Статті в журналах: "Acidic tumor microenvironment"

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Böhme, Ines, and Anja Katrin Bosserhoff. "Acidic tumor microenvironment in human melanoma." Pigment Cell & Melanoma Research 29, no. 5 (July 5, 2016): 508–23. http://dx.doi.org/10.1111/pcmr.12495.

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Feng, Liangzhu, Ziliang Dong, Danlei Tao, Yicheng Zhang, and Zhuang Liu. "The acidic tumor microenvironment: a target for smart cancer nano-theranostics." National Science Review 5, no. 2 (June 24, 2017): 269–86. http://dx.doi.org/10.1093/nsr/nwx062.

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Abstract The acidic tumor microenvironment (TME), which mainly results from the high glycolytic rate of tumor cells, has been characterized as a hallmark of solid tumors and found to be a pivotal factor participating in tumor progression. Recently, due to the increasing understanding of the acidic TME, it has been shown that the acidic TME could be utilized as a multifaceted target during the design of various pH-responsive nanoscale theranostic platforms for the precise diagnosis and effective treatment of cancers. In this article, we will give a focused overview on the latest progress in utilizing this characteristic acidic TME as the target of nano-theranostics to enable cancer-specific imaging and therapy. The future perspectives in the development of acidic TME-targeting nanomedicine strategies will be discussed afterwards.

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Jin, Haojie, Ning Wang, Cun Wang, and Wenxin Qin. "MicroRNAs in hypoxia and acidic tumor microenvironment." Chinese Science Bulletin 59, no. 19 (April 12, 2014): 2223–31. http://dx.doi.org/10.1007/s11434-014-0273-y.

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Liu, Yu-Cheng, Zhi-Xian Wang, Jing-Yi Pan, Ling-Qi Wang, Xin-Yi Dai, Ke-Fei Wu, Xue-Wei Ye, and Xiao-Ling Xu. "Recent Advances in Imaging Agents Anchored with pH (Low) Insertion Peptides for Cancer Theranostics." Molecules 28, no. 5 (February 26, 2023): 2175. http://dx.doi.org/10.3390/molecules28052175.

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The acidic extracellular microenvironment has become an effective target for diagnosing and treating tumors. A pH (low) insertion peptide (pHLIP) is a kind of peptide that can spontaneously fold into a transmembrane helix in an acidic microenvironment, and then insert into and cross the cell membrane for material transfer. The characteristics of the acidic tumor microenvironment provide a new method for pH-targeted molecular imaging and tumor-targeted therapy. As research has increased, the role of pHLIP as an imaging agent carrier in the field of tumor theranostics has become increasingly prominent. In this paper, we describe the current applications of pHLIP-anchored imaging agents for tumor diagnosis and treatment in terms of different molecular imaging methods, including magnetic resonance T1 imaging, magnetic resonance T2 imaging, SPECT/PET, fluorescence imaging, and photoacoustic imaging. Additionally, we discuss relevant challenges and future development prospects.

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Boedtkjer, Ebbe, and Stine F. Pedersen. "The Acidic Tumor Microenvironment as a Driver of Cancer." Annual Review of Physiology 82, no. 1 (February 10, 2020): 103–26. http://dx.doi.org/10.1146/annurev-physiol-021119-034627.

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Acidic metabolic waste products accumulate in the tumor microenvironment because of high metabolic activity and insufficient perfusion. In tumors, the acidity of the interstitial space and the relatively well-maintained intracellular pH influence cancer and stromal cell function, their mutual interplay, and their interactions with the extracellular matrix. Tumor pH is spatially and temporally heterogeneous, and the fitness advantage of cancer cells adapted to extracellular acidity is likely particularly evident when they encounter less acidic tumor regions, for instance, during invasion. Through complex effects on genetic stability, epigenetics, cellular metabolism, proliferation, and survival, the compartmentalized pH microenvironment favors cancer development. Cellular selection exacerbates the malignant phenotype, which is further enhanced by acid-induced cell motility, extracellular matrix degradation, attenuated immune responses, and modified cellular and intercellular signaling. In this review, we discuss how the acidity of the tumor microenvironment influences each stage in cancer development, from dysplasia to full-blown metastatic disease.

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Sharma, Vishal, та Jagdeep Kaur. "Acidic environment could modulate the interferon-γ expression: Implication on modulation of cancer and immune cells’ interactions". Asian Biomedicine 17, № 2 (1 квітня 2023): 72–83. http://dx.doi.org/10.2478/abm-2023-0047.

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Abstract Background In rapidly growing solid tumors, insufficient vascularization and poor oxygen supply result in an acidic tumor microenvironment, which can alter immune response. Objective To investigate the role of the acidic microenvironment in immune response modulation along with cancer and immune cells’ interactions. Method To mimic the tumor microenvironment conditions, T cells (Jurkat), macrophages (THP-1), and HeLa (cervical) cells were cultured under acidic conditions (pH 6.9, pH 6.5) and physiological pH (7.4). The HeLa cell culture medium was exploited as a tumor cell conditioned medium. Real-time PCR was carried out to quantify the mRNA levels, while flow cytometry and western blot hybridization was carried out to ascertain the levels of different proteins. Results The acidic microenvironment around the T cells (Jurkat) and macrophage cells (THP-1) could lead to the downregulation of the interferon gamma (IFN-γ). An increase in IFN-γ expression was observed when Jurkat and macrophage cells were cultured in HeLa cells conditioned medium (HCM) at low pH (pH 6.9, pH 6.5). The HeLa cells under acidic environment (pH 6.9, pH 6.5) upregulated interleukin 18 levels and secreted it as exosome anchored. Additionally, enhanced nuclear localization of NF-κB was observed in Jurkat and THP-1 cells cultured in HCM (pH 6.9, pH 6.5). Jurkat and THP-1 cultured in HCM revealed enhanced cytotoxicity against the HeLa cells upon reverting the pH of the medium from acidic to physiological pH (pH 7.4). Conclusion Collectively, these results suggest that the acidic microenvironment acted as a key barrier to cancer and immune cells’ interactions.

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Xu, Jingyong, Yao Li, Zhe Li, Weiwei Shao, Jinghai Song, and Junmin Wei. "Acidic Tumor Microenvironment Promotes Pancreatic Cancer through miR-451a/MEF2D Axis." Journal of Oncology 2022 (January 12, 2022): 1–12. http://dx.doi.org/10.1155/2022/3966386.

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Pancreatic cancer (PC), as a highly malignant and aggressive solid tumor, is common in the digestive system. The acidic microenvironment is one of the critical markers of cancer. Nonetheless, there are few studies on how the acidic microenvironment affects the development of PC. This study focused on investigating the specific molecular mechanisms of the acidic microenvironment in PC. In our study, qRT-PCR was conducted for examining microRNA (miR)-451a and myocyte enhancer factor 2D (MEF2D) expressions in PANC-1 cells. Then, detailed functional effects of an acidic environment on miR-451a and MEF2D in PANC-1 cells were detected by CCK-8, colony formation, flow cytometry, wound healing, transwell, mitochondrial functionality measurement, JC-1 staining, DCFH-DA staining, and sphere formation assays. The relationship between miR-451a and MEF2D was confirmed by luciferase reporter analysis. Under acidic conditions, the increase of proliferation, migration, and invasion of PANC-1 cells was observed. Moreover, the mitochondrial oxidative respiration-related gene miR-451a was reduced in acidic conditions. In addition, we found that, in PANC-1 cells under an acidic environment, miR-451a overexpression enhanced oxygen consumption, mitochondrial membrane potential (MMP) loss, and ROS generation and inhibited proliferation, migration, invasion, and stemness via sponging MEF2D. In a word, our results revealed that the acidic microenvironment regulated PC progression by affecting the miR-451a/MEF2D axis, indicating a novel avenue for the future treatment of PC.

