About this Research Topic
Most human cancers develop as a result of transformation of normal cells into cancer cells. Transformed cells lose control over contact inhibition, programmed cell death and acquire unlimited proliferative potential. Developing tumor potentiates its own vasculature to achieve unabated supply of growth factors and nutrients. Differentiated cancer cells, stromal cells, cancer stem cells, together with infiltrating immune cells, and other accessory cells constitute what is known as tumor microenvironment (TME). TME is a dynamic environment that not only provides specialized niche to cancer stem cells, but also creates immune-suppressive state whereby tumor infiltrating immune cells lose their effector function and become exhausted or tolerant or immune-suppressive themselves, further exacerbating the TME. Understanding the composition as well as interplay of different cellular and molecular constituents of TME, and their contribution to maintenance and progression of tumor growth is critical to devise effective strategies to reprogram TME conducive to immunotherapy conducive microenvironment.
Several cellular components of tumor microenvironment have been identified, and several underlying molecular mechanisms that play essential roles in establishment of TME have been deciphered. Among these, exosomes-mediated cellular signaling has gained special attention. These micro-vesicles can carry molecular signals in the form of small RNAs, for example via microRNAs and long non-coding RNAs (LNC RNAs), to name a few. Furthermore, cellular metabolism also plays a significant role not only in tumor growth, but also in the establishment of TME. Highly proliferative cancer cells require constant supply of energy, which is achieved by channeling glucose through oxidative glycolysis, that converts glucose into lactate, in spite of functioning mitochondria. The metabolic shift not only allows cancer cells to use most of available glucose faster, it also turns TME acidic, facilitating differentiation of macrophages towards M2 route, allowing establishment of immune-suppressive TME.
This Research Topic welcomes Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial and Opinion articles. Topics of interest includes, but not limited to the following areas:
• Articles addressing composition of TME, interplay of cellular and molecular constituents of TME in the maintenance of immunosuppressive TME.
• Articles addressing modulation of metabolism of cancer cells as well as tumor infiltrating immune cells that can prevent or further augment tumor growth by modulating TME towards immune competent or tolerant/immune suppressive state.
• Special interest is extended to articles on novel strategies for reprogramming cancer cell metabolism as well as metabolism of tumor resident immune cells in order to mitigate immune suppressive TME, and facilitate recruitment of functional immune effectors to tumor site, to improve efficacy of T cell and B cell-based cancer immunotherapy strategies.
Dr. David K. Han declares significant financial interest in Hans Health Inc. The other Topic Editors declare no competing interests with regards to the Research Topic theme.
Several cellular components of tumor microenvironment have been identified, and several underlying molecular mechanisms that play essential roles in establishment of TME have been deciphered. Among these, exosomes-mediated cellular signaling has gained special attention. These micro-vesicles can carry molecular signals in the form of small RNAs, for example via microRNAs and long non-coding RNAs (LNC RNAs), to name a few. Furthermore, cellular metabolism also plays a significant role not only in tumor growth, but also in the establishment of TME. Highly proliferative cancer cells require constant supply of energy, which is achieved by channeling glucose through oxidative glycolysis, that converts glucose into lactate, in spite of functioning mitochondria. The metabolic shift not only allows cancer cells to use most of available glucose faster, it also turns TME acidic, facilitating differentiation of macrophages towards M2 route, allowing establishment of immune-suppressive TME.
This Research Topic welcomes Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial and Opinion articles. Topics of interest includes, but not limited to the following areas:
• Articles addressing composition of TME, interplay of cellular and molecular constituents of TME in the maintenance of immunosuppressive TME.
• Articles addressing modulation of metabolism of cancer cells as well as tumor infiltrating immune cells that can prevent or further augment tumor growth by modulating TME towards immune competent or tolerant/immune suppressive state.
• Special interest is extended to articles on novel strategies for reprogramming cancer cell metabolism as well as metabolism of tumor resident immune cells in order to mitigate immune suppressive TME, and facilitate recruitment of functional immune effectors to tumor site, to improve efficacy of T cell and B cell-based cancer immunotherapy strategies.
Dr. David K. Han declares significant financial interest in Hans Health Inc. The other Topic Editors declare no competing interests with regards to the Research Topic theme.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
