mestastases (CLM) misc Biology (General)
topic_browse	misc QH301-705.5 misc liver cancer misc cellular senescence misc senescence-associated secretory phenotype misc hepatocellular carcinoma (HCC) misc cholangiocarcinoma (CCA) misc colorectal liver mestastases (CLM) misc Biology (General)
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	Biomedicines
hierarchy_parent_id	750370483
hierarchy_top_title	Biomedicines
isfreeaccess_txt	true
familylinks_str_mv	(DE-627)750370483 (DE-600)2720867-9
title	Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies
ctrlnum	(DE-627)DOAJ096197560 (DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f
title_full	Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies
author_sort	Aurora Gazzillo
journal	Biomedicines
journalStr	Biomedicines
callnumber-first-code	Q
lang_code	eng
isOA_bool	true
recordtype	marc
publishDateSort	2023
contenttype_str_mv	txt
author_browse	Aurora Gazzillo Camilla Volponi Cristiana Soldani Michela Anna Polidoro Barbara Franceschini Ana Lleo Eduardo Bonavita Matteo Donadon
container_volume	12
class	QH301-705.5
format_se	Elektronische Aufsätze
author-letter	Aurora Gazzillo
doi_str_mv	10.3390/biomedicines12010026
author2-role	verfasserin
title_sort	cellular senescence in liver cancer: how dying cells become “zombie” enemies
callnumber	QH301-705.5
title_auth	Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies
abstract	Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance.
abstractGer	Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance.
abstract_unstemmed	Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 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_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	1, p 26
title_short	Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies
url	https://doi.org/10.3390/biomedicines12010026 https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f https://www.mdpi.com/2227-9059/12/1/26 https://doaj.org/toc/2227-9059
remote_bool	true
author2	Camilla Volponi Cristiana Soldani Michela Anna Polidoro Barbara Franceschini Ana Lleo Eduardo Bonavita Matteo Donadon
author2Str	Camilla Volponi Cristiana Soldani Michela Anna Polidoro Barbara Franceschini Ana Lleo Eduardo Bonavita Matteo Donadon
ppnlink	750370483
callnumber-subject	QH - Natural History and Biology
mediatype_str_mv	c
isOA_txt	true
hochschulschrift_bool	false
doi_str	10.3390/biomedicines12010026
callnumber-a	QH301-705.5
up_date	2024-07-03T18:49:57.960Z
_version_	1803584901445844992
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">DOAJ096197560</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240413143954.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240413s2023 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3390/biomedicines12010026</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ096197560</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ96048340d86a4c5f9e56cebe65104a6f</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">QH301-705.5</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Aurora Gazzillo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2023</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">Liver cancer represents the fourth leading cause of cancer-associated death worldwide. The heterogeneity of its tumor microenvironment (TME) is a major contributing factor of metastasis, relapse, and drug resistance. Regrettably, late diagnosis makes most liver cancer patients ineligible for surgery, and the frequent failure of non-surgical therapeutic options orientates clinical research to the investigation of new drugs. In this context, cellular senescence has been recently shown to play a pivotal role in the progression of chronic inflammatory liver diseases, ultimately leading to cancer. Moreover, the stem-like state triggered by senescence has been associated with the emergence of drug-resistant, aggressive tumor clones. In recent years, an increasing number of studies have emerged to investigate senescence-associated hepatocarcinogenesis and its derived therapies, leading to promising results. In this review, we intend to provide an overview of the recent evidence that unveils the role of cellular senescence in the most frequent forms of primary and metastatic liver cancer, focusing on the involvement of this mechanism in therapy resistance.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">liver cancer</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">cellular senescence</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">senescence-associated secretory phenotype</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">hepatocellular carcinoma (HCC)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">cholangiocarcinoma (CCA)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">colorectal liver mestastases (CLM)</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biology (General)</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Camilla Volponi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Cristiana Soldani</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Michela Anna Polidoro</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Barbara Franceschini</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Ana Lleo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Eduardo Bonavita</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Matteo Donadon</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">Biomedicines</subfield><subfield code="d">MDPI AG, 2014</subfield><subfield code="g">12(2023), 1, p 26</subfield><subfield code="w">(DE-627)750370483</subfield><subfield code="w">(DE-600)2720867-9</subfield><subfield code="x">22279059</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:12</subfield><subfield code="g">year:2023</subfield><subfield code="g">number:1, p 26</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3390/biomedicines12010026</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/96048340d86a4c5f9e56cebe65104a6f</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.mdpi.com/2227-9059/12/1/26</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2227-9059</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">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_74</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_206</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_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_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">12</subfield><subfield code="j">2023</subfield><subfield code="e">1, p 26</subfield></datafield></record></collection>
score	7.4022093

Nicht das Richtige dabei?

Schreiben Sie uns!

Cellular Senescence in Liver Cancer: How Dying Cells Become “Zombie” Enemies

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?