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Noack, Anne-Kathrin, Henrike Lucas, Petr Chytil, Tomáš Etrych, Karsten Mäder, and Thomas Mueller. "Intratumoral Distribution and pH-Dependent Drug Release of High Molecular Weight HPMA Copolymer Drug Conjugates Strongly Depend on Specific Tumor Substructure and Microenvironment." International Journal of Molecular Sciences 21, no. 17 (August 21, 2020): 6029. http://dx.doi.org/10.3390/ijms21176029.

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Stimulus-sensitive polymer drug conjugates based on high molecular weight N-(2-hydroxypropyl) methacrylamide (HPMA) copolymers carrying doxorubicin via a pH-dependent cleavable bond (pHPMA-Dox) were previously shown to be able to overcome multi-drug resistance. Nevertheless, a tumor type dependent differential response was observed. Although an improved and more selective tumor accumulation of pHPMA-Dox is generally achieved due to the enhanced permeability and retention (EPR) effect, little is known about the fate of these conjugates upon entering the tumor tissue, which could explain the different responses. In this study, we compared in vitro and in vivo accumulation and Dox-activation of pHPMA-Dox in three cancer cell line models (1411HP, A2780cis, HT29) and derived xenograft tumors using a near-infrared fluorescence-labeled pHPMA-Dox conjugate. Firstly, cytotoxicity assays using different pH conditions proved a stepwise, pH-dependent increase in cytotoxic activity and revealed comparable sensitivity among the cell lines. Using multispectral fluorescence microscopy, we were able to track the distribution of drug and polymeric carrier simultaneously on cellular and histological levels. Microscopic analyses of cell monolayers confirmed the assumed mechanism of cell internalization of the whole conjugate followed by intracellular cleavage and nuclear accumulation of Dox in all three cell lines. In contrast, intratumoral distribution and drug release in xenograft tumors were completely different and were associated with different tissue substructures and microenvironments analyzed by Azan- and Hypoxisense®-staining. In 1411HP tumors, large vessels and less hypoxic/acidic microenvironments were associated with a pattern resulting from consistent tissue distribution and cellular uptake as whole conjugate followed by intracellular drug release. In A2780cis tumors, an inconsistent pattern of distribution partly resulting from premature drug release was associated with a more hypoxic/acidic microenvironment, compacted tumor tissue with compressed vessels and specific pre-damaged tissue structures. A completely different distribution pattern was observed in HT29 tumors, resulting from high accumulation of polymer in abundant fibrotic structures, with small embedded vessels featuring this tumor type together with pronounced premature drug release due to the strongly hypoxic/acidic microenvironment. In conclusion, the pattern of intratumoral distribution and drug release strongly depends on the tumor substructure and microenvironment and may result in different degrees of therapeutic efficacy. This reflects the pronounced heterogeneity observed in the clinical application of nanomedicines and can be exploited for the future design of such conjugates.

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Mbugua, Simon Ngigi. "Targeting Tumor Microenvironment by Metal Peroxide Nanoparticles in Cancer Therapy." Bioinorganic Chemistry and Applications 2022 (December 16, 2022): 1–20. http://dx.doi.org/10.1155/2022/5041399.

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Solid tumors have a unique tumor microenvironment (TME), which includes hypoxia, low acidity, and high hydrogen peroxide and glutathione (GSH) levels, among others. These unique factors, which offer favourable microenvironments and nourishment for tumor development and spread, also serve as a gateway for specific and successful cancer therapies. A good example is metal peroxide structures which have been synthesized and utilized to enhance oxygen supply and they have shown great promise in the alleviation of hypoxia. In a hypoxic environment, certain oxygen-dependent treatments such as photodynamic therapy and radiotherapy fail to respond and therefore modulating the hypoxic tumor microenvironment has been found to enhance the antitumor impact of certain drugs. Under acidic environments, the hydrogen peroxide produced by the reaction of metal peroxides with water not only induces oxidative stress but also produces additional oxygen. This is achieved since hydrogen peroxide acts as a reactive substrate for molecules such as catalyse enzymes, alleviating tumor hypoxia observed in the tumor microenvironment. Metal ions released in the process can also offer distinct bioactivity in their own right. Metal peroxides used in anticancer therapy are a rapidly evolving field, and there is good evidence that they are a good option for regulating the tumor microenvironment in cancer therapy. In this regard, the synthesis and mechanisms behind the successful application of metal peroxides to specifically target the tumor microenvironment are highlighted in this review. Various characteristics of TME such as angiogenesis, inflammation, hypoxia, acidity levels, and metal ion homeostasis are addressed in this regard, together with certain forms of synergistic combination treatments.

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Vernucci, Enza, Jaime Abrego, Venugopal Gunda, Surendra K. Shukla, Aneesha Dasgupta, Vikrant Rai, Nina Chaika, et al. "Metabolic Alterations in Pancreatic Cancer Progression." Cancers 12, no. 1 (December 18, 2019): 2. http://dx.doi.org/10.3390/cancers12010002.

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Pancreatic cancer is the third leading cause of cancer-related deaths in the USA. Pancreatic tumors are characterized by enhanced glycolytic metabolism promoted by a hypoxic tumor microenvironment and a resultant acidic milieu. The metabolic reprogramming allows cancer cells to survive hostile microenvironments. Through the analysis of the principal metabolic pathways, we identified the specific metabolites that are altered during pancreatic cancer progression in the spontaneous progression (KPC) mouse model. Genetically engineered mice exhibited metabolic alterations during PanINs formation, even before the tumor development. To account for other cells in the tumor microenvironment and to focus on metabolic adaptations concerning tumorigenic cells only, we compared the metabolic profile of KPC and orthotopic tumors with those obtained from KPC-tumor derived cell lines. We observed significant upregulation of glycolysis and the pentose phosphate pathway metabolites even at the early stages of pathogenesis. Other biosynthetic pathways also demonstrated a few common perturbations. While some of the metabolic changes in tumor cells are not detectable in orthotopic and spontaneous tumors, a significant number of tumor cell-intrinsic metabolic alterations are readily detectable in the animal models. Overall, we identified that metabolic alterations in precancerous lesions are maintained during cancer development and are largely mirrored by cancer cells in culture conditions.

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Dharmaratne, Nayanthara U., Alanna R. Kaplan, and Peter M. Glazer. "Targeting the Hypoxic and Acidic Tumor Microenvironment with pH-Sensitive Peptides." Cells 10, no. 3 (March 4, 2021): 541. http://dx.doi.org/10.3390/cells10030541.

