Dina Morein
A5041643185- Cytokine Signaling Pathways and Interactions
- Cancer Immunotherapy and Biomarkers
- Cancer Cells and Metastasis
- Chemokine receptors and signaling
- Cancer, Stress, Anesthesia, and Immune Response
- Immune cells in cancer
- Immunotherapy and Immune Responses
- Bioactive Compounds and Antitumor Agents
- Monoclonal and Polyclonal Antibodies Research
- Psoriasis: Treatment and Pathogenesis
- Inflammasome and immune disorders
- Synthesis and Reactions of Organic Compounds
- Urticaria and Related Conditions
- Immune Cell Function and Interaction
- Inflammatory Biomarkers in Disease Prognosis
- Inflammatory mediators and NSAID effects
- Mesenchymal stem cell research
Compugen (Israel)
2024
Tel Aviv University
2019-2022
The tumor microenvironment (TME) plays key roles in promoting disease progression the aggressive triple-negative subtype of breast cancer (TNBC; Basal/Basal-like). Here, we took an integrative approach and determined impact tumor-stroma-inflammation networks on pro-metastatic phenotypes TNBC. With TCGA dataset found that pro-inflammatory cytokines necrosis factor α (TNFα) interleukin 1β (IL-1β), as well their target chemokines CXCL8 (IL-8), CCL2 (MCP-1), CCL5 (RANTES) were expressed at...
Stromal cells and pro-inflammatory cytokines play key roles in promoting the aggressiveness of triple-negative breast cancers (TNBC; Basal/Basal-like). In our previous study we demonstrated that stimulation TNBC mesenchymal stem (MSCs) co-cultures by cytokine tumor necrosis factor α (TNFα) has led to increased metastasis-related properties vitro vivo. this context, elevated release pro-metastatic chemokines CXCL8 (IL-8) CCL5 (RANTES) was noted TNFα- interleukin-1β (IL-1β)-stimulated TNBC:MSC...
The pro-inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β) are expressed simultaneously have tumor-promoting roles in breast cancer. In parallel, mesenchymal stem cells (MSCs) undergo conversion at the site to cancer-associated fibroblasts (CAFs), which generally connected enhanced progression. Here, we determined impact of consistent inflammatory stimulation on stromal cell plasticity. MSCs that were persistently stimulated by TNFα + IL-1β (generally 14–18...
Recombinant cytokines have limited anticancer efficacy mostly due to a narrow therapeutic window and systemic adverse effects. IL18 is an inflammasome-induced proinflammatory cytokine, which enhances T- NK-cell activity stimulates IFNγ production. The of naturally blocked by high-affinity endogenous binding protein (IL18BP). IL18BP induced in the tumor microenvironment (TME) response upregulation negative feedback mechanism. In this study, we found that upregulated TME compared with...
Therapies targeting the PD-L1/PD-1 axis have recently been introduced to triple-negative breast cancer (TNBC) with limited efficacy, suggesting that this promotes tumor progression through mechanisms other than immune suppression. Here, we over-expressed WT-PD-L1 in human TNBC cells (express endogenous PD-L1) and luminal-A (no PD-L1 expression) demonstrated cell-autonomous activities lead increased cell growth, invasion release of pro-metastatic factors (CXCL8, sICAM-1, GM-CSF). These were...
Chronic inflammation promotes cancer progression by affecting the tumor cells and their microenvironment. Here, we demonstrate that a continuous stimulation (~6 weeks) of triple-negative breast (TNBC) proinflammatory cytokines necrosis factor α (TNFα) + interleukin 1β (IL-1β) changed expression hundreds genes, skewing towards phenotype. While not stemness, TNFα IL-1β has increased cell dispersion induced hybrid metabolic phenotype in TNBC cells; this was indicated transcription-independent...
Abstract IL-18 is an inflammasome induced proinflammatory cytokine that augments T and NK cell activity stimulates IFNγ production. The of naturally blocked by a high affinity endogenous binding protein (IL-18BP). IL-18BP in the tumor microenvironment (TME) response to upregulation negative feedback mechanism. By evaluating 88 human specimens serum samples we were able show upregulated TME (median 11.2ng/gr) compared 0.3ng/ml). Moreover, showed most bound IL-18BP. IL-18BP-bound levels...
<p>Supplemental Figure S5. IL-18BP blockade alters the immune infiltrate composition of E0771 tumors.</p>
<p>Supplemental Figure S5. IL-18BP blockade alters the immune infiltrate composition of E0771 tumors.</p>
<p>Supplemental Figure S2. COM503 releases IL-18 activity in biochemical and functional assays.</p>
<p>Supplemental Figure S3. Antitumor activity of anti-mouse-IL-18BP Ab in mice studies.</p>
<div>Abstract<p>Recombinant cytokines have limited anticancer efficacy mostly due to a narrow therapeutic window and systemic adverse effects. IL18 is an inflammasome-induced proinflammatory cytokine, which enhances T- NK-cell activity stimulates IFNγ production. The of naturally blocked by high-affinity endogenous binding protein (IL18BP). IL18BP induced in the tumor microenvironment (TME) response upregulation negative feedback mechanism. In this study, we found that...
<p>Supplemental Figure S1. IL-18BP is a potential soluble immune checkpoint in cancer.</p>
<p>Supplemental Figure S4. Anti-IL-18BP Ab induced immunogenic memory response in E0771 tumor model.</p>
<p>Supplemental Figure S1. IL-18BP is a potential soluble immune checkpoint in cancer.</p>
<p>Supplemental Figure S3. Antitumor activity of anti-mouse-IL-18BP Ab in mice studies.</p>
<p>Supplemental Figure S4. Anti-IL-18BP Ab induced immunogenic memory response in E0771 tumor model.</p>
<p>Supplemental Figure S2. COM503 releases IL-18 activity in biochemical and functional assays.</p>
<div>Abstract<p>Recombinant cytokines have limited anticancer efficacy mostly due to a narrow therapeutic window and systemic adverse effects. IL18 is an inflammasome-induced proinflammatory cytokine, which enhances T- NK-cell activity stimulates IFNγ production. The of naturally blocked by high-affinity endogenous binding protein (IL18BP). IL18BP induced in the tumor microenvironment (TME) response upregulation negative feedback mechanism. In this study, we found that...
<p>Supplementary Methods</p>
<p>Supplementary Methods</p>
Accumulating evidence substantiates potent pro-malignancy roles for stromal cells, such as bone marrow-derived mesenchymal stem cells and cancer-associated fibroblasts, in breast cancer. In parallel, the tumor microenvironment (TME) is enriched with pro-inflammatory cytokines that play causative promoting disease course. Focusing on aggressive triple negative subtype of cancer (TNBC), we have analyzed by patient dataset studies, vitro co-culture experiments vivo model systems interactions...