Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts
Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While imm...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Alguacil-Núñez, Cristina [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
9 |
|---|
| Übergeordnetes Werk: |
Enthalten in: miR-214 in stroma cells and tumor progression - Dettori, D. ELSEVIER, 2016, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:125 ; year:2018 ; pages:102-110 ; extent:9 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.critrevonc.2018.02.015 |
|---|
| Katalog-ID: |
ELV042623472 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV042623472 | ||
| 003 | DE-627 | ||
| 005 | 20230626001910.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180726s2018 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.critrevonc.2018.02.015 |2 doi | |
| 028 | 5 | 2 | |a GBV00000000000194A.pica |
| 035 | |a (DE-627)ELV042623472 | ||
| 035 | |a (ELSEVIER)S1040-8428(17)30456-0 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 610 |q VZ |
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.52 |2 bkl | ||
| 100 | 1 | |a Alguacil-Núñez, Cristina |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts |
| 264 | 1 | |c 2018transfer abstract | |
| 300 | |a 9 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. | ||
| 520 | |a Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. | ||
| 650 | 7 | |a ALK |2 Elsevier | |
| 650 | 7 | |a HH |2 Elsevier | |
| 650 | 7 | |a NSCLC |2 Elsevier | |
| 650 | 7 | |a HGF |2 Elsevier | |
| 650 | 7 | |a SDF-1 |2 Elsevier | |
| 650 | 7 | |a CAF |2 Elsevier | |
| 650 | 7 | |a IGF |2 Elsevier | |
| 650 | 7 | |a EMT |2 Elsevier | |
| 650 | 7 | |a EGFR |2 Elsevier | |
| 650 | 7 | |a CSC |2 Elsevier | |
| 650 | 7 | |a CRC |2 Elsevier | |
| 650 | 7 | |a KRAS |2 Elsevier | |
| 650 | 7 | |a MSC |2 Elsevier | |
| 700 | 1 | |a Ferrer-Ortiz, Inés |4 oth | |
| 700 | 1 | |a García-Verdú, Elena |4 oth | |
| 700 | 1 | |a López- Pirez, Pilar |4 oth | |
| 700 | 1 | |a Llorente-Cortijo, Irene Maria |4 oth | |
| 700 | 1 | |a Sainz, Bruno |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Dettori, D. ELSEVIER |t miR-214 in stroma cells and tumor progression |d 2016 |g Amsterdam [u.a.] |w (DE-627)ELV019637179 |
| 773 | 1 | 8 | |g volume:125 |g year:2018 |g pages:102-110 |g extent:9 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.critrevonc.2018.02.015 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a GBV_ILN_11 | ||
| 912 | |a GBV_ILN_20 | ||
| 912 | |a GBV_ILN_70 | ||
| 912 | |a GBV_ILN_100 | ||
| 912 | |a GBV_ILN_2006 | ||
| 912 | |a GBV_ILN_2009 | ||
| 912 | |a GBV_ILN_2014 | ||
| 912 | |a GBV_ILN_2015 | ||
| 912 | |a GBV_ILN_2016 | ||
| 912 | |a GBV_ILN_2048 | ||
| 936 | b | k | |a 44.52 |j Therapie |x Medizin |q VZ |
| 951 | |a AR | ||
| 952 | |d 125 |j 2018 |h 102-110 |g 9 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
c a n can |
|---|---|
| matchkey_str |
alguacilnezcristinaferrerortizinsgarcave:2018----:urnprpcieoterstlbtenugacrtmeladac |
| hierarchy_sort_str |
2018transfer abstract |
| bklnumber |
44.52 |
| publishDate |
2018 |
| allfields |
10.1016/j.critrevonc.2018.02.015 doi GBV00000000000194A.pica (DE-627)ELV042623472 (ELSEVIER)S1040-8428(17)30456-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.52 bkl Alguacil-Núñez, Cristina verfasserin aut Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts 2018transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC Elsevier Ferrer-Ortiz, Inés oth García-Verdú, Elena oth López- Pirez, Pilar oth Llorente-Cortijo, Irene Maria oth Sainz, Bruno oth Enthalten in Elsevier Science Dettori, D. ELSEVIER miR-214 in stroma cells and tumor progression 2016 Amsterdam [u.a.] (DE-627)ELV019637179 volume:125 year:2018 pages:102-110 extent:9 https://doi.org/10.1016/j.critrevonc.2018.02.015 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_20 GBV_ILN_70 GBV_ILN_100 GBV_ILN_2006 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2048 44.52 Therapie Medizin VZ AR 125 2018 102-110 9 045F 610 |
| spelling |
10.1016/j.critrevonc.2018.02.015 doi GBV00000000000194A.pica (DE-627)ELV042623472 (ELSEVIER)S1040-8428(17)30456-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.52 bkl Alguacil-Núñez, Cristina verfasserin aut Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts 2018transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC Elsevier Ferrer-Ortiz, Inés oth García-Verdú, Elena oth López- Pirez, Pilar oth Llorente-Cortijo, Irene Maria oth Sainz, Bruno oth Enthalten in Elsevier Science Dettori, D. ELSEVIER miR-214 in stroma cells and tumor progression 2016 Amsterdam [u.a.] (DE-627)ELV019637179 volume:125 year:2018 pages:102-110 extent:9 https://doi.org/10.1016/j.critrevonc.2018.02.015 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_20 GBV_ILN_70 GBV_ILN_100 GBV_ILN_2006 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2048 44.52 Therapie Medizin VZ AR 125 2018 102-110 9 045F 610 |