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The delivery of cancer therapeutics can be limited by pharmacological issues such as poor bioavailability and high toxicity to healthy tissue. pH-low insertion peptides (pHLIPs) represent a promising tool to overcome these limitations. pHLIPs allow for the selective delivery of agents to tumors on the basis of pH, taking advantage of the acidity of the hypoxic tumor microenvironment. This review article highlights the various applications in which pHLIPs have been utilized for targeting and treating diseases in hypoxic environments, including delivery of small molecule inhibitors, toxins, nucleic acid analogs, fluorescent dyes, and nanoparticles.

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Sheng, Liangju, Xuanlei Zhu, Miao Sun, Zhe Lan, Yong Yang, Yuanrong Xin, and Yuefeng Li. "Tumor Microenvironment-Responsive Magnetic Nanofluid for Enhanced Tumor MRI and Tumor multi-treatments." Pharmaceuticals 16, no. 2 (January 23, 2023): 166. http://dx.doi.org/10.3390/ph16020166.

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We prepared a tumor microenvironment-responsive magnetic nanofluid (MNF) for improving tumor targeting, imaging and treatment simultaneously. For this purpose, we synthesized sulfonamide-based amphiphilic copolymers with a suitable pKa at 7.0; then, we utilized them to prepare the tumor microenvironment-responsive MNF by self-assembly of the sulfonamide-based amphiphilic copolymers and hydrophobic monodispersed Fe3O4 nanoparticles at approximately 8 nm. After a series of characterizations, the MNF showed excellent application potential due to the fact of its high stability under physiological conditions and its hypersensitivity toward tumor stroma by forming aggregations within neutral or weak acidic environments. Due to the fact of its tumor microenvironment-responsiveness, the MNF showed great potential for accumulation in tumors, which could enhance MNF-mediated magnetic resonance imaging (MRI), magnetic hyperthermia (MH) and Fenton reaction (FR) in tumor. Moreover, in vitro cell experiment did not only show high biocompatibility of tumor microenvironment-responsive MNF in physiological environment, but also exhibit high efficacy on inhibiting cell proliferation by MH-dependent chemodynamic therapy (CDT), because CDT was triggered and promoted efficiently by MH with increasing strength of alternating magnetic field. Although the current research is limited to in vitro study, these positive results still suggest the great potential of the MNF on effective targeting, diagnosis, and therapy of tumor.

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Zhang, Lingling, Yang Song, Xiaoyan Dai, Wenwen Xu, Mengxia Li та Yuxi Zhu. "Inhibition of IDH3α Enhanced the Efficacy of Chemoimmunotherapy by Regulating Acidic Tumor Microenvironments". Cancers 15, № 6 (16 березня 2023): 1802. http://dx.doi.org/10.3390/cancers15061802.

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In recent years, chemoimmunotherapy has become effective in some advanced cancers, but its effect is still limited. Transcriptional upregulation of isocitrate dehydrogenase 3α (IDH3α) can promote tumor initiation and progression. However, it is not clear whether the aberrant expression of IDH3α is related to the efficacy of chemoimmunotherapy in cancers. Here, we found that IDH3α was elevated in uterine cervical cancer (UCC) and lung adenocarcinoma (LUAD) samples by using public databases. High expression of IDH3α could promote the epithelial–mesenchymal transition (EMT), alter the intracellular redox status, promote glycolysis, and induce an acidic microenvironments in cancer cells. Furthermore, we found that inhibition of IDH3α combined with chemoimmunotherapy (cisplatin and programmed cell death ligand 1 (PD-L1) antibodies) activated the cGAS–STING pathway, promoted CD8+ T cell infiltration, and decreased tumor growth in mouse models of cervical cancer. In conclusion, our data indicate that silencing IDH3α sensitizes tumors to chemoimmunotherapy by modulating the acidic microenvironment and activating the cGAS–STING pathway.

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He, Yongju, Xingyu Fan, Xiaozan Wu, Taishun Hu, Fangfang Zhou, Songwen Tan, Botao Chen, Anqiang Pan, Shuquan Liang, and Hui Xu. "pH-Responsive size-shrinkable mesoporous silica-based nanocarriers for improving tumor penetration and therapeutic efficacy." Nanoscale 14, no. 4 (2022): 1271–84. http://dx.doi.org/10.1039/d1nr07513f.

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To overcome the nanomedicine penetration barrier across the dense tumor matrix, acidic tumor microenvironment-responsive size-shrinkable mesoporous silica-based nanomedicine is developed for enhancing drug tumor penetration and therapeutic efficacy.

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Wang, Joy X., Stephen Y. C. Choi, Xiaojia Niu, Ning Kang, Hui Xue, James Killam, and Yuzhuo Wang. "Lactic Acid and an Acidic Tumor Microenvironment suppress Anticancer Immunity." International Journal of Molecular Sciences 21, no. 21 (November 7, 2020): 8363. http://dx.doi.org/10.3390/ijms21218363.

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Immune evasion and altered metabolism, where glucose utilization is diverted to increased lactic acid production, are two fundamental hallmarks of cancer. Although lactic acid has long been considered a waste product of this alteration, it is now well accepted that increased lactic acid production and the resultant acidification of the tumor microenvironment (TME) promotes multiple critical oncogenic processes including angiogenesis, tissue invasion/metastasis, and drug resistance. We and others have hypothesized that excess lactic acid in the TME is responsible for suppressing anticancer immunity. Recent studies support this hypothesis and provide mechanistic evidence explaining how lactic acid and the acidic TME impede immune cell functions. In this review, we consider lactic acid’s role as a critical immunoregulatory molecule involved in suppressing immune effector cell proliferation and inducing immune cell de-differentiation. This results in the inhibition of antitumor immune responses and the activation of potent, negative regulators of innate and adaptive immune cells. We also consider the role of an acidic TME in suppressing anticancer immunity. Finally, we provide insights to help translate this new knowledge into impactful anticancer immune therapies.

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Wojtkowiak, Jonathan W., Daniel Verduzco, Karla J. Schramm, and Robert J. Gillies. "Drug Resistance and Cellular Adaptation to Tumor Acidic pH Microenvironment." Molecular Pharmaceutics 8, no. 6 (October 26, 2011): 2032–38. http://dx.doi.org/10.1021/mp200292c.

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Sun, Xiao, Guilong Zhang, and Zhengyan Wu. "Nanostructures for pH-sensitive Drug Delivery and Magnetic Resonance Contrast Enhancement Systems." Current Medicinal Chemistry 25, no. 25 (August 30, 2018): 3036–57. http://dx.doi.org/10.2174/0929867324666170406110642.

