Mara De Martino

ORCID: 0000-0002-3049-6495
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About
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Research Areas
  • HER2/EGFR in Cancer Research
  • Monoclonal and Polyclonal Antibodies Research
  • Glycosylation and Glycoproteins Research
  • Cancer Immunotherapy and Biomarkers
  • Cancer Cells and Metastasis
  • TGF-β signaling in diseases
  • Cancer, Lipids, and Metabolism
  • Cancer, Hypoxia, and Metabolism
  • Immune cells in cancer
  • interferon and immune responses
  • Peroxisome Proliferator-Activated Receptors
  • Immune Cell Function and Interaction
  • Immunotherapy and Immune Responses
  • Cancer Research and Treatments
  • Cytokine Signaling Pathways and Interactions
  • Breast Lesions and Carcinomas
  • Cancer-related molecular mechanisms research
  • Glioma Diagnosis and Treatment
  • Metabolomics and Mass Spectrometry Studies
  • Breast Cancer Treatment Studies
  • Pancreatic and Hepatic Oncology Research
  • Telomeres, Telomerase, and Senescence
  • Cell Adhesion Molecules Research
  • Inflammatory mediators and NSAID effects
  • Epigenetics and DNA Methylation

Cornell University
2019-2025

Weill Cornell Medicine
2020-2025

Experimental Medicine and Biology Institute
2015-2022

Consejo Nacional de Investigaciones Científicas y Técnicas
2015-2022

Although trastuzumab administration improved the outcome of HER2-positive breast cancer patients, resistance events hamper its clinical benefits. We