Mannose Receptor–positive Macrophage Infiltration Correlates with Prostate Cancer Onset and Metastatic Castration-resistant Disease

Zarif, Jelani C.; Valle, Javier Baena-Del; Hicks, Jessica L.; Heaphy, Christopher M.; Vidal, Igor; Luo, Jacob; Lotan, Tamara L.; Hooper, Jody E.; Isaacs, William B.; Pienta, Kenneth J.; Marzo, Angelo M. De

doi:10.1016/j.euo.2018.09.014

Cited by 52 publications

(67 citation statements)

References 29 publications

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“…63 In addition, tumor-associated macrophages (TAMs) are an important component of tumor microenvironment. Recently Zarif et al 64 showed that TAM can reprogram tumor phenotype and play a major role in the emergence of a neuroendocrine phenotype in prostate cancers. Targeting these signals in the prostate cancer microenvironment could potentially augment immunotherapeutic approaches in NEPC.…”

Section: Lineage Plasticity Driving Development Of Nepcmentioning

confidence: 99%

Epigenetic modulations and lineage plasticity in advanced prostate cancer

et al. 2020

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Prostate cancer is the most common cancer and second leading cause of cancer-related death in American men. Antiandrogen therapies are part of the standard of therapeutic regimen for advanced or metastatic prostate cancers; however, patients who receive these treatments are more likely to develop castration-resistant prostate cancer (CRPC) or neuroendocrine prostate cancer (NEPC). In the development of CRPC or NEPC, numerous genetic signaling pathways have been under preclinical investigations and in clinical trials. Accumulated evidence shows that DNA methylation, chromatin integrity, and accessibility for transcriptional regulation still play key roles in prostate cancer initiation and progression. Better understanding of how epigenetic change regulates the progression of prostate cancer and the interaction between epigenetic and genetic modulators driving NEPC may help develop a better risk stratification and more effective treatment regimens for prostate cancer patients.

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Section: Lineage Plasticity Driving Development Of Nepcmentioning

confidence: 99%

Epigenetic modulations and lineage plasticity in advanced prostate cancer

et al. 2020

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“…Macrophages positive for CD206, a biomarker for the M2/TAM macrophage phenotype, 12,42 were observed in rat prostates showing early proliferative lesions, even before malignancy was established. Similar findings have been reported previously in breast tissue 43 and the prostate 12 .…”

Section: Discussionmentioning

confidence: 99%

Tumor‐Associated Macrophages (TAM) are recruited to the aging prostate epithelial lesions and become intermingled with basal cells

et al. 2020

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Background Prostate cancer remains one of the most common cancers in men. Macrophages are thought to be important regulators in cancers, and their potential involvement in prostate cancer should not be overlooked. Therefore, the association between macrophages and the pre‐tumorous changes in prostate epithelium during aging deserves further investigation. Objectives We sought to investigate whether macrophages would be recruited into the prostate epithelium that display pathological lesions commonly found during aging. Materials and methods Prostates of aging rats, with and without treatment with a combination of testosterone and estradiol, were examined for premalignant and malignant epithelial lesions. For comparison, prostates of castrated rats were also investigated. Results Intraepithelial macrophages were found restricted to areas of premalignant and malignant lesions. An unprecedented interaction between macrophages and basal cells was observed in the aging pathological lesions. The intraepithelial macrophages were associated with autophagy, in contrast to those found after castration. In prostate lesions, the intraepithelial macrophages had TAM phenotype (CD68+/iNOS+/CD206+/ARG+), denoting a possible involvement in cancer progression. However, M2 macrophages (CD68+/CD163+) were recruited into the epithelium after castration, possibly to phagocytize cells undergoing apoptosis. Discussion and conclusion In conclusion, macrophages were recruited into the prostate epithelium and presented diverse phenotypes and morphology, consistent with changes reflected in the hormonal environment. Macrophages with the TAM phenotype were found restricted to areas of premalignant and malignant lesions in aging prostates, denoting a possible involvement in cancer progression. In contrast, M2 macrophages were found in the regressed epithelium after castration.

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“…Cancer cells and M2-like macrophages occupy a substantial part of the tumor habitat and have marked influence on the tumor ecosystem as a whole. [30][31][32] Cancer cells and macrophages support each other by secreting factors that stimulate the others' growth, survival, and, importantly, support tumorpromoting ecosystem engineering (Figure 2A). The ecosystem engineering of the cancer cells, the primary invader population, recruits secondary invasion of M2 macrophages by releasing cytokines that recruit and polarize M2 macrophages.…”

Section: Cooperative Invasive Ecosystem Engineersmentioning

confidence: 99%

Cancer Cells and M2 Macrophages: Cooperative Invasive Ecosystem Engineers

Myers

Pienta

Amend³

2020

Cancer Control

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Many aspects of cancer can be explained utilizing well-defined ecological principles. Applying these principles to cancer, cancer cells are an invasive species to a healthy organ ecosystem. In their capacity as ecosystem engineers, cancer cells release cytokines that recruit monocytes to the tumor and polarize them to M2-like protumor macrophages. Macrophages, recruited by the cancer cells, act as a secondary invasive species. The ecosystem engineering functions of M2-macrophages in turn support and stimulate cancer cell survival and proliferation. The cooperative ecosystem engineering of both the primary invasive species of the cancer cell and the secondary invasive species of the M2-macrophage thus creates a vicious cycle of tumor promotion. Targeting a specific aspect of this tumor-promoting ecosystem engineering, such as blocking efferocytosis by M2-like macrophages, may improve the response to standard-of-care anticancer therapies. This strategy has the potential to redirect cooperative protumor ecosystem engineering toward an antitumor ecosystem engineering strategy.

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Mannose Receptor–positive Macrophage Infiltration Correlates with Prostate Cancer Onset and Metastatic Castration-resistant Disease

Abstract: Background: M2 tumor-associated macrophages (M2-TAMs) can suppress inflammation in the tumor microenvironment and have been reported to modulate cancer progression. We and others have previously reported M2-TAM infiltration in metastatic castration-resistant prostate cancer (mCRPC).

Cited by 52 publications

References 29 publications

Epigenetic modulations and lineage plasticity in advanced prostate cancer

Epigenetic modulations and lineage plasticity in advanced prostate cancer

Tumor‐Associated Macrophages (TAM) are recruited to the aging prostate epithelial lesions and become intermingled with basal cells

Cancer Cells and M2 Macrophages: Cooperative Invasive Ecosystem Engineers

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