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According to the differences of microenvironments between tumors and healthy tissues, if the anticancer drugs or magnetic resonance contrast agents (MRCAs) can be controlled to precisely match physiological needs at targeted tumor sites, it is expected to acquire better therapeutic efficacy and more accurate diagnosis. Over the decade, stimuli-responsive nanomaterials have been a research hotspot for cancer treatment and diagnosis because they show many excellent functions, such as in vivo imaging, combined targeting drug delivery and systemic controlled release, extended circulation time, etc. Among the various stimuli nanosystems, pH-stimuli mode is regarded as the most general strategy because of solid tumors acidosis. When exposed to weakly acidic tumor microenvironment, pH-responsive nanoplatforms can generate physicochemical changes for their structure and surface characteristics, causing drug release or contrast enhancement. In this review, we focused on the designs of various pH-responsive nanoplatforms and discussed the mechanisms of controlled drug release or switch on-off in MRCAs. This review also discussed the efficacy of cellular internalization for these nanoplatforms via endocytosis of acidic tumor cell. Meanwhile, nanoplatforms response to acidic intracellular pH (such as endosome, lysosome) are discussed, along with approaches for improving drug release performance and magnetic resonance contrast enhancement. A greater understanding of these pH-responsive nanoplatforms will help design more efficient nanomedicine to address the challenges encountered in conventional diagnosis and chemotherapy.

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Reuss, Anna Maria, Dominik Groos, Michael Buchfelder, and Nicolai Savaskan. "The Acidic Brain—Glycolytic Switch in the Microenvironment of Malignant Glioma." International Journal of Molecular Sciences 22, no. 11 (May 24, 2021): 5518. http://dx.doi.org/10.3390/ijms22115518.

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Malignant glioma represents a fatal disease with a poor prognosis and development of resistance mechanisms against conventional therapeutic approaches. The distinct tumor zones of this heterogeneous neoplasm develop their own microenvironment, in which subpopulations of cancer cells communicate. Adaptation to hypoxia in the center of the expanding tumor mass leads to the glycolytic and angiogenic switch, accompanied by upregulation of different glycolytic enzymes, transporters, and other metabolites. These processes render the tumor microenvironment more acidic, remodel the extracellular matrix, and create energy gradients for the metabolic communication between different cancer cells in distinct tumor zones. Escape mechanisms from hypoxia-induced cell death and energy deprivation are the result. The functional consequences are more aggressive and malignant behavior with enhanced proliferation and survival, migration and invasiveness, and the induction of angiogenesis. In this review, we go from the biochemical principles of aerobic and anaerobic glycolysis over the glycolytic switch, regulated by the key transcription factor hypoxia-inducible factor (HIF)-1α, to other important metabolic players like the monocarboxylate transporters (MCTs)1 and 4. We discuss the metabolic symbiosis model via lactate shuttling in the acidic tumor microenvironment and highlight the functional consequences of the glycolytic switch on glioma malignancy. Furthermore, we illustrate regulation by micro ribonucleic acids (miRNAs) and the connection between isocitrate dehydrogenase (IDH) mutation status and glycolytic metabolism. Finally, we give an outlook about the diagnostic and therapeutic implications of the glycolytic switch and the relation to tumor immunity in malignant glioma.

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Bhattacharya, Saswati, Jasmina Khanam, Pradipta Sarkar, and Tapan Kumar Pal. "A chemotherapeutic approach targeting the acidic tumor microenvironment: combination of a proton pump inhibitor and paclitaxel for statistically optimized nanotherapeutics." RSC Advances 9, no. 1 (2019): 240–54. http://dx.doi.org/10.1039/c8ra08924h.

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Sun, Yu, Zekun Wang, Pu Zhang, Jingyuan Wang, Ying Chen, Chenyang Yin, Weiyun Wang, Cundong Fan, and Dongdong Sun. "Mesoporous silica integrated with Fe3O4 and palmitoyl ascorbate as a new nano-Fenton reactor for amplified tumor oxidation therapy." Biomaterials Science 8, no. 24 (2020): 7154–65. http://dx.doi.org/10.1039/d0bm01738h.

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Wang, Heng, Beilei Wang, Jie Jiang, Yi Wu, Anning Song, Xiaoyu Wang, Chenlu Yao, et al. "SnSe Nanosheets Mimic Lactate Dehydrogenase to Reverse Tumor Acid Microenvironment Metabolism for Enhancement of Tumor Therapy." Molecules 27, no. 23 (December 5, 2022): 8552. http://dx.doi.org/10.3390/molecules27238552.

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The acidic tumor microenvironment (TME) is unfriendly to the activity and function of immune cells in the TME. Here, we report inorganic nanozymes (i.e., SnSe NSs) that mimic the catalytic activity of lactate dehydrogenase to degrade lactate to pyruvate, contributing to the metabolic treatment of tumors. As found in this study, SnSe NSs successfully decreased lactate levels in cells and tumors, as well as reduced tumor acidity. This is associated with activation of the immune response of T cells, thus alleviating the immunosuppressive environment of the TME. More importantly, the nanozyme successfully inhibited tumor growth in mutilate mouse tumor models. Thus, SnSe NSs show a promising result in lactate depletion and tumor suppression, which exemplifies its potential strategy in targeting lactate for metabolic therapy.

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Lei, Yanli, Xiaoxiao He, Jinlu Tang, Hui Shi, Dinggeng He, Lv’an Yan, Jianbo Liu, Yu Zeng, and Kemin Wang. "Ultra-pH-responsive split i-motif based aptamer anchoring strategy for specific activatable imaging of acidic tumor microenvironment." Chemical Communications 54, no. 73 (2018): 10288–91. http://dx.doi.org/10.1039/c8cc04420a.

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Andreucci, Elena, Silvia Peppicelli, Jessica Ruzzolini, Francesca Bianchini, Alessio Biagioni, Laura Papucci, Lucia Magnelli, Benedetta Mazzanti, Barbara Stecca, and Lido Calorini. "The acidic tumor microenvironment drives a stem-like phenotype in melanoma cells." Journal of Molecular Medicine 98, no. 10 (August 15, 2020): 1431–46. http://dx.doi.org/10.1007/s00109-020-01959-y.

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Abstract Acidosis characterizes the microenvironment of most solid tumors and is considered a new hallmark of cancer. It is mainly caused by both “aerobic” and “anaerobic” glycolysis of differently adapted cancer cells, with the final product lactic acid being responsible of the extracellular acidification. Many evidences underline the role of extracellular acidosis in tumor progression. Among the different findings, we demonstrated that acidosis-exposed cancer cells are characterized by an epithelial-to-mesenchymal transition phenotype with high invasive ability, high resistance to apoptosis, anchorage-independent growth, and drug therapy. Acidic melanoma cells over-express SOX2, which is crucial for the maintenance of their oxidative metabolism, and carbonic anhydrase IX, that correlates with poor prognosis of cancer patients. Considering these evidences, we realized that the profile outlined for acid cancer cells inevitably remind us the stemness profile. Therefore, we wondered whether extracellular acidosis might induce in cancer cells the acquisition of stem-like properties and contribute to the expansion of the cancer stem cell sub-population. We found that a chronic adaptation to acidosis stimulates in cancer cells the expression of stem-related markers, also providing a high in vitro/in vivo clonogenic and trans-differentiating ability. Moreover, we observed that the acidosis-induced stem-like phenotype of melanoma cells was reversible and related to the EMT induction. These findings help to characterize a further aspect of stem cell niche, contributing to the sustainment and expansion of cancer stem cell subpopulation. Thus, the usage of agents controlling tumor extracellular acidosis might acquire great importance in the clinic for the treatment of aggressive solid tumor. Key messages • Extracellular acidosis up-regulates EMT and stem-related markers in melanoma cells • Acidic medium up-regulates in vitro self-renewal capacity of melanoma cells • Chronic acidosis adaptation induces trans-differentiation ability in melanoma cells • Melanoma cells adapted to acidosis show higher tumor-initiating potential than control cells • Extracellular acidosis promotes a stem-like phenotype in prostate and colorectal carcinoma cells

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Walter, Sebastian Gottfried, Peter Knöll, Peer Eysel, Alexander Quaas, Christopher Gaisendrees, Robert Nißler, and Lena Hieggelke. "Molecular In-Depth Characterization of Chondrosarcoma for Current and Future Targeted Therapies." Cancers 15, no. 9 (April 29, 2023): 2556. http://dx.doi.org/10.3390/cancers15092556.

