Tumor Microenvironment

Publication Title: 
PloS One

There is growing evidence and a consensus in the field that most pediatric brain tumors originate from stem cells, of which radial glial cells constitute a subtype. Here we show that orthotopic transplantation of human radial glial (RG) cells to the subventricular zone of the 3rd ventricle--but not to other transplantation sites--of the brain in immunocompromised NOD-SCID mice, gives rise to tumors that have the hallmarks of CNS primitive neuroectodermal tumors (PNETs). The resulting mouse model strikingly recapitulates the phenotype of PNETs.

Author(s): 
Malchenko, Sergey
Sredni, Simone Treiger
Hashimoto, Hitoshi
Kasai, Atsushi
Nagayasu, Kazuki
Xie, Jianping
Margaryan, Naira V.
Seiriki, Kaoru
Lulla, Rishi R.
Seftor, Richard E. B.
Pachman, Lauren M.
Meltzer, Herbert Y.
Hendrix, Mary J. C.
Soares, Marcelo B.
Publication Title: 
Journal of Stem Cells

Cancer stem cells (CSCs) are stem-like tumor populations that are reported to contribute towards tumor growth, maintenance and recurrence after therapy. Hypoxia increases CSC fraction and promotes acquisition of a stem-cell-like state. Cancer stem cells are critically dependant on the hypoxia-inducible factor-1 (HIF-1) for survival, self-renewal, tumor growth and maintenance of their undifferentiated phenotype.

Author(s): 
Bhargav, Hemant
Metri, Kashinath
Raghuram, Nagarathna
Ramarao, Nagendra Hongasandra
Koka, Prasad S.
Publication Title: 
The American Journal of Pathology

Exosomes released from tumor cells having been shown to induce interleukin-6 release from myeloid-derived suppressor cells in a Toll-like receptor 2/Stat3-dependent manner. In this study, we show that exosomes released from tumor cells re-isolated from syngeneic mice are capable of inducing interleukin-6 in a Toll-like receptor 2-independent manner, whereas the data generated from exosomes of tumor cells having undergone numerous in vitro passages induce interleukin-6 in a Toll-like receptor 2-dependent manner.

Author(s): 
Xiang, Xiaoyu
Liu, Yuelong
Zhuang, Xiaoyin
Zhang, Shuangqin
Michalek, Sue
Taylor, Douglas D.
Grizzle, William
Zhang, Huang-Ge
Publication Title: 
BioFactors (Oxford, England)

For the past 100 years, vitamin A has been implicated as an essential dietary component in host resistance to infectious disease. However, only recently have studies begun to elucidate the cellular and molecular mechanisms of how vitamin A regulates cell-mediated and humoral-mediated immunity. In this review, we present an overview of the recent discoveries of the role that vitamin A and its metabolite, retinoic acid (RA), play in the regulation of immune cells.

Author(s): 
Pino-Lagos, Karina
Guo, Yanxia
Noelle, Randolph J.
Publication Title: 
BMC cancer

BACKGROUND: The glycolytic nature of malignant tumors contributes to high levels of extracellular acidity in the tumor microenvironment. Tumor acidity is a driving force in invasion and metastases. Recently, it has been shown that buffering of extracellular acidity through systemic administration of oral bicarbonate can inhibit the spread of metastases in a mouse model for metastatic breast cancer. While these findings are compelling, recent assessments into the use of oral bicarbonate as a cancer intervention reveal limitations.

Author(s): 
Robey, Ian F.
Martin, Natasha K.
Publication Title: 
Cancer Research

While vitamin A has been implicated in host resistance to infectious disease, little is known about the role of vitamin A and its active metabolite, retinoic acid (RA) in host defenses against cancer. Here, we show that local RA production within the tumor microenvironment (TME) is increased up to 5-fold as compared with naïve surrounding tissue, with a commensurate increase in RA signaling to regionally infiltrating tumor-reactive T cells.

Author(s): 
Guo, Yanxia
Pino-Lagos, Karina
Ahonen, Cory A.
Bennett, Kathy A.
Wang, Jinshan
Napoli, Joseph L.
Blomhoff, Rune
Sockanathan, Shanthini
Chandraratna, Roshantha A.
Dmitrovsky, Ethan
Turk, Mary Jo
Noelle, Randolph J.
Publication Title: 
Journal of Immunology (Baltimore, Md.: 1950)

The macrophage migration inhibitory factor (MIF), an inflammatory cytokine, is overexpressed in many solid tumors and is associated with poor prognosis. We previously identified inhibitors of MIF within a class of natural products with demonstrated anti-cancer activities. We therefore sought to determine how MIF contributes to tumor growth and progression.

Author(s): 
Simpson, Kendra D.
Templeton, Dennis J.
Cross, Janet V.
Publication Title: 
Cancer Research

Chemoresistance due to heterogeneity of the tumor microenvironment (TME) hampers the long-term efficacy of first-line therapies for lung cancer. Current combination therapies for lung cancer provide only modest improvement in survival, implicating necessity for novel approaches that suppress malignant growth and stimulate long-term antitumor immunity. Oxidative stress in the TME promotes immunosuppression by tumor-infiltrating myeloid-derived suppressor cells (MDSC), which inhibit host protective antitumor immunity.

Author(s): 
Sawant, Anandi
Schafer, Cara C.
Jin, Tong Huan
Zmijewski, Jaroslaw
Tse, Hubert M.
Roth, Justin
Sun, Zhihuan
Siegal, Gene P.
Thannickal, Victor J.
Grant, Stefan C.
Ponnazhagan, Selvarangan
Deshane, Jessy S.
Publication Title: 
Journal of Stem Cells

Cancer stem cells (CSCs) are stem-like tumor populations that are reported to contribute towards tumor growth, maintenance and recurrence after therapy. Hypoxia increases CSC fraction and promotes acquisition of a stem-cell-like state. Cancer stem cells are critically dependant on the hypoxia-inducible factor-1 (HIF-1) for survival, self-renewal, tumor growth and maintenance of their undifferentiated phenotype.

Author(s): 
Bhargav, Hemant
Metri, Kashinath
Raghuram, Nagarathna
Ramarao, Nagendra Hongasandra
Koka, Prasad S.
Publication Title: 
Genes & Development

Metabolism generates oxygen radicals, which contribute to oncogenic mutations. Activated oncogenes and loss of tumor suppressors in turn alter metabolism and induce aerobic glycolysis. Aerobic glycolysis or the Warburg effect links the high rate of glucose fermentation to cancer. Together with glutamine, glucose via glycolysis provides the carbon skeletons, NADPH, and ATP to build new cancer cells, which persist in hypoxia that in turn rewires metabolic pathways for cell growth and survival.

Author(s): 
Dang, Chi V.

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