Category: Scientific Posters

Tissue-derived peripheral biomarkers that reflect activity of T-cells, macrophages, and neutrophils in patients with solid tumors

Introduction

By identifying and quantifying specific extracellular protein fragments with neo-epitopes that are generated by proteolytic cleavage and post-translational modifications specific for T-cells, neutrophils and macrophages, respectively, it is possible to develop peripheral biomarkers that reflect the activity of these immune cells.

Poster

Conclusion

Tissue-derived peripheral biomarkers that reflect the activity of T-cells (C4G), macrophages (VICM) and neutrophils (nordicCPa9-HNE™) has biomarker potential in solid tumors and may serve as prognostic, predictive and pharmacodynamic biomarkers in clinical trials investigating cancer immunotherapy.

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Serological assessment of cancer associated myo-fibroblast (myCAF) activity by collagen pro-peptide biomarkers provides high prognostic power

Introduction

Myofibroblast Cancer Associated Fibroblasts (myCAFs) are the main tumor fibrosis drivers and hence different from inflammatory CAFs (iCAFs). CAFs produce type III, V, VI and XI collagen that are the essential components of tumor fibrosis. Pro-peptides of these collagens can be quantified both in serum with the nordicPRO-C3™, PRO-C5, nordicPRO-C6™ and PRO-C11 biomarkers where they are prognostic for poor overall survival in patients with various solid tumor types and may be applied in vitro.

In this study we investigated the association and difference between myCAFs and iCAFs and their collagen expression profile and related that to data available data on serological assessments of nordicPRO-C3™, PRO-C5, nordicPRO-C6™ and PRO-C11, and cultured CAFs.

Poster

Conclusion

Profiling collagen expression in fibroblast from PDAC and NSCLC reveals that type V collagen and type XI collagen are found in myCAF. Biomarkers of these collagens can be measured in serum from cancer patients and are prognostic for poor overall survival. Thus, these data suggest that cancer associated myo-fibroblast (myCAF) activity can be assessed non-invasively by specific collagen pro-peptide biomarkers.

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Introduction

Pancreatic ductal adenocarcinoma (PDAC) patients have poor prognosis partly due to excessive activity of cancer-associated fibroblasts (CAFs). CAFs drive the fibrosis that causes excessive type III collagen and extracellular matrix deposition that in turn reduces drug response resulting in poor survival. High levels of the type III collagen serum biomarker nordicPRO-C3™ correlates with poor survival in PDAC. While TGF-β is thought to be one of the main drivers of nordicPRO-C3™ and tumor fibrosis, cytokines such as Interleukin 1 (IL-1) play a key role in the pancreatic tumor microenvironment and may play a significant role in also tumor fibrosis.
In this study, we first investigated the potential of IL-1 in activating fibroblasts to drive fibrosis and produce nordicPRO-C3™. Subsequently, we established a co-culture of pancreatic cancer cells and pancreatic CAFs to investigate the anti-fibrotic properties of nadunolimab, a fully humanized ADCC-enhanced monoclonal IgG1 antibody that targets IL1RAP and disrupts both IL-1α and IL-1β signaling.

Poster

Conclusion

Co-cultures of pancreatic tumor cells and CAFs induced formation, including collagen type III formation, and nadunolimab inhibited the collagen type III formation, suggesting anti-fibrotic properties. Activated fibroblasts had induced type III collagen formation (nordicPRO-C3™) suggesting that IL-1 is a driver of tumor fibrosis in PDAC. Nadunolimab, which is currently in clinical development for treatment of pancreatic cancer, has the potential to counteract the detrimental, fibrotic progression in tumors by targeting IL1RAP and blocking both IL-1α and IL-1β signaling. These findings suggest that nordicPRO-C3™ could potentially be used for prognostic/predictive enrichment and as a pharmacodynamic marker in future studies evaluating anti-IL-1 modalities in PDAC.