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Chondrosarcoma (CHS) are heterogenous, but as a whole, represent the second most common primary malignant bone tumor entity. Although knowledge on tumor biology has grown exponentially during the past few decades, surgical resection remains the gold standard for the treatment of these tumors, while radiation and differentiated chemotherapy do not result in sufficient cancer control. An in-depth molecular characterization of CHS reveals significant differences compared to tumors of epithelial origin. Genetically, CHS are heterogenous, but there is no characteristic mutation defining CHS, and yet, IDH1 and IDH2 mutations are frequent. Hypovascularization, extracellular matrix composition of collagen, proteoglycans, and hyaluronan create a mechanical barrier for tumor suppressive immune cells. Comparatively low proliferation rates, MDR-1 expression and an acidic tumor microenvironment further limit therapeutic options in CHS. Future advances in CHS therapy depend on the further characterization of CHS, especially the tumor immune microenvironment, for improved and better targeted therapies.

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Liu, Xiaodong, Qian Chen, Guangbao Yang, Lifen Zhang, Zhuang Liu, Zhenping Cheng, and Xiulin Zhu. "Magnetic nanomaterials with near-infrared pH-activatable fluorescence via iron-catalyzed AGET ATRP for tumor acidic microenvironment imaging." Journal of Materials Chemistry B 3, no. 14 (2015): 2786–800. http://dx.doi.org/10.1039/c5tb00070j.

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This work provides a fluorescent/magnetic iron oxide nanomaterials prototype to visualize the solid tumor in vivo by sensing the tumor acidic microenvironment, and a satisfactory tumor-to-normal tissue signal ratio (T/N ratio) and a prolonged time-window for 4T1 tumor visualization were observed in vivo.

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Peppicelli, Silvia, Elena Andreucci, Jessica Ruzzolini, Anna Laurenzana, Francesca Margheri, Gabriella Fibbi, Mario Del Rosso, Francesca Bianchini, and Lido Calorini. "The acidic microenvironment as a possible niche of dormant tumor cells." Cellular and Molecular Life Sciences 74, no. 15 (March 22, 2017): 2761–71. http://dx.doi.org/10.1007/s00018-017-2496-y.

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Shen, Ming, Yongzhuo Huang, Limei Han, Jing Qin, Xiaoling Fang, Jianxin Wang, and Victor C. Yang. "Multifunctional drug delivery system for targeting tumor and its acidic microenvironment." Journal of Controlled Release 161, no. 3 (August 2012): 884–92. http://dx.doi.org/10.1016/j.jconrel.2012.05.013.

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Choi, Joung-Woo, Soo-Jung Jung, Dayananda Kasala, June Kyu Hwang, Jun Hu, You Han Bae, and Chae-Ok Yun. "pH-sensitive oncolytic adenovirus hybrid targeting acidic tumor microenvironment and angiogenesis." Journal of Controlled Release 205 (May 2015): 134–43. http://dx.doi.org/10.1016/j.jconrel.2015.01.005.

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Xie, Yunong, Stephanie Ma, and Man Tong. "Metabolic Plasticity of Cancer Stem Cells in Response to Microenvironmental Cues." Cancers 14, no. 21 (October 29, 2022): 5345. http://dx.doi.org/10.3390/cancers14215345.

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An increasing body of evidence suggests that cancer stem cells (CSCs) utilize reprogrammed metabolic strategies to adapt to a hostile tumor microenvironment (TME) for survival and stemness maintenance. Such a metabolic alteration in CSCs is facilitated by microenvironmental cues including metabolites such as glucose, amino acids and lipids, and environmental properties such as hypoxic and acidic TME. Similarly, metabolites uptake from the diet exerts critical imprints to the metabolism profile of CSCs and directly influence the maintenance of the CSC population. Moreover, CSCs interact with tumor-infiltrating cells inside the CSC niche to promote cancer stemness, ultimately contributing to tumor development and progression. Understanding the underlying mechanisms of how CSCs employ metabolic plasticity in response to different microenvironmental cues represents a therapeutic opportunity for better cancer treatment.

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Clark, Amelia M., and Brian J. Altman. "Circadian control of macrophages in the tumor microenvironment." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 165.06. http://dx.doi.org/10.4049/jimmunol.208.supp.165.06.

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Abstract Introduction All leukocytes tested to date have functional circadian clocks, and nearly every arm of the immune response is subject to circadian regulation. Circadian clocks instruct the time-of-day-dependent, rhythmic expression of genes in a tissue- and cell-specific manner. In macrophages (mΦs), the circadian clock regulates several factors that are critical to executing effective immune responses. Tumor-associated mΦs are major contributors to immune suppression in the tumor microenvironment (TME). Evidence suggests that metabolically stressful factors in the TME such as acidic pH and nutrient limitation promote mΦ-mediated immune suppression, and recent data point to dysregulation of the circadian clock downstream of metabolic stress. Methods We study the effect of TME-associated metabolic stress on the circadian clock of mΦs in vitro by culturing bone marrow-derived mΦs in conditions mimicking acidic pH and nutrient limitations that have been observed in the TME. To study the impact of mΦ-intrinsic circadian rhythms on tumorigenesis in vivo, we use mice genetically engineered to have a myeloid cell-specific disruption of the circadian clock via deletion of the key clock protein BMAL1. Results Oscillation of core clock proteins is altered in mΦs subjected to TME-associated metabolic stress. Additionally, we observe increased tumor growth in mice co-injected with mΦs whose circadian clocks were disrupted compared to mice co-injected with mΦs whose circadian clocks were functional. Conclusion Our data suggests that stressful conditions associated with the TME can alter the mΦ circadian clock, and that a functional circadian clock in mΦs can suppress tumor growth in a syngeneic murine tumor model of pancreatic cancer. This research has been supported by the following fellowships and grants: 2021-Current: Wilmot Predoctoral Cancer Research Fellowship, Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, NY 2020-2021: NIH T32 Training Grant in Cellular, Biochemical & Molecular Sciences, University of Rochester Medical Center, Rochester, NY

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Zhan, Yuan, Mara Gonçalves, Panpan Yi, Débora Capelo, Yuhong Zhang, João Rodrigues, Changsheng Liu, Helena Tomás, Yulin Li, and Peixin He. "Thermo/redox/pH-triple sensitive poly(N-isopropylacrylamide-co-acrylic acid) nanogels for anticancer drug delivery." Journal of Materials Chemistry B 3, no. 20 (2015): 4221–30. http://dx.doi.org/10.1039/c5tb00468c.

