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Volume 3, Issue 9, pp. 284 - 309, September 2019

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Cover: This month in Cell Stress: Myelopoiesis and immunosurveillance in cancer cell stress. Fluorescence image of HeLa cells stained with the actin binding toxin phalloidin (orange), microtubules (blue) and cell nuclei (violet). Public domain image by National Institutes of Health (NIH) - National Institutes of Health (NIH), Public Domain, Modified by Cell Stress. The cover is published under the CC BY 4.0 license. Enlarge issue cover


Myelopoiesis, metabolism and therapy: a crucial crossroads in cancer progression

Antonio Sica, Valentina Guarneri and Alessandra Gennari

page 284-294 | 10.15698/cst2019.09.197 | Full text | PDF | Abstract

Cancers promote immunological stresses that induce alterations of the myelopoietic output, defined as emergency myelopoiesis, which lead to the generation of different myeloid populations endowed with tumor-promoting activities. New evidence indicates that acquisition of this tumor-promoting phenotype by myeloid cells is the result of a multistep process, encompassing initial events originating into the bone marrow and later steps operating in the tumor microenvironment. The careful characterization of these sequential mechanisms is likely to offer new potential therapeutic opportunities. Here, we describe relevant mechanisms of myeloid cells reprogramming that instate immune dysfunctions and limit effective responses to anticancer therapy and discuss the influence that metabolic events, as well as chemotherapy, elicit on such events.

Immunosurveillance of cancer cell stress

Seila Lorenzo-Herrero, Christian Sordo-Bahamonde, Segundo González and Alejandro López-Soto

page 295-309 | 10.15698/cst2019.09.198 | Full text | PDF | Abstract

Cancer development is tightly controlled by effector immune responses that recognize and eliminate malignantly transformed cells. Nonetheless, certain immune subsets, such as tumor-associated macrophages, have been described to promote tumor growth, unraveling a double-edge role of the immune system in cancer. Cell stress can modulate the crosstalk between immune cells and tumor cells, reshaping tumor immunogenicity and/or immune function and phenotype. Infiltrating immune cells are exposed to the challenging conditions typically present in the tumor microenvironment. In return, the myriad of signaling pathways activated in response to stress conditions may tip the balance toward stimulation of antitumor responses or immune-mediated tumor progression. Here, we explore how distinct situations of cellular stress influence innate and adaptive immunity and the consequent impact on cancer establishment and progression.

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