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Grant category: Research Grants in open competition

Year: 2022

Geography: USA

Cutaneous T-cell lymphoma (CTCL), a cancer of white blood cells, can look like atopic dermatitis. This project from Larisa Geskin aims to develop and validate a screening test for patients with atopic dermatitis (AD) which will aid in identifying undiagnosed CTCL in these patients.

Interleukin-4 (IL-4) and interleukin-13 (IL-13) are essential cytokines (i.e., signaling molecules released from cells to the environment in order to affect other cells), in the pathogenesis of AD. Targeting these cytokines with antibodies such as dupilumab or tralokinumab has proven to be highly effective for therapy of AD.

However, patients with AD may have an increased risk for lymphoma, especially CTCL. There are numerous reports of patients with AD who received dupilumab and later developed CTCL, lethal in some cases. Therefore, therapies targeting IL-4/IL-13 are currently contraindicated for patients with CTCL. However, differentiation between AD and CTCL is difficult because of similar manifestations in the skin and lack of specific markers (i.e., molecules that are uniquely present or expressed in a given condition) for these diseases.

In their preliminary studies Larisa and her team have screened the blood of patients with biopsy-confirmed CTCL and AD for 18 highly selected potential biomarkers using an efficient screening method. Of the 18 tested biomarkers, 9 demonstrated sensitivity and specificity potentially adequate to differentiate CTCL from benign dermatoses. These data serve as a proof of principle and justify further studies, as described in this proposed project, to test a broader set of biomarkers to find the most promising biomarker panel with the highest sensitivity and specificity to develop a simple, robust and inexpensive test, which may be widely accessible to all treating physicians before initiating therapy for AD.

Grant category: Research Grants in open competition

Year: 2019

Geography: Denmark

The survival rate of patients with advanced melanoma has improved in recent years due to the clinical application of immune checkpoint inhibitors, as well as kinase inhibitors in BRAF/RAS-mutated melanoma cases.

However, melanoma remains a fatal diagnosis as a consequence of emerging resistance mechanisms and the absence of reliable biomarkers that identify high-risk tumour subsets, therefore impacting the stratification of these subsets for novel adjuvant therapies.

In the search for novel oncosuppressors that are altered in melanoma, we have found a promising candidate in the protein called AMBRA1. AMBRA1 has a fundamental role in the positive regulation of autophagy – a process which can elicit both pro- and anti-tumorigenic roles. Additionally, AMBRA1 finely modulates other crucial oncogenic processes, such as cell proliferation, cell invasion, and cell death.

Our preliminary research in a mouse model of melanoma has proven Ambra1 to be a crucial oncosuppressor, whose expression has been found highly altered in a number of human melanoma cells. Thus, by applying melanoma cell and mouse models in combination with systems biology approaches and state-of-the-art technologies, we aim to decipher the response of Ambra1-deficient melanomas to the current therapies.

Moreover, we will investigate the role of Ambra1 in regulating lipid metabolism in melanoma, which has recently been shown to profoundly affect its progression. Additionally, our aim is to assess the prognostic relevance of AMBRA1 in human cohorts of melanoma patients and understand whether AMBRA1 expression correlates with disease progression and whether it influences treatment.

Outcomes from this project will pave the way for novel clinical insight into the prognosis and treatment of melanoma patients.

This project is co-supported by a Young Investigator award from the Melanoma Research Alliance (MRA) in the USA of 224,500 USD (https://www.curemelanoma.org/research/grants/).