| allfields_unstemmed |
10.1016/j.critrevonc.2018.02.015 doi GBV00000000000194A.pica (DE-627)ELV042623472 (ELSEVIER)S1040-8428(17)30456-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.52 bkl Alguacil-Núñez, Cristina verfasserin aut Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts 2018transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC Elsevier Ferrer-Ortiz, Inés oth García-Verdú, Elena oth López- Pirez, Pilar oth Llorente-Cortijo, Irene Maria oth Sainz, Bruno oth Enthalten in Elsevier Science Dettori, D. ELSEVIER miR-214 in stroma cells and tumor progression 2016 Amsterdam [u.a.] (DE-627)ELV019637179 volume:125 year:2018 pages:102-110 extent:9 https://doi.org/10.1016/j.critrevonc.2018.02.015 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_20 GBV_ILN_70 GBV_ILN_100 GBV_ILN_2006 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2048 44.52 Therapie Medizin VZ AR 125 2018 102-110 9 045F 610 |
| allfieldsGer |
10.1016/j.critrevonc.2018.02.015 doi GBV00000000000194A.pica (DE-627)ELV042623472 (ELSEVIER)S1040-8428(17)30456-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.52 bkl Alguacil-Núñez, Cristina verfasserin aut Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts 2018transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC Elsevier Ferrer-Ortiz, Inés oth García-Verdú, Elena oth López- Pirez, Pilar oth Llorente-Cortijo, Irene Maria oth Sainz, Bruno oth Enthalten in Elsevier Science Dettori, D. ELSEVIER miR-214 in stroma cells and tumor progression 2016 Amsterdam [u.a.] (DE-627)ELV019637179 volume:125 year:2018 pages:102-110 extent:9 https://doi.org/10.1016/j.critrevonc.2018.02.015 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_20 GBV_ILN_70 GBV_ILN_100 GBV_ILN_2006 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2048 44.52 Therapie Medizin VZ AR 125 2018 102-110 9 045F 610 |
| allfieldsSound |
10.1016/j.critrevonc.2018.02.015 doi GBV00000000000194A.pica (DE-627)ELV042623472 (ELSEVIER)S1040-8428(17)30456-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.52 bkl Alguacil-Núñez, Cristina verfasserin aut Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts 2018transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC Elsevier Ferrer-Ortiz, Inés oth García-Verdú, Elena oth López- Pirez, Pilar oth Llorente-Cortijo, Irene Maria oth Sainz, Bruno oth Enthalten in Elsevier Science Dettori, D. ELSEVIER miR-214 in stroma cells and tumor progression 2016 Amsterdam [u.a.] (DE-627)ELV019637179 volume:125 year:2018 pages:102-110 extent:9 https://doi.org/10.1016/j.critrevonc.2018.02.015 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_20 GBV_ILN_70 GBV_ILN_100 GBV_ILN_2006 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2048 44.52 Therapie Medizin VZ AR 125 2018 102-110 9 045F 610 |
| language |
English |
| source |
Enthalten in miR-214 in stroma cells and tumor progression Amsterdam [u.a.] volume:125 year:2018 pages:102-110 extent:9 |
| sourceStr |
Enthalten in miR-214 in stroma cells and tumor progression Amsterdam [u.a.] volume:125 year:2018 pages:102-110 extent:9 |
| format_phy_str_mv |
Article |
| bklname |
Therapie |
| institution |
findex.gbv.de |
| topic_facet |
ALK HH NSCLC HGF SDF-1 CAF IGF EMT EGFR CSC CRC KRAS MSC |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
miR-214 in stroma cells and tumor progression |
| authorswithroles_txt_mv |
Alguacil-Núñez, Cristina @@aut@@ Ferrer-Ortiz, Inés @@oth@@ García-Verdú, Elena @@oth@@ López- Pirez, Pilar @@oth@@ Llorente-Cortijo, Irene Maria @@oth@@ Sainz, Bruno @@oth@@ |
| publishDateDaySort_date |
2018-01-01T00:00:00Z |
| hierarchy_top_id |
ELV019637179 |
| dewey-sort |
3610 |
| id |
ELV042623472 |
| 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">ELV042623472</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626001910.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180726s2018 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.critrevonc.2018.02.015</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000194A.