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Doxorubicin is effectively loaded into disulfide-crosslinked poly(N-isopropylacrylamide-co-acrylic acid) nanogels, which can be triggerably released in a heating or reducing acidic tumor microenvironment.

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Voss, Ninna C. S., Thomas Dreyer, Mikkel B. Henningsen, Pernille Vahl, Bent Honoré, and Ebbe Boedtkjer. "Targeting the Acidic Tumor Microenvironment: Unexpected Pro-Neoplastic Effects of Oral NaHCO3 Therapy in Murine Breast Tissue." Cancers 12, no. 4 (April 6, 2020): 891. http://dx.doi.org/10.3390/cancers12040891.

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The acidic tumor microenvironment modifies malignant cell behavior. Here, we study consequences of the microenvironment in breast carcinomas. Beginning at carcinogen-based breast cancer induction, we supply either regular or NaHCO3-containing drinking water to female C57BL/6j mice. We evaluate urine and blood acid-base status, tumor metabolism (microdialysis sampling), and tumor pH (pH-sensitive microelectrodes) in vivo. Based on freshly isolated epithelial organoids from breast carcinomas and normal breast tissue, we assess protein expression (immunoblotting, mass spectrometry), intracellular pH (fluorescence microscopy), and cell proliferation (bromodeoxyuridine incorporation). Oral NaHCO3 therapy increases breast tumor pH in vivo from 6.68 ± 0.04 to 7.04 ± 0.09 and intracellular pH in breast epithelial organoids by ~0.15. Breast tumors develop with median latency of 85.5 ± 8.2 days in NaHCO3-treated mice vs. 82 ± 7.5 days in control mice. Oral NaHCO3 therapy does not affect tumor growth, histopathology or glycolytic metabolism. The capacity for cellular net acid extrusion is increased in NaHCO3-treated mice and correlates negatively with breast tumor latency. Oral NaHCO3 therapy elevates proliferative activity in organoids from breast carcinomas. Changes in protein expression patterns—observed by high-throughput proteomics analyses—between cancer and normal breast tissue and in response to oral NaHCO3 therapy reveal complex influences on metabolism, cytoskeleton, cell-cell and cell-matrix interaction, and cell signaling pathways. We conclude that oral NaHCO3 therapy neutralizes the microenvironment of breast carcinomas, elevates the cellular net acid extrusion capacity, and accelerates proliferation without net effect on breast cancer development or tumor growth. We demonstrate unexpected pro-neoplastic consequences of oral NaHCO3 therapy that in breast tissue cancel out previously reported anti-neoplastic effects.

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Palma, Susana I. C. J., Alexandra R. Fernandes, and Ana C. A. Roque. "An affinity triggered MRI nanoprobe for pH-dependent cell labeling." RSC Advances 6, no. 114 (2016): 113503–12. http://dx.doi.org/10.1039/c6ra17217b.

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The pH-sensitive affinity pair composed by neutravidin and iminobiotin was used to develop a multilayered Magnetic Resonance Imaging (MRI) nanoprobe responsive to the acidic pH of tumor microenvironment.

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Lv, Shuxin, Wei Long, Junchi Chen, Qinjuan Ren, Junying Wang, Xiaoyu Mu, Haile Liu, Xiao-Dong Zhang, and Ruiping Zhang. "Dual pH-triggered catalytic selective Mn clusters for cancer radiosensitization and radioprotection." Nanoscale 12, no. 2 (2020): 548–57. http://dx.doi.org/10.1039/c9nr08192e.

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Mn clusters with pH-triggered catalytic selective capacity could optimize the effects of radiotherapy in the acidic tumor microenvironment, while protecting normal tissues from radiation in neutral circumstances simultaneously.

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Si, Zhan, Cuiyun Huang, Xihui Gao, and Cong Li. "pH-responsive near-infrared nanoprobe imaging metastases by sensing acidic microenvironment." RSC Adv. 4, no. 98 (2014): 55548–55. http://dx.doi.org/10.1039/c4ra07984a.

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A pH responsive near-infrared fluorescence nanoprobe was developed and visualized pulmonary metastases in a mouse model with a volume as small as 0.5 mm³ by sensing the acidic tumor microenvironment.

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Wang, Sheng, Jiaji Mao, Hong Liu, Shihui Huang, Jiali Cai, Wentao Gui, Jun Wu, Junyao Xu, Jun Shen, and Zhiyong Wang. "pH-Sensitive nanotheranostics for dual-modality imaging guided nanoenzyme catalysis therapy and phototherapy." Journal of Materials Chemistry B 8, no. 22 (2020): 4859–69. http://dx.doi.org/10.1039/c9tb02731a.

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A theranostic nanosystem with a pH-sensitive structure showed charge conversion properties in the tumor acidic microenvironment. It could perform dual-modality imaging diagnosis and carry out catalysis therapy and phototherapy.

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Yoneda, Toshiyuki N/A, Masahiro N/A Hiasa, Yuki N/A Nagata, Matthew S. Ripsch, Fletcher A. White, and G. David Roodman. "Acidic Extracellular Microenvironment in Myeloma-Colonized Bone Contributes to Bone Pain." Blood 124, no. 21 (December 6, 2014): 3397. http://dx.doi.org/10.1182/blood.v124.21.3397.3397.

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Abstract Multiple myeloma (MM) bone disease results in devastating bone pain and fractures, which are the major cause of morbidity, and contribute to increased mortality and diminish the quality of life in MM patients. Current treatments for MM bone pain do not completely control the pain and have serious side effects. Thus, new therapies are needed to control myeloma bone pain. However, the mechanisms responsible for MM-associated bone pain are poorly understood. Specific osteoclast inhibitors (bisphosphonates and denosumab) can reduce bone pain in MM patients, suggesting that factors released at the tumor-bone interface during osteoclastic bone resorption may be important contributors to bone pain.Bone-resorbing osteoclasts release protons to dissolve bone minerals and aggressively proliferating tumor cells also release protons/lactate as a consequenece of aerobic glycolysis. Since acidosis is algogenic for primary afferent sensory neurons, we reasoned that an acidic extracellular microenvironment created by the release of protons by osteoclasts and MM cells play a critical role in the pathophysiology of bone pain. To investigate the mechanism of bone pain associated with MM, we used an animal model in which the JJN3 human MM cells were inoculated into the tibiae of SCID mice. Control mice received PBS. Bone pain was assessed by determining tactile hypersensitivity and thermal hyperalgesia of JJN3-bearing mice using von Frey and plantar tests. Administration of the pH probe acridine orange to JJN3-bearing mice revealed that resorption pits beneath bone-resorbing osteoclasts and JJN3-colonized tibiae are acidic. Mice bearing JJN3 MM in their tibiae displayed progressive tactile hypersensitivity and thermal hyperalgesia as the tumor grew. Of note, the bisphosphonate zoledronic acid significantly reduced the progression of the tactile hypersensitivity and thermal hyperalgesia, suggesting that these nociceptive behaviors of JJN3-bearing mice are due to osteoclast-mediated bone pain. Importantly, the non-selective proton pump inhibitor bafilomycin A1 inhibited the creation of the acidic extracellular microenvironment in JJN3-colonized bone and significantly prevented the progression of the nociceptive behaviors. These results support that the acidic extracellular microenvironment is responsible for evoking bone pain. Immunohistochemical examination to identify acid-sensing mechanisms present in bone showed that the calcitonin gene-related peptide (CGRP)-positive sensory neurons innervating bone are adjacent to osteoclasts with co-expression of the acid-sensing nociceptor, the transient receptor potential vanilloid subfamily member 1 (TRPV1). To determine the role of TRPV1 in the excitation of sensory neurons, primary sensory neuron cells isolated from dorsal root ganglion (DRG) were exposed to acidic medium (pH 6.5) and examined for intracellular Ca2+ mobilization using Fura 2 AM calcium imaging assays. Acidic medium induced Ca2+ influx in DRG sensory neuron cells and the induced Ca2+ influx was blocked in the presence of the specific TRPV1 antagonist SB366791, while the specific TRPV4 antagonist RN1734 showed no effect. Further, the specific antagonist for the acid-sensing ion channel 3 (ASIC3), APETx2, also blocked the induction of Ca2+ influx. Neutral medium (pH 7.4) did not induce Ca2+ influx. Taken together, these results suggest that TRPV1 and ASIC3 play an important role in the excitation of sensory neurons exposed to acidic extracellular microenvironment. Our results suggest that the acidic extracellular microenvironments created by protons released from osteoclasts and MM cells excite sensory neurons associated with bone via the acid-sensing nociceptors, TRPV1 and ASIC3, to evoke bone pain. TRPV1 and ASIC3 may be potential targets for ameliorating bone pain in MM. Disclosures Roodman: Eli Lilly and Co.: Research Funding.

