Special Issue "Inflammation and Cancer"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (16 April 2018)

Special Issue Editor

Guest Editor
Dr. Shairaz Baksh

Department of Pediatrics, Cancer Research Institute of Northern Alberta, University of Alberta, Edmonton, AB, Canada
Website | E-Mail
Phone: +001 780 492 3494
Interests: apoptosis; cancer; epigenetics; design and synthesis of novel anti-inflammatories; animal models; 3D intestinal organoid model

Special Issue Information

Dear Colleagues,

Inflammation is a complex defense mechanism against biological and chemical insults. Although beneficial, persistent inflammation can cause cellular damage resulting in many diseases including obesity, diabetes, inflammatory bowel disease (IBD), cancer, schizophrenia and recently, Parkinson’s Disease. It is estimated that about 15–20% of all cancer cases are preceded by chronic inflammation, including lung, colon and pancreatic cancers to mention a few. Hanahan and Weinberg in 2011 categorized “tumor inflammation” and “avoiding immune detection” as “Hallmarks of Cancer”. Thus, there is a great need to understand how inflammation is regulated - both modulation of the threshold of activation and factors effectively deactivating it, in a timely manner, when not needed.

Some of the molecular drivers of inflammation have been repeatedly demonstrated to influence cell death, growth and metabolic pathways of a pre-cancer or cancer cell. The challenge is to understand how these molecular drivers differ from their function in normal cells and in homeostatic regulation. If key molecular drivers of inflammation to cancer can be identified, novel therapies can be obtained to selectively target their abnormal function in “inflammatory phase” prior to pre-cancer or cancer cells. This Special Issue on “Inflammation and Cancer” will provide an open-source sharing of significant articles describing the role for new and emerging players in regulating inflammation and how these players may impinge of the cell death, metabolic and growth characteristics of a pre-cancer or cancer cell (to mention a few).

Topics of this Special Issue include, but are not limited to:

  1. The Use of Organoids to explore inflammation and cancer
  2. Targeting tumor-promoting inflammation through lysophosphatidate signaling in cancer therapy
  3. Oncometabolism and Inflammation
  4. Inflammation as a driver of development of hematologic malignancies
  5. Roles for Siglecs in Modulating Inflammation in Cancer
  6. The relationship between malnutrition, inflammation and immune suppression in cancer
  7. The role for non-receptor protein tyrosine kinases, HPK1, in immunocheckpoint control
  8. RIPK2: New Elements in Modulating Inflammatory Breast Cancer Pathogenesis
  9. The complex interplay between chronic inflammation, the microbiome and cancer: understanding disease progression and what we can do to prevent it

If you have a topic that you would like to contribute to this Special Issue, please email Dr. Shairaz Baksh at [email protected] and we will do our best to incorporate it into our Special Issue. Thanks for your time.

Dr. Shairaz Baksh
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Tumor suppressor protein
  • inflammation
  • NFkB
  • Metabolic syndrome
  • 3D orgaonids/spheroids
  • Microbiome
  • AMPK
  • MCT1
  • Cell death
  • GTPase
  • WNT/β-catenin

Published Papers (6 papers)

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Research

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Open AccessFeature PaperArticle RIPK2: New Elements in Modulating Inflammatory Breast Cancer Pathogenesis
Cancers 2018, 10(6), 184; https://doi.org/10.3390/cancers10060184
Received: 29 March 2018 / Revised: 29 May 2018 / Accepted: 4 June 2018 / Published: 5 June 2018
Cited by 2 | PDF Full-text (4041 KB) | HTML Full-text | XML Full-text
Abstract
Inflammatory breast cancer (IBC) is a rare and aggressive form of breast cancer that is associated with significantly high mortality. In spite of advances in IBC diagnoses, the prognosis is still poor compared to non-IBC. Due to the aggressive nature of the disease, [...] Read more.
Inflammatory breast cancer (IBC) is a rare and aggressive form of breast cancer that is associated with significantly high mortality. In spite of advances in IBC diagnoses, the prognosis is still poor compared to non-IBC. Due to the aggressive nature of the disease, we hypothesize that elevated levels of inflammatory mediators may drive tumorigenesis and metastasis in IBC patients. Utilizing IBC cell models and patient tumor samples, we can detect elevated NF-κB activity and hyperactivation of non-canonical drivers of NF-κB (nuclear factor kappaB)-directed inflammation such as tyrosine phosphorylated receptor-interacting protein kinase 2 (pY RIPK2), when compared to non-IBC cells or patients. Interestingly, elevated RIPK2 activity levels were present in a majority of pre-chemotherapy samples from IBC patients at the time of diagnosis to suggest that patients at diagnosis had molecular activation of NF-κB via RIPK2, a phenomenon we define as “molecular inflammation”. Surprisingly, chemotherapy did cause a significant increase in RIPK2 activity and thus molecular inflammation suggesting that chemotherapy does not resolve the molecular activation of NF-κB via RIPK2. This would impact on the metastatic potential of IBC cells. Indeed, we can demonstrate that RIPK2 activity correlated with advanced tumor, metastasis, and group stage as well as body mass index (BMI) to indicate that RIPK2 might be a useful prognostic marker for IBC and advanced stage breast cancer. Full article
(This article belongs to the Special Issue Inflammation and Cancer)
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Review