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV042623472</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1040-8428(17)30456-0</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="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.52</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Alguacil-Núñez, Cristina</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ALK</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HH</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NSCLC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HGF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SDF-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CAF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IGF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">EMT</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">EGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CSC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CRC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">KRAS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MSC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ferrer-Ortiz, Inés</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">García-Verdú, Elena</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">López- Pirez, Pilar</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Llorente-Cortijo, Irene Maria</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sainz, Bruno</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Dettori, D. ELSEVIER</subfield><subfield code="t">miR-214 in stroma cells and tumor progression</subfield><subfield code="d">2016</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV019637179</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:125</subfield><subfield code="g">year:2018</subfield><subfield code="g">pages:102-110</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.critrevonc.2018.02.015</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</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_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_100</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2006</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2009</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_2015</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2016</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2048</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.52</subfield><subfield code="j">Therapie</subfield><subfield code="x">Medizin</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">125</subfield><subfield code="j">2018</subfield><subfield code="h">102-110</subfield><subfield code="g">9</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Alguacil-Núñez, Cristina |
| spellingShingle |
Alguacil-Núñez, Cristina ddc 610 bkl 44.52 Elsevier ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts |
| authorStr |
Alguacil-Núñez, Cristina |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV019637179 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 610 VZ 44.52 bkl Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC Elsevier |
| topic |
ddc 610 bkl 44.52 Elsevier ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC |
| topic_unstemmed |
ddc 610 bkl 44.52 Elsevier ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC |
| topic_browse |
ddc 610 bkl 44.52 Elsevier ALK Elsevier HH Elsevier NSCLC Elsevier HGF Elsevier SDF-1 Elsevier CAF Elsevier IGF Elsevier EMT Elsevier EGFR Elsevier CSC Elsevier CRC Elsevier KRAS Elsevier MSC |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| hierarchy_parent_title |
miR-214 in stroma cells and tumor progression |
| hierarchy_parent_id |
ELV019637179 |
| dewey-tens |
610 - Medicine & health |
| hierarchy_top_title |
miR-214 in stroma cells and tumor progression |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV019637179 |
| title |
Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts |
| ctrlnum |
(DE-627)ELV042623472 (ELSEVIER)S1040-8428(17)30456-0 |
| title_full |
Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts |
| author_sort |
Alguacil-Núñez, Cristina |
| journal |
miR-214 in stroma cells and tumor progression |
| journalStr |
miR-214 in stroma cells and tumor progression |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2018 |
| contenttype_str_mv |
zzz |
| container_start_page |
102 |
| author_browse |
Alguacil-Núñez, Cristina |
| container_volume |
125 |
| physical |
9 |
| class |
610 610 DE-600 610 VZ 44.52 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Alguacil-Núñez, Cristina |
| doi_str_mv |
10.1016/j.critrevonc.2018.02.015 |
| dewey-full |
610 |
| title_sort |
current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts |
| title_auth |
Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts |
| abstract |
Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. |
| abstractGer |
Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. |
| abstract_unstemmed |
Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_20 GBV_ILN_70 GBV_ILN_100 GBV_ILN_2006 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2048 |
| title_short |
Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts |
| url |
https://doi.org/10.1016/j.critrevonc.2018.02.015 |
| remote_bool |
true |
| author2 |
Ferrer-Ortiz, Inés García-Verdú, Elena López- Pirez, Pilar Llorente-Cortijo, Irene Maria Sainz, Bruno |
