Cessation of CCL2 inhibition accelerates breast cancer metastasis by promoting angiogenesis

By Laura Bonapace, Marie-May Coissieux, J. Wyckoff, K. Mertz, Z. Varga, T. Junt, M. Bentires‐Alj. Nature, 2014

648 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/bd57ef355ebda74066463e7b2481786bd80fac7f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. A. Mantovani
2. J. Pollard
3. R. Weinberg
4. P. Allavena
5. R. Noy
6. Binzhi Qian
7. Zena Werb
8. Jiu-feng Li

In Oncology

1. A. Mantovani
2. R. Weinberg
3. J. Pollard
4. Zena Werb
5. P. Allavena
6. D. Pattabiraman
7. Arthur W. Lambert
8. R. Noy

Citations in the corpus

• The interaction of anticancer therapies with tumor-associated macrophages (2015, result): “Recent results caution against the possibility that interruption of antiCCL2 therapy may lead to enhanced metastasis (Bonapace et al., 2014).”
• Progress in tumor-associated macrophage (TAM)-targeted therapeutics (2017, positive): “Anti-CCL2 antibodies have been shown to prevent metastasis in breast and prostate cancer models [111][112].”
• Roles of the immune system in cancer: from tumor initiation to metastatic progression (2018, background): “The role of CCL2 in cancer is more controversial, as previous studies have shown contradictory findings (Rollins and Sunday 1991; Manome et al. 1995; Lu and Kang 2009; Takahashi et al. 2009; Granot et al. 2011; Qian et al. 2011; Bonapace et al. 2014; Espinosa et al. 2014; Headley et al. 2016; Long e”
• Tumor-associated macrophages in tumor metastasis: biological roles and clinical therapeutic applications (2019, background): “Hence, digging into the respective roles of those components of TME and modeling their intricate interactions evolving along with the metastasis by system biology approaches may be the avenues for future research [162].”
• Microenvironment-induced PTEN loss by exosomal microRNA primes brain metastasis outgrowth (2015, background): “Notably, although clinical application of CCL2 inhibitor for metastasis treat-ment requires careful design 26 , our data of brain metastasis inhibition by stable ablation of PTEN-loss-induced CCL2 demonstrated the potential of CCL2-targeting for therapeutic intervention of life-threatening brain…”
• CCL2-induced chemokine cascade promotes breast cancer metastasis by enhancing retention of metastasis-associated macrophages (2015, background): “A recent paper also suggests a risk of anti-CCL2 therapy as there is a rebound increase of prometastatic myeloid cells after cessation of the therapy that accelerates the metastatic diseases (Bonapace et al., 2014).”