Cancer-related inflammation

被引：10305

作者：

Mantovani, Alberto ^{[1
,2
]}

Allavena, Paola ^{[1
]}

Sica, Antonio ^{[3
]}

Balkwill, Frances ^{[4
,5
]}

机构：

[1] IRCCS, Ist Clin Humanitas, I-20089 Milan, Italy

[2] Univ Milan, Ist Patol Gen, I-20133 Milan, Italy

[3] Fdn Humanitas Ric, I-20089 Milan, Italy

[4] Ctr Canc & Inflammat, Inst Canc, London EC1M 6BQ, England

[5] Univ London St Bartholomews Hosp Med Coll, Sch Med & Dent, Canc Res UK Clin Ctr, London EC1M 6BQ, England

来源：

NATURE | 2008年 / 454卷 / 7203期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1038/nature07205

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 [理学]; 0710 [生物学]; 09 [农学];

摘要：

The mediators and cellular effectors of inflammation are important constituents of the local environment of tumours. In some types of cancer, inflammatory conditions are present before a malignant change occurs. Conversely, in other types of cancer, an oncogenic change induces an inflammatory microenvironment that promotes the development of tumours. Regardless of its origin, 'smouldering' inflammation in the tumour microenvironment has many tumour-promoting effects. It aids in the proliferation and survival of malignant cells, promotes angiogenesis and metastasis, subverts adaptive immune responses, and alters responses to hormones and chemotherapeutic agents. The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.

引用

收藏

页码：436 / 444

页数：9

相关论文

共 98 条

[1]

Toll-like receptor 4-dependent contribution of the immune system to anticancer chemotherapy and radiotherapy [J].

Apetoh, Lionel ;

Ghiringhelli, Francois ;

Tesniere, Antoine ;

Obeid, Michel ;

Ortiz, Carla ;

Criollo, Alfredo ;

Mignot, Gregoire ;

Maiuri, M. Chiara ;

Ullrich, Evelyn ;

Saulnier, Patrick ;

Yang, Huan ;

Amigorena, Sebastian ;

Ryffel, Bernard ;

Barrat, Franck J. ;

Saftig, Paul ;

Levi, Francis ;

Lidereau, Rosette ;

Nogues, Catherine ;

Mira, Jean-Paul ;

Chompret, Agnes ;

Joulin, Virginie ;

Clavel-Chapelon, Francoise ;

Bourhis, Jean ;

Andre, Fabrice ;

Delaloge, Suzette ;

Tursz, Thomas ;

Kroemer, Guido ;

Zitvogel, Laurence .

NATURE MEDICINE, 2007, 13 (09) :1050-1059

[2]

Cancer and the chemokine network [J].

Balkwill, F .

NATURE REVIEWS CANCER, 2004, 4 (07) :540-550

[3]

Smoldering and polarized inflammation in the initiation and promotion of malignant disease [J].

Balkwill, F ;

Charles, KA ;

Mantovani, A .

CANCER CELL, 2005, 7 (03) :211-217

[4]

Inflammation and cancer: back to Virchow? [J].

Balkwill, F ;

Mantovani, A .

LANCET, 2001, 357 (9255) :539-545

[5]

Tumor necrosis factor-α stimulates the epithelial-to-mesenchymal transition of human colonic organoids [J].

Bates, RC ;

Mercurio, AM .

MOLECULAR BIOLOGY OF THE CELL, 2003, 14 (05) :1790-1800

[6]

Beatson GT., 1896, LANCET, V148, P104, DOI DOI 10.1016/S0140-6736(01)72307-0

[7]

Celecoxib for the prevention of sporadic colorectal adenomas [J].

Bertagnolli, Monica M. ;

Eagle, Craig J. ;

Zauber, Ann G. ;

Redston, Mark ;

Solomon, Scott D. ;

Kim, KyungMann ;

Tang, Jie ;

Rosenstein, Rebecca B. ;

Wittes, Janet ;

Corle, Donald ;

Hess, Timothy M. ;

Woloj, G. Mabel ;

Boisserie, Frederic ;

Anderson, William F. ;

Viner, Jaye L. ;

Bagheri, Donya ;

Burn, John ;

Chung, Daniel C. ;

Dewar, Thomas ;

Foley, T. Raymond ;

Hoffman, Neville ;

Macrae, Finlay ;

Pruitt, Ronald E. ;

Saltzman, John R. ;

Salzberg, Bruce ;

Sylwestrowicz, Thomas ;

Gordon, Gary B. ;

Hawk, Ernest T. .

NEW ENGLAND JOURNAL OF MEDICINE, 2006, 355 (09) :873-884

[8]

Human cancers express a mutator phenotype [J].

Bielas, Jason H. ;

Loeb, Keith R. ;

Rubin, Brian P. ;

True, Lawrence D. ;

Loeb, Lawrence A. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (48) :18238-18242

[9]

TGF-β and cancer [J].

Bierie, B ;

Moses, HL .

CYTOKINE & GROWTH FACTOR REVIEWS, 2006, 17 (1-2) :29-40

[10]

A distinct and unique transcriptional program expressed by tumor-associated macrophages (defective NF-κB and enhanced IRF-3/STAT1 activation) [J].

Biswas, SK ;

Gangi, L ;

Paul, S ;

Schioppa, T ;

Saccani, A ;

Sironi, M ;

Bottazzi, B ;

Doni, A ;

Vincenzo, B ;

Pasqualini, F ;

Vago, L ;

Nebuloni, M ;

Mantovani, A ;

Sica, A .

BLOOD, 2006, 107 (05) :2112-2122

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