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Shiba, Hiroya, Misaki Nishio, Mei Sawada, Mamiko Tamaki, Masataka Michigami, Shinya Nakai, Ikuhiko Nakase, Ikuo Fujii, Akikazu Matsumoto, and Chie Kojima. "Carboxy-terminal dendrimers with phenylalanine for a pH-sensitive delivery system into immune cells including T cells." Journal of Materials Chemistry B 10, no. 14 (2022): 2463–70. http://dx.doi.org/10.1039/d1tb01980e.

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Dendrimers with phenylalanine (Phe) and cyclohexanedicarboxylic acid (CHex) showed higher uptake into various cells including T cells via endocytosis. The cell association was enhanced under weak acidic conditions observed in tumor microenvironment.

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Bogdanov, A. A., An A. Bogdanov, and V. M. Moiseyenko. "Alkalinization of the tumor microenvironment: are there prospects as a therapeutic objective?" Practical oncology 23, no. 3 (September 30, 2022): 143–59. http://dx.doi.org/10.31917/2303143.

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Tumor acidity is one of the hallmarks of cancer. The use of glycolysis as the main source of ATP production due to the metabolic reprogramming of cancer cells makes their intracellular pH alkaline and extracellular pH acidic. This metabolic reprogramming and acidification are part of the general defenses that allow malignant cells to survive, multiply, spread, and become resistant to therapies. Tumor acidity may also be associated with a poor prognosis for cancer patients, and clinicians should consider this when diagnosing and determining optimal treatment. On the other hand, the inversion of the pH gradient in tumors could be a weakness, which will allow the development of new promising therapies. Pharmacological inhibition of pH regulation pathways and alkalinization of the tumor appear to be prospective therapeutic options for cancer treatment. Alkalization therapy does not contradict standard treatment methods and can be used in combination to increase effectiveness. Here, we have tried to summarize the basic knowledge about tumor acidity and related potential cancer treatment options.

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Qi, Guohua, Bo Wang, Xiangfu Song, Haijuan Li, and Yongdong Jin. "A green, efficient and precise hydrogen therapy of cancer based on in vivo electrochemistry." National Science Review 7, no. 3 (December 5, 2019): 660–70. http://dx.doi.org/10.1093/nsr/nwz199.

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Abstract By combined use of traditional Chinese acupuncture Fe needle electrode and in vivo electrochemistry, we achieved in vivo H2 generation in tumors in a controllable manner and exploited it for effective and green therapy of tumors for the first time. The cathodic acupuncture electrodes working under an applied voltage of ∼3 V (with minimal damage to the living body) undergo effective electrochemical reactions in the acidic tumor area that produce sufficient H2 locally to cause cancer cells to burst and die. Due to puncture positioning, the acidic tumor microenvironment and gas diffusion effect, the developed H2 generation electrochemotherapy (H2-ECT) strategy enables precise and large-scale tumor therapy, as demonstrated by in vivo treatment of diseased mice (glioma and breast cancers). Such green H2-ECT is simple, highly efficient and minimally invasive, requiring no expensive medical equipment or nano materials and medication, and is therefore very promising for potential clinical applications.

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Tsai, Ming-Hsien, Cheng-Liang Peng, Cheng-Jung Yao, and Ming-Jium Shieh. "Enhanced efficacy of chemotherapeutic drugs against colorectal cancer using ligand-decorated self-breakable agents." RSC Advances 5, no. 112 (2015): 92361–70. http://dx.doi.org/10.1039/c5ra16175d.

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Targeting self-breakable micelles could facilitate Caco2 cancer cells in acidic tumor microenvironment to take up SN38 which the micelle loaded with and trigger drug release in cancer cells, resulting in enhanced drug efficacy.

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Larijani, Nazanin Rohani, Marielle Huot, Anne Lenferink, and Noël R. Raynal. "Abstract B041: Mimicking tumor acidic and hypoxic microenvironment in vitro towards generation of more predictive screening platform for solid tumors." Cancer Research 82, no. 10_Supplement (May 15, 2022): B041. http://dx.doi.org/10.1158/1538-7445.evodyn22-b041.

