Search Results for: tumour microenvironment

Tumour microenvironment – ameloblastomas

Following our post on tumour microenvironment and glioblastoma, we will focus today on ameloblastomas.

Ameloblastomas are benign tumours that occur in the jawbone, and invade bone. This type of tumour is treated by surgery and can cause various problems, including changes in facial countenance and mastication disorders.1-s2.0-S0006291X14X00355-cov150h

Ameloblastomas have abundant tumor stroma, including fibroblasts and immune cells. Cell-to-cell interactions in ameloblastoma have not been fully investigated yet. A recent publication by Fuchigami et al.  has investigated the soluble factors (i.e. secretome) involved in the formation and progression of ameloblastoma.

Using the Q-plex technology in a human ameloblastoma cell line (AM-3), as well as human fibroblasts (HFF-2) and primary-culture fibroblasts from human ameloblastoma tissues, they analysed the effect of ameloblastoma-associated cell-to-cell communications. Q-plex was used to study the cytokine secretion, namely IL-1alpha, IL-6, IL-8. Fuchigami et al. conclude that ameloblastoma cells and stromal fibroblasts behave interactively via these cytokines to create a tumour microenvironment (TME) that leads to the extension of this type of tumours.

32_Q_Plex__multiplex_ELISA_by_QuansysWould you like to know more about the Q-plex technology? We recently organised a webinar on this technology. Contact us if you want to receive a link with the recorded version or the PDF with the presentation!


Tumour microenvironment – the kinome (II)

In a previous post, we discussed  kinome studies in the tumour microenvironment (TME). We described some solutions to study known markers, but we did not look at those cases in which the biomarkers associated to the kinome are unkown, and therefore some exploration is needed. [Read more…]

Tumour microenvironment and kinome studies

We all react to external factors, even the most cold-blooded person. We might hide our emotions, but there they are.

The same happens in cancer. Cells (both the tumour cells and the normal ones) react to the environment in one direction or another. In this post, we will see how “kinome” analysis might help Researchers in better understanding cellular interactions in tumour microenvironment (TME).

[Read more…]

Tumour microenvironment – exosomes

Following our series of posts on the tumour microenvironment (TME), we will put our spotlight today on exosomes.


Proposed immunological functions of tumour-derived exosomes. Taken from Ref. 3

TME is composed on myofibroblasts, extracellular matrix and many other cell types. The tumour communicates with its microenvironment through cytokines, growth factors, chemokines, miRNAs, etc, as previously seen. Exosomes are nanosized extracellular vesicles (EVs) that allow communication between cells. They seem to play a role in the progression of some cancers (e.g. prostate cancer, glioblastoma), as well as in resistance to cancer therapies (1, 2). In fact, they modulate the immune response, explaining their role in either fighting the tumour or helping the tumour cells evade the immune system (3). [Read more…]

Tumour microenvironment and miRNA biomarkers

In previous posts, we have seen the role of inflammation and glycosylation in the tumour microenvironment (TME). All these are mainly factors at the protein level causing the tumour cells to evade the immune system and metastasise. But what about other factors?

One of the areas that has raised quite some interest recently are microRNAs (miRNAs). If you’d like to brush up your knowledge on miRNAs, you might be interested in this post by my colleague Paola Vecino. miRNAs are becoming trendy, as they seem to be involved in several disease mechanisms (not only in cancer, but also in some other pathologies, including some inflammatory diseases), and they can be used as diagnostic and/or prognostic biomarkers.

[Read more…]

Tumour microenvironment – glioblastoma

Tumour microenvironment – glycosylation

Cancer research is increasingly focusing on the tumour microenvironment (TME). Several studies have shown that tumours depend on external signals for maintenance and expansion. It is therefore needed to have a deeper knowledge of the cross-talk between tumour cells in the stroma (fibroblasts, adipocytes, endothelial cells and macrophages) and their microenvironment which also includes the study of interactions between cancer cells and cancer stem cells. TME studies also involve soluble factors, signaling molecules, extracellular matrix proteins (ECM) and other factors that help the tumour grow and invade other tissues, protect it from the host immune system, and contributes to therapeutic resistance in some cases (1). In a previous post, we discussed the role of Cox-2 signaling and PGE2 in TME. Also, we have already discussed the role of inflammation and the modification of the host’s immune response by cancer cells.

Today, we would like to focus on how TME affects the glycosylation of proteins involved in tumour progression.

[Read more…]

Tumour microenvironment – inflammation and immunity

Following our series of posts on tumour microenvironment (TME) and the role of Cox-2/PGE2 signaling, I’d like today to focus on inflammation and immunity.

TME is a dynamic milieu influenced by numerous changes favoring the emergence of a tumour-promoting inflammatory environment (eg. tissue remodeling, metabolic alterations, recruitment of stromal cells (including immune cells)…). Extracellular matrix (ECM) also participate in this inflammatory environment by promoting pro-inflammatory cytokines expression (CCL2, GM-CSF). Tumour cell progression seems to be mediated by adaptative and immune cells, where differential cytokine and chemokine expression changes the balance between Th1 (anti-tumour) and Th2 (pro-tumour) phenotypes. Microbiota also influences cancer progression by regulating the inflammatory components of TME, though how this is done needs further investigation (1).

[Read more…]

Tumour microenvironment – the dark side of PGE2

PGE2 (Prostaglandin E2) is a lipid mediator with key links to inflammation and cancer.  PGE2 is produced by a wide variety of tissues and in several pathological conditions, including inflammation, arthritis, fever, tissue injury, endometriosis, and a variety of cancers. Recombinant prostaglandins are also used as therapy for different conditions (pulmonary hypertension, glaucoma, ulcers… even to make eyelashes grow!). So PGE2 has, as many things in life, a bright and a dark side.

Let’s talk about the dark side of PGE2 today. Reports indicate that its overexpression in cancer cells promotes angiogenesis and metastasis, by influencing the immune response (1). In brief, cyclooxygenases (COXs) convert arachidonic acid to PGE2 and thromboxane. PGE2 binds to its receptors and activates signaling pathways controlling cell proliferation, migration, apoptosis and/or angiogenesis. A few drugs are intended to target and inhibit some types of COXs, but they might have undesirable side effects and may not be efficient in some patient groups.

For example, non-steroidal anti-inflammatory drugs (NSAIDs) such as celecoxib (Celebrex®),  and rofecoxib (Vioxx®) in the past,  have shown to possibly cause a significant increase in cardiovascular risk (2) (3).

Nevertheless, several studies highlight the need to reduce PGE2 levels in cancer, and focus on its catabolism to find new therapeutic targets (4). The COX-2/PGE2 pathway has a key influence on tumour expansion and it might even be relevant in tumour initiation (5). [Read more…]

Cancer stem cells – friend or foe in the fight against cancer?

Today, following our series on Tumour Microenvironment (TME), and leading on from three recent publications, let’s discuss Cancer Stem Cells (CSCs).

CSCs are part of the TME, as they reside in niches where they can survive from immune surveillance, maintain plasticity and facilitate cancer metastasis (1). They can also circulate around the body. Which makes them so interesting. Their worse effect is that they can expand cancer to other organs in the body, thus helping metastasic. The good thing is that their early detection is a very powerful biomarker for cancer, allowing an early treatment. [Read more…]