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Non-invasive biomarkers of ECM turnover are prognostic for combinations of checkpoint inhibition immunotherapy in solid tumors

Introduction

Immune checkpoint inhibitors (ICIs) are being investigated in many different combinations (Table 1) but only a fraction of patients respond. This highlights the need for prognostic biomarkers that can help identify patients most likely to respond. Tumor fibrosis and the high collagen/ECM turnover in the tumor microenvironment – processes are closely related to response to ICIs and survival outcomes.

In this study we investigated the clinical utility of non-invasive biomarkers of collagen-1 (reC1M), collagen-III (nordicPRO-C3™), collagen-4 (C4M), collagen-19 (PRO-C19), collagen-20 (PRO-C20) and TGF-β activity in metastatic cancer patients treated with ICIs.

Poster

Conclusion

Across a diverse cohort of patients with metastatic cancer treated with different checkpoint inhibition regimens, non-invasive biomarkers associated with tumor fibrosis and collagen/ECM turnover (nordicPRO-C3™, PRO-C19, PRO-C20, TGF-β, reC1M and C4M) could identify cancer patients with poor prognosis.

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Unraveling collagen signatures in cancer-associated fibroblasts: A biomarker-driven approach

Introduction

The tumor microenvironment (TME) plays a crucial role in driving tumor development. Among the constituents of the tumor stroma, cancer-associated fibroblasts (CAFs) are a pivotal component.
CAFs are actively involved in tumor progression by modulating the architecture of the TME through increased deposition of various collagens resulting in tumor fibrosis. Several studies have shown that CAFs have heterogeneity within, and between, individual tissues. TGF-β is thought to be the main driver of tumor fibrosis, however, the field lacks a characterization of the specific collagen deposition of CAFs from different tissues.

In this study, we investigated the fibrotic activity of CAFs from various tissues by measuring the production of three specific collagen peptides in vitro by use of non-invasive clinically validated biomarkers.

Poster

Conclusion

These findings underscore the heterogeneity in collagen production among CAFs from different indications, providing valuable insights into the ECM dynamics within distinct TMEs. Collagen-based non-invasive biomarkers further demonstrate the capability to differentiate between the fibrotic activity of CAFs isolated from different tissues. These insights support the utility of this model as a useful tool for anti-fibrotic drug screening.

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Novel tissue turnover biomarkers are associated with prolonged QTc and pulmonary arterial hypertension in patients with systemic sclerosis

Introduction

Systemic sclerosis (SSc) is characterized by vasculopathy and fibrosis of the skin and internal organs. Cardiovascular involvement is a frequent and significant contributor to morbidity and mortality in SSc. They can develop clinically silent and be difficult to detect. Novel tissue turnover biomarkers hold the potential to detect the manifestations before clinical overt disease, identify risk patients and monitor the disease course as well as improve our understanding of the pathophysiology in SSc.

The objective of this study is to measure a panel of collagen biomarkers in SSc and explore associations to cardiac involvement detected by ECG and to PAH.

Poster

Conclusion

Patients with SSc and prolonged ECG presented an altered tissue turnover, by an increased level of nordicPRO-C3™ and nordicPRO-C6™. In addition, SSc patients with presence of PAH had increased levels of nordicPRO-C3™ and nordicPRO-C6™ as well. presented an altered tissue turnover in presence of PAH, and with a QTc>450 ms. Our study indicates that they could serve as biomarkers of these manifestations and warrant further studies in cardiac disease in SSc.

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TNF-α and TGF-β Synergistically Promote Fibrogenesis in a In Vitro Model of Fibro-inflammation

Introduction

Systemic sclerosis (SSc) is a skin disease characterized by chronic inflammation leading to
fibrosis, a process called fibro-inflammation. TNF-α is an inflammatory cytokine driving chronic inflammation in SSc, while TGF-β activation is a hallmark of fibrotic pathology. Fibrogenesis (wound healing) is characterized by granulation tissue formation consisting of mainly type III collagen.

