The Role of Tumor Inflammatory Microenvironment in Lung Cancer

Tan, Zhaofeng; Xue, Hai-Bin; Sun, Yi; Zhang, Chuanlong; Song, Yonglei; Qi, Yuanfu

doi:10.3389/fphar.2021.688625

Cited by 91 publications

(62 citation statements)

References 114 publications

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“…It also includes exosomes and apoptotic bodies in which they are known as an extracellular vehicle (EVs). Moreover, TME has special unique features including hypoxia and acidic environment [20][21][22]. The lung TME plays an imminent role in cancer cell resistance by interfering with the pharmacokinetic distribution of the anti-cancer agent [23].…”

Section: Tumor Microenvironmentmentioning

confidence: 99%

Nanomedicine Strategies for Management of Drug Resistance in Lung Cancer

Haider¹,

Sherbeny²,

Pittalà³

et al. 2022

Preprint

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Lung cancer (LC) is one of the leading causes of cancer occurrence and mortality worldwide. Treatment of patients with advanced and metastatic LC presents a significant challenge as malignant cells use different mechanisms to resist chemotherapy. Drug resistance (DR) is a complex process that occurs due to a variety of genetic and acquired factors. Identifying the mechanisms underlying DR in LC patients and possible therapeutic alternatives for more efficient therapy is a central goal of LC research. Advances in nanotechnology resulted in the development of targeted and multifunctional nanoscale drug constructs. The possible modulation of the components of nanomedicine, their surface functionalization, and encapsulation of various active therapeutics provide promising tools to bypass crucial biological barriers. These attributes enhance the delivery of multiple therapeutic agents directly to the tumor microenvironment (TME), resulting in reversal of LC resistance to anticancer treatment. This review provides a broad framework for understanding the different molecular mechanisms of DR in lung cancer; presents novel nanomedicine therapeutics aimed to improve the efficacy of treatment of various forms of resistant LC; outlines current challenges in using nanotechnology for reversing DR; and discusses the future directions for clinical application of nanomedicine in management of LC resistance.

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Section: Tumor Microenvironmentmentioning

confidence: 99%

Nanomedicine Strategies for Management of Drug Resistance in Lung Cancer

Haider¹,

Sherbeny²,

Pittalà³

et al. 2022

Preprint

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“…TME consists of a heterogeneous population of cancer cells, immune cells, vessels, stroma, signaling mediators and extracellular matrix proteins (8). The presence of a chronic inflammatory environment in lung cancer (9) may alter or deviate immune cell differentiation, resulting in an imbalance of anti-tumor activity, thus favoring tumor evasion (8) and later on, resistance to ICI (10). In this context, TME might represent a relevant source of predictive biomarkers for ICIs, as well as a potential target for novel therapeutic strategies.…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Implications of Tumor Microenvironment in Lung Cancer: Focus on Immune Checkpoint Blockade

et al. 2022

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In the last decade, the treatment of non-small cell lung cancer (NSCLC) has been revolutionized by the introduction of immune checkpoint inhibitors (ICI) directed against programmed death protein 1 (PD-1) and its ligand (PD-L1), or cytotoxic T lymphocyte antigen 4 (CTLA-4). In spite of these improvements, some patients do not achieve any benefit from ICI, and inevitably develop resistance to therapy over time. Tumor microenvironment (TME) might influence response to immunotherapy due to its prominent role in the multiple interactions between neoplastic cells and the immune system. Studies investigating lung cancer from the perspective of TME pointed out a complex scenario where tumor angiogenesis, soluble factors, immune suppressive/regulatory elements and cells composing TME itself participate to tumor growth. In this review, we point out the current state of knowledge involving the relationship between tumor cells and the components of TME in NSCLC as well as their interactions with immunotherapy providing an update on novel predictors of benefit from currently employed ICI or new therapeutic targets of investigational agents. In first place, increasing evidence suggests that TME might represent a promising biomarker of sensitivity to ICI, based on the presence of immune-modulating cells, such as Treg, myeloid derived suppressor cells, and tumor associated macrophages, which are known to induce an immunosuppressive environment, poorly responsive to ICI. Consequently, multiple clinical studies have been designed to influence TME towards a pro-immunogenic state and subsequently improve the activity of ICI. Currently, the mostly employed approach relies on the association of “classic” ICI targeting PD-1/PD-L1 and novel agents directed on molecules, such as LAG-3 and TIM-3. To date, some trials have already shown promising results, while a multitude of prospective studies are ongoing, and their results might significantly influence the future approach to cancer immunotherapy.

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“…Epidemiological and clinical studies have shown a strong relationship between lung cancer, inflammatory microenvironment, and chronic infection [39], as well as between colorectal cancer and chronic inflammatory diseases [24]. In pancreatic cancer, an extensive stromal remodeling, with inflammatory cells and fibrotic scars, is also a hallmark of this type of cancer.…”

Section: Introductionmentioning

confidence: 99%

KRAS as a Modulator of the Inflammatory Tumor Microenvironment: Therapeutic Implications

Pereira

Ferreira

Reis

et al. 2022

Cells

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KRAS mutations are one of the most frequent oncogenic mutations of all human cancers, being more prevalent in pancreatic, colorectal, and lung cancers. Intensive efforts have been encouraged in order to understand the effect of KRAS mutations, not only on tumor cells but also on the dynamic network composed by the tumor microenvironment (TME). The relevance of the TME in cancer biology has been increasing due to its impact on the modulation of cancer cell activities, which can dictate the success of tumor progression. Here, we aimed to clarify the pro- and anti-inflammatory role of KRAS mutations over the TME, detailing the context and the signaling pathways involved. In this review, we expect to open new avenues for investigating the potential of KRAS mutations on inflammatory TME modulation, opening a different vision of therapeutic combined approaches to overcome KRAS-associated therapy inefficacy and resistance in cancer.

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The Role of Tumor Inflammatory Microenvironment in Lung Cancer

Cited by 91 publications

References 114 publications

Nanomedicine Strategies for Management of Drug Resistance in Lung Cancer

Nanomedicine Strategies for Management of Drug Resistance in Lung Cancer

Therapeutic Implications of Tumor Microenvironment in Lung Cancer: Focus on Immune Checkpoint Blockade

KRAS as a Modulator of the Inflammatory Tumor Microenvironment: Therapeutic Implications

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