Liver prometastatic reaction : Stimulating factors and responsive cancer phenotypes
Copyright © 2020 Elsevier Ltd. All rights reserved..
Cancer is first a localized tissue disorder, whose soluble and exosomal molecules and invasive cells induce a host response providing the stromal components of the primary tumor microenvironment (TME). Once the TME is developed, cancer-derived molecules and cells can more efficiently spread out and a whole-body response takes place, whose pathophysiological changes may result in a paraneoplastic syndrome. Remote organ-specific prometastatic reactions may also occur at this time, facilitating metastatic activities of circulating tumor cells (CTCs) through premetastatic niche development at targeted organs. However, additional signaling factors from the inter-organ communication network involved in the pathophysiology and comorbidities of cancer patients may also regulate prometastatic reaction-stimulating effects of cancer and non-cancer tissue factors. This article provides a conceptual overview of our ongoing clinical research on the liver prometastatic reaction (LPR) of patients with colorectal cancer (CRC), their portal vein- and hepatic artery-driven LPR-Stimulating Factors (LPR-SF), and their resulting LPR-derived Metastasis-Stimulating Factors (LPR-MSF) acting on liver-invading CRC cells. In addition, we also provide new insights on the molecular subtyping of LPR-responsive cancer phenotypes in patients with CRC and melanoma; and on how to investigate and interpret the prometastatic infrastructure in the real pathophysiological context of patients with cancer undergoing surgical procedures and receiving pharmacological treatments with multiple side effects, including those affecting the LPR, its stimulating factors and responsive cancer phenotypes.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2021 |
|---|---|
| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:71 |
|---|---|
| Enthalten in: |
Seminars in cancer biology - 71(2021) vom: 15. Juni, Seite 122-133 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Vidal-Vanaclocha, Fernando [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 03.03.2022 Date Revised 03.03.2022 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.semcancer.2020.08.001 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM313799636 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM313799636 | ||
| 003 | DE-627 | ||
| 005 | 20231225151339.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231225s2021 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.semcancer.2020.08.001 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1045.xml |
| 035 | |a (DE-627)NLM313799636 | ||
| 035 | |a (NLM)32805395 | ||
| 035 | |a (PII)S1044-579X(20)30171-1 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Vidal-Vanaclocha, Fernando |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Liver prometastatic reaction |b Stimulating factors and responsive cancer phenotypes |
| 264 | 1 | |c 2021 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 03.03.2022 | ||
| 500 | |a Date Revised 03.03.2022 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2020 Elsevier Ltd. All rights reserved. | ||
| 520 | |a Cancer is first a localized tissue disorder, whose soluble and exosomal molecules and invasive cells induce a host response providing the stromal components of the primary tumor microenvironment (TME). Once the TME is developed, cancer-derived molecules and cells can more efficiently spread out and a whole-body response takes place, whose pathophysiological changes may result in a paraneoplastic syndrome. Remote organ-specific prometastatic reactions may also occur at this time, facilitating metastatic activities of circulating tumor cells (CTCs) through premetastatic niche development at targeted organs. However, additional signaling factors from the inter-organ communication network involved in the pathophysiology and comorbidities of cancer patients may also regulate prometastatic reaction-stimulating effects of cancer and non-cancer tissue factors. This article provides a conceptual overview of our ongoing clinical research on the liver prometastatic reaction (LPR) of patients with colorectal cancer (CRC), their portal vein- and hepatic artery-driven LPR-Stimulating Factors (LPR-SF), and their resulting LPR-derived Metastasis-Stimulating Factors (LPR-MSF) acting on liver-invading CRC cells. In addition, we also provide new insights on the molecular subtyping of LPR-responsive cancer phenotypes in patients with CRC and melanoma; and on how to investigate and interpret the prometastatic infrastructure in the real pathophysiological context of patients with cancer undergoing surgical procedures and receiving pharmacological treatments with multiple side effects, including those affecting the LPR, its stimulating factors and responsive cancer phenotypes | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Review | |
| 650 | 4 | |a Biomarkers | |
| 650 | 4 | |a Colorectal cancer | |
| 650 | 4 | |a Exosomal proteins | |
| 650 | 4 | |a Gene expression profiling | |
| 650 | 4 | |a Inter-organ prometastatic communication | |
| 650 | 4 | |a Liver metastasis | |
| 650 | 4 | |a Liver prometastatic reaction | |
| 650 | 4 | |a Melanoma | |
| 650 | 4 | |a Premetastatic niche | |
| 650 | 4 | |a Tumor microenvironment | |
| 700 | 1 | |a Crende, Olatz |e verfasserin |4 aut | |
| 700 | 1 | |a García de Durango, Cira |e verfasserin |4 aut | |
| 700 | 1 | |a Herreros-Pomares, Alejandro |e verfasserin |4 aut | |
| 700 | 1 | |a López-Doménech, Sandra |e verfasserin |4 aut | |
| 700 | 1 | |a González, Álvaro |e verfasserin |4 aut | |
| 700 | 1 | |a Ruiz-Casares, Eva |e verfasserin |4 aut | |
| 700 | 1 | |a Vilboux, Thierry |e verfasserin |4 aut | |
| 700 | 1 | |a Caruso, Riccardo |e verfasserin |4 aut | |
| 700 | 1 | |a Durán, Hipólito |e verfasserin |4 aut | |
| 700 | 1 | |a Gil, Antonio |e verfasserin |4 aut | |
| 700 | 1 | |a Ielpo, Benedetto |e verfasserin |4 aut | |
| 700 | 1 | |a Lapuente, Fernando |e verfasserin |4 aut | |
| 700 | 1 | |a Quijano, Yolanda |e verfasserin |4 aut | |
| 700 | 1 | |a Vicente, Emilio |e verfasserin |4 aut | |
| 700 | 1 | |a Vidal-Lartitegui, Leticia |e verfasserin |4 aut | |
| 700 | 1 | |a Sotomayor, Eduardo M |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Seminars in cancer biology |d 1991 |g 71(2021) vom: 15. Juni, Seite 122-133 |w (DE-627)NLM012641944 |x 1096-3650 |7 nnns |
| 773 | 1 | 8 | |g volume:71 |g year:2021 |g day:15 |g month:06 |g pages:122-133 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.semcancer.2020.08.001 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 71 |j 2021 |b 15 |c 06 |h 122-133 | ||