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Open AccessReview Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities
Cancers 2018, 10(6), 207; https://doi.org/10.3390/cancers10060207
Received: 31 May 2018 / Revised: 13 June 2018 / Accepted: 14 June 2018 / Published: 18 June 2018
Cited by 7 | PDF Full-text (1433 KB) | HTML Full-text | XML Full-text
Abstract
Cell surface glycosylation is dynamic and often changes in response to cellular differentiation under physiological or pathophysiological conditions. Altered glycosylation on cancers cells is gaining attention due its wide-spread occurrence across a variety of cancer types and recent studies that have documented functional [...] Read more.
Cell surface glycosylation is dynamic and often changes in response to cellular differentiation under physiological or pathophysiological conditions. Altered glycosylation on cancers cells is gaining attention due its wide-spread occurrence across a variety of cancer types and recent studies that have documented functional roles for aberrant glycosylation in driving cancer progression at various stages. One change in glycosylation that can correlate with cancer stage and disease prognosis is hypersialylation. Increased levels of sialic acid are pervasive in cancer and a growing body of evidence demonstrates how hypersialylation is advantageous to cancer cells, particularly from the perspective of modulating immune cell responses. Sialic acid-binding receptors, such as Siglecs and Selectins, are well-positioned to be exploited by cancer hypersialylation. Evidence is also mounting that Siglecs modulate key immune cell types in the tumor microenvironment, particularly those responsible for maintaining the appropriate inflammatory environment. From these studies have come new and innovative ways to block the effects of hypersialylation by directly reducing sialic acid on cancer cells or blocking interactions between sialic acid and Siglecs or Selectins. Here we review recent works examining how cancer cells become hypersialylated, how hypersialylation benefits cancer cells and tumors, and proposed therapies to abrogate hypersialylation of cancer. Full article
(This article belongs to the Special Issue Inflammation and Cancer)
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Open AccessReview Organoids Provide an Important Window on Inflammation in Cancer
Cancers 2018, 10(5), 151; https://doi.org/10.3390/cancers10050151
Received: 17 April 2018 / Revised: 17 May 2018 / Accepted: 17 May 2018 / Published: 21 May 2018
Cited by 3 | PDF Full-text (892 KB) | HTML Full-text | XML Full-text
Abstract
Inflammation is a primary driver of cancer initiation and progression. However, the complex and dynamic nature of an inflammatory response make this a very difficult process to study. Organoids are a new model system where complex multicellular structures of primary cells can be [...] Read more.
Inflammation is a primary driver of cancer initiation and progression. However, the complex and dynamic nature of an inflammatory response make this a very difficult process to study. Organoids are a new model system where complex multicellular structures of primary cells can be grown in a 3D matrix to recapitulate the biology of the parent tissue. This experimental model offers several distinct advantages over alternatives including the ability to be genetically engineered, implanted in vivo and reliably derived from a wide variety of normal and cancerous tissue from patients. Furthermore, long-term organoid cultures reproduce many features of their source tissue, including genetic and epigenetic alterations and drug sensitivity. Perhaps most significantly, cancer organoids can be cocultured in a variety of different systems with a patients’ own immune cells, uniquely permitting the study of autologous cancer-immune cell interactions. Experiments with such systems promise to shed light on the mechanisms governing inflammation-associated cancer while also providing prognostic information on an individual patient’s responsiveness to immunotherapeutic anti-cancer drugs. Thanks to their ability to capture important features of the complex relationship between a cancer and its microenvironment, organoids are poised to become an essential tool for unraveling the mechanisms by which inflammation promotes cancer. Full article
(This article belongs to the Special Issue Inflammation and Cancer)
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Open AccessReview The Critical Role of Inflammation in the Pathogenesis and Progression of Myeloid Malignancies
Cancers 2018, 10(4), 104; https://doi.org/10.3390/cancers10040104
Received: 1 March 2018 / Revised: 23 March 2018 / Accepted: 2 April 2018 / Published: 3 April 2018
Cited by 2 | PDF Full-text (7575 KB) | HTML Full-text | XML Full-text
Abstract
Hematopoietic stem cells (HSCs) maintain an organism’s immune system for a lifetime, and derangements in HSC proliferation and differentiation result in hematologic malignancies. Chronic inflammation plays a contributory if not causal role in HSC dysfunction. Inflammation induces HSC exhaustion, which promotes the emergence [...] Read more.