The aim of this study was to investigate if primary human dermal fibroblasts treated with TNF-α
and TGF-β1 had increased fibrogenesis compared to fibroblasts treated only with TGF-β1.

Poster

Conclusion

Inflammatory TNF-α stimulation increases TGF-β driven fibrogenesis in dermal fibroblasts, by promoting their formation of type III collagen and fibronectin. Consequently, biomarkers of type III collagen formation and fibronectin formation may be markers of early fibrosis in fibro-inflammatory skin disease.

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Is Skin Disease a Local Manifestation of Systemic Tissue Turnover? Serological Collagen Biomarkers Provide Important Information on Skin Diseases Arising from Mutations in Collagen Genes

Introduction

Collagens are the main constituents of the skin. Genetic mutations in type VI, VII, and XVII collagen cause skin diseases, such as atopic dermatitis, epidermolysis bullosa, and bullous pemphigoid. These are all
characterized as systemic diseases, with local manifestations. Novel collagen biomarkers hold the potential to detect skin manifestations, monitor the disease course, as well as improve our understanding of the pathophysiology.

The aim of this study was to develop blood-based biomarkers of type VI, VII, and XVII collagen, and investigate their diagnostic potential for skin pathologies, including systemic sclerosis.

Poster

Conclusion

These biomarkers reflect the downstream effect of different genetic mutations leading to skin disease and may be useful to determine skin involvement in rheumatic diseases, including systemic sclerosis and psoriatic arthritis.

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Serum biomarkers of proteolytic tissue destruction, formation and macrophage activity can discern patients with IBD according to infliximab treatment non-response or response

Introduction

Characterized by chronic inflammation, patients with Inflammatory Bowel Disease (IBD) experience detrimental remodeling of their intestinal extracellular matrix (ECM). Treatment with anti-inflammatory drugs can reduce inflammation, leading to remission and tissue healing. However, adequate monitoring of patients is critical to ensure and maintain treatment response.

As potential surrogate markers of ECM remodeling, we investigated blood-based biomarkers of type III and -VII collagen and posttranslational modifications of vimentin in patients with IBD. Our aim was to determine the value of the C3M, PRO-C7, and VICM biomarkers for identifying and monitoring response to infliximab (IFX).

Poster

Conclusion

Quantifying a combination of non-invasive biomarkers of ECM remodeling and macrophage activity provided AUCs of 0.684 to 0.797 identifying responders to IFX treatment. Each biomarker provided value at the three different visits (Visit 1, 2, and 3). Combining all three biomarkers measured at each visit
resulted in an AUC of 0.797 identifying responders to IFX treatment.

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Immune-cell specific biomarker of early intestinal inflammation: Neutrophil elastase degraded fragment of type III collagen is elevated in patients with inflammatory bowel disease

Introduction

Inflammatory Bowel Disease (IBD) is characterized by epithelial barrier injury of the gastrointestinal (GI) tract and is driven by abnormal immune responses and excessive secretion of proteases from immune cells. Among these, neutrophils are the first to migrate into the inflamed interstitial matrix, where type III collagen is significantly deposited. Early detection of mucosal inflammation is crucial to prevent cumulative clinical damage, as a delayed diagnosis can hinder effective treatment.

In this study we aimed to develop a biomarker that reflects early intestinal inflammation prior to it becoming medically evident; allowing us to distinguish patients that would benefit from an anti-inflammatory treatment.

Poster

Conclusion

C3-HNE levels are elevated in patients with IBD compared with HD. This increase is also observed in conditioned media from primary neutrophils activated with lipopolysaccharide (LPS) for six hours. Importantly, C3-HNE reflects the early stages of clinically apparent mucosal damage in experimental models of colitis. As such, this biomarker holds promise for identifying early mucosal injury or acute inflammation in the gastrointestinal tract. Nevertheless, additional studies are needed to evaluate its clinical validity.

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