| author2Str |
Ferrer-Ortiz, Inés García-Verdú, Elena López- Pirez, Pilar Llorente-Cortijo, Irene Maria Sainz, Bruno |
| ppnlink |
ELV019637179 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth |
| doi_str |
10.1016/j.critrevonc.2018.02.015 |
| up_date |
2024-07-06T16:40:17.041Z |
| _version_ |
1803848533453832192 |
| 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">ELV042623472</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626001910.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180726s2018 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.critrevonc.2018.02.015</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000194A.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV042623472</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1040-8428(17)30456-0</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="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.52</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Alguacil-Núñez, Cristina</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Current perspectives on the crosstalk between lung cancer stem cells and cancer-associated fibroblasts</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Lung cancer, in particular non-small cell lung carcinoma (NSCLC), is the second most common cancer in both men and women and the leading cause of cancer-related deaths worldwide. Its prognosis and diagnosis are determined by several driver mutations and diverse risk factors (e.g. smoking). While immunotherapy has proven effective in some patients, treatment of NSCLC using conventional chemotherapy is largely ineffective. The latter is believed to be due to the existence of a subpopulation of stem-like, highly tumorigenic and chemoresistant cells within the tumor population known as cancer stem cells (CSC). To complicate the situation, CSCs interact with the tumor microenvironment, which include cancer-associated fibroblasts (CAFs), immune cells, endothelial cells, growth factors, cytokines and connective tissue components, which via a dynamic crosstalk, composed of proteins and exosomes, activates the CSC compartment. In this review, we analyze the crosstalk between CSCs and CAFs, the primary component of the NSCLC microenvironment, at the molecular and extracellular level and contemplate therapies to disrupt this communication.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">ALK</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HH</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NSCLC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">HGF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SDF-1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CAF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">IGF</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">EMT</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">EGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CSC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CRC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">KRAS</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MSC</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ferrer-Ortiz, Inés</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">García-Verdú, Elena</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">López- Pirez, Pilar</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Llorente-Cortijo, Irene Maria</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sainz, Bruno</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Dettori, D. ELSEVIER</subfield><subfield code="t">miR-214 in stroma cells and tumor progression</subfield><subfield code="d">2016</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV019637179</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:125</subfield><subfield code="g">year:2018</subfield><subfield code="g">pages:102-110</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.critrevonc.2018.02.015</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</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_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_100</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2006</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2009</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_2015</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2016</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2048</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.52</subfield><subfield code="j">Therapie</subfield><subfield code="x">Medizin</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">125</subfield><subfield code="j">2018</subfield><subfield code="h">102-110</subfield><subfield code="g">9</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.3986187 |