Hematopoietic stem cells (HSCs) maintain an organism’s immune system for a lifetime, and derangements in HSC proliferation and differentiation result in hematologic malignancies. Chronic inflammation plays a contributory if not causal role in HSC dysfunction. Inflammation induces HSC exhaustion, which promotes the emergence of mutant clones that may be resistant to an inflammatory microenvironment; this likely promotes the onset of a myeloid hematologic malignancy. Inflammatory cytokines are characteristically high in patients with myeloid malignancies and are linked to disease initiation, symptom burden, disease progression, and worsened prognostic survival. This review will cover our current understanding of the role of inflammation in the initiation, progression, and complications of myeloid hematologic malignancies, drawing from clinical studies as well as murine models. We will also highlight inflammation as a therapeutic target in hematologic malignancies. Full article
(This article belongs to the Special Issue Inflammation and Cancer)
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Open AccessReview The Complex Interplay between Chronic Inflammation, the Microbiome, and Cancer: Understanding Disease Progression and What We Can Do to Prevent It
Received: 1 March 2018 / Revised: 15 March 2018 / Accepted: 15 March 2018 / Published: 20 March 2018
Cited by 7 | PDF Full-text (1260 KB) | HTML Full-text | XML Full-text
Abstract
Cancer is a multifaceted condition, in which a senescent cell begins dividing in an irregular manner due to various factors such as DNA damage, growth factors and inflammation. Inflammation is not typically discussed as carcinogenic; however, a significant percentage of cancers arise from [...] Read more.
Cancer is a multifaceted condition, in which a senescent cell begins dividing in an irregular manner due to various factors such as DNA damage, growth factors and inflammation. Inflammation is not typically discussed as carcinogenic; however, a significant percentage of cancers arise from chronic microbial infections and damage brought on by chronic inflammation. A hallmark cancer-inducing microbe is Helicobacter pylori and its causation of peptic ulcers and potentially gastric cancer. This review discusses the recent developments in understanding microbes in health and disease and their potential role in the progression of cancer. To date, microbes can be linked to almost every cancer, including colon, pancreatic, gastric, and even prostate. We discuss the known mechanisms by which these microbes can induce cancer growth and development and how inflammatory cells may contribute to cancer progression. We also discuss new treatments that target the chronic inflammatory conditions and their associated cancers, and the impact microbes have on treatment success. Finally, we examine common dietary misconceptions in relation to microbes and cancer and how to avoid getting caught up in the misinterpretation and over inflation of the results. Full article
(This article belongs to the Special Issue Inflammation and Cancer)
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Open AccessFeature PaperReview Coming of Age for Autotaxin and Lysophosphatidate Signaling: Clinical Applications for Preventing, Detecting and Targeting Tumor-Promoting Inflammation
Received: 23 February 2018 / Revised: 10 March 2018 / Accepted: 12 March 2018 / Published: 15 March 2018
Cited by 9 | PDF Full-text (834 KB) | HTML Full-text | XML Full-text
Abstract
A quarter-century after the discovery of autotaxin in cell culture, the autotaxin-lysophosphatidate (LPA)-lipid phosphate phosphatase axis is now a promising clinical target for treating chronic inflammatory conditions, mitigating fibrosis progression, and improving the efficacy of existing cancer chemotherapies and radiotherapy. Nearly half of [...] Read more.
A quarter-century after the discovery of autotaxin in cell culture, the autotaxin-lysophosphatidate (LPA)-lipid phosphate phosphatase axis is now a promising clinical target for treating chronic inflammatory conditions, mitigating fibrosis progression, and improving the efficacy of existing cancer chemotherapies and radiotherapy. Nearly half of the literature on this axis has been published during the last five years. In cancer biology, LPA signaling is increasingly being recognized as a central mediator of the progression of chronic inflammation in the establishment of a tumor microenvironment which promotes cancer growth, immune evasion, metastasis, and treatment resistance. In this review, we will summarize recent advances made in understanding LPA signaling with respect to chronic inflammation and cancer. We will also provide perspectives on the applications of inhibitors of LPA signaling in preventing cancer initiation, as adjuncts extending the efficacy of current cancer treatments by blocking inflammation caused by either the cancer or the cancer therapy itself, and by disruption of the tumor microenvironment. Overall, LPA, a simple molecule that mediates a plethora of biological effects, can be targeted at its levels of production by autotaxin, LPA receptors or through LPA degradation by lipid phosphate phosphatases. Drugs for these applications will soon be entering clinical practice. Full article
(This article belongs to the Special Issue Inflammation and Cancer)
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