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Abstract The drug discovery process in oncology relies mainly on screening and preclinical validation platforms that use human cancer cells that are grown in standard monolayer (2D) cultures. However, 2D monolayer cell culture methods poorly reflect the tumor microenvironment (TME) and the transcriptome and epigenome attributes of the cancer cells in vivo, leading to inaccurate estimate of drug efficacy in clinic. The TME of solid tumors is complex yet it consist of generic hallmarks such as hypoxia and extracellular acidosis that are common across tumor types and directly modulate gene expression and epigenome. Here we hypothesized that in vitro culture systems that recapitulate the acidic and hypoxic features of the solid TME, more accurately reflect the gene expression profile of cells in in vivo tumors, and thus serve as improved drug screening platform that reliably determine drug efficacies. Here we surveyed systematically the impact on transcriptome and epigenome hallmarks of exposure to hypoxia and acidosis on 2D and 3D cultures of A549 lung adenocarcinoma cell line as a model for solid tumor. To recapitulate naturally occurring hypoxia in vitro, A549 cells were adapted over several passages to growth in 3D. Transcriptome data derived from cells adapted to 3D, when compared to 2D and patient tumor datasets suggested that time spent in 3D increased the concordance of transcriptome profile with tumors from patients. Furthermore adaptation to 3D revealed emergence of hypoxia hallmarks when compared to 2D. To model the combined effect of hypoxia and acidosis, the 3D adapted A549 spheroids were additionally exposed to low pH conditions (6.4) for a duration of 5 days. The additional exposure to low pH led to enhanced tumor progressive phenotypes as evidenced by enrichment in genes associated with hallmarks of inflammation, epithelial mesenchymal transition (EMT), cell invasion and drug resistance. To determine the impact of hypoxic and acidic TME on cytotoxic response to anti-cancer drugs, the 2D and 3D adapted spheroids with or without additional exposure to low pH were screened against a library consisting of 184 anti-cancer drugs. Additional exposure to low pH led to an overall increase in drug resistance. However the combined hypoxic and acidic conditions in 3D revealed novel susceptibilities for compounds that belong to the family of Aurora kinase inhibitors. These results provide indications that accurate modeling of hypoxic and acidic TME in vitro could reveal expected resistance mechanisms and specific drug susceptibilities. This study introduces a 3D screening platform that recapitulates the acidosis and hypoxia of solid TME and captures the transcriptomic profile in vitro that is highly concordant with tumors in patients. This model allows the study of resistance mechanisms and unravel novel susceptibilities that is otherwise undiscovered in standard 2D conditions and could result in the identification of anticancer drugs that are more clinically relevant. Citation Format: Nazanin Rohani Larijani, Marielle Huot, Anne Lenferink, Noël R. Raynal. Mimicking tumor acidic and hypoxic microenvironment in vitro towards generation of more predictive screening platform for solid tumors [abstract]. In: Proceedings of the AACR Special Conference on the Evolutionary Dynamics in Carcinogenesis and Response to Therapy; 2022 Mar 14-17. Philadelphia (PA): AACR; Cancer Res 2022;82(10 Suppl):Abstract nr B041.

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Sun, Yanting, Yuling Li, Shuo Shi, and Chunyan Dong. "Exploiting a New Approach to Destroy the Barrier of Tumor Microenvironment: Nano-Architecture Delivery Systems." Molecules 26, no. 9 (May 5, 2021): 2703. http://dx.doi.org/10.3390/molecules26092703.

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Recent findings suggest that tumor microenvironment (TME) plays an important regulatory role in the occurrence, proliferation, and metastasis of tumors. Different from normal tissue, the condition around tumor significantly altered, including immune infiltration, compact extracellular matrix, new vasculatures, abundant enzyme, acidic pH value, and hypoxia. Increasingly, researchers focused on targeting TME to prevent tumor development and metastasis. With the development of nanotechnology and the deep research on the tumor environment, stimulation-responsive intelligent nanostructures designed based on TME have attracted much attention in the anti-tumor drug delivery system. TME-targeted nano therapeutics can regulate the distribution of drugs in the body, specifically increase the concentration of drugs in the tumor site, so as to enhance the efficacy and reduce adverse reactions, can utilize particular conditions of TME to improve the effect of tumor therapy. This paper summarizes the major components and characteristics of TME, discusses the principles and strategies of relevant nano-architectures targeting TME for the treatment and diagnosis systematically.

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Matsumoto, A., A. J. Stephenson-Brown, T. Khan, T. Miyazawa, H. Cabral, K. Kataoka, and Y. Miyahara. "Heterocyclic boronic acids display sialic acid selective binding in a hypoxic tumor relevant acidic environment." Chemical Science 8, no. 9 (2017): 6165–70. http://dx.doi.org/10.1039/c7sc01905j.

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A group of heterocyclic boronic acids demonstrating unusually high affinity and selectivity for sialic acids are described, with strong interactions under the weakly acidic pH conditions associated with a hypoxic tumoral microenvironment.

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Meng, Xianfu, Yan Yi, Yun Meng, Guanglei Lv, Xingwu Jiang, Yelin Wu, Wei Yang, Yefeng Yao, Huixiong Xu, and Wenbo Bu. "Self-Enhanced Acoustic Impedance Difference Strategy for Detecting the Acidic Tumor Microenvironment." ACS Nano 16, no. 3 (March 7, 2022): 4217–27. http://dx.doi.org/10.1021/acsnano.1c10173.

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Tong, Zhiqian, Wenhong Luo, Yanqing Wang, Fei Yang, Ying Han, Hui Li, Hongjun Luo, et al. "Tumor Tissue-Derived Formaldehyde and Acidic Microenvironment Synergistically Induce Bone Cancer Pain." PLoS ONE 5, no. 4 (April 21, 2010): e10234. http://dx.doi.org/10.1371/journal.pone.0010234.

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Iwaizumi, Moriya, Stephanie Tseng-Rogenski, and John M. Carethers. "Acidic tumor microenvironment downregulates hMLH1 but does not diminish 5-fluorouracil chemosensitivity." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 747-748 (July 2013): 19–27. http://dx.doi.org/10.1016/j.mrfmmm.2013.04.006.

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Nagae, Maho, Toru Hiraga, and Toshiyuki Yoneda. "Acidic microenvironment created by osteoclasts causes bone pain associated with tumor colonization." Journal of Bone and Mineral Metabolism 25, no. 2 (February 26, 2007): 99–104. http://dx.doi.org/10.1007/s00774-006-0734-8.

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Lu, Yudie, Jie Feng, Zhiyu Liang, Xuanyi Lu, Shuai Guo, Lin Huang, Wei Xiong, et al. "A tumor microenvironment dual responsive contrast agent for contrary contrast-magnetic resonance imaging and specific chemotherapy of tumors." Nanoscale Horizons 7, no. 4 (2022): 403–13. http://dx.doi.org/10.1039/d1nh00632k.

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A smart MRI contrast agent that is almost not responsive to normal physiological conditions, but highly responsive to acidic and reductive TME, realized CC-MRI, and significantly enhanced the MRI contrast between tumors and livers.

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Dailey, K. M., R. I. Jacobson, J. Kim, S. Mallik, and A. E. Brooks. "PROBING CLINICAL RELEVANCE: ESTABLISHING THE EFFICACY OF C. NOVYI AGAINST A PANEL OF 2D CULTURED PANCREATIC CANCER CELLS." Biomedical Sciences Instrumentation 57, no. 2 (April 1, 2021): 92–99. http://dx.doi.org/10.34107/yhpn9422.0492.

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Pancreatic cancer presents a unique challenge for the development of effective oncotherapies. The tumor microenvironment (TME) of this type of tumor typically contains a dense desmoplastic barrier composed of aberrant extracellular matrix proteins, as well as an acidic, hypoxic and necrotic core. Additionally, the immune system surrounding this type of tumor has often been suppressed by the TME. Hence, choosing the correct model of the tumor microenvironment within which to test a potential anti-cancer therapy is a critical experimental design decision. While the typical solid tumor contains a complex microenvironment including both phenotypic and genotypic heterogeneity, the methods used to model this disease state often do not reflect this complexity. This simplistic approach may have contributed to stagnant five-year survival rates experienced over the past four decades. Oncolytic bacteria, a class of bacteria with the innate ability to seek and destroy solid tumors has been revived from historical anecdotes in an attempt to overcome these challenges. Regardless of the promise of oncolytic bacteria, accurate assessment of their potential requires choosing the proper tumor model. This study explores the impact of cancer cell lines co-cultured with Wild-Type C. novyi to establish the efficacy of this oncolytic bacteria in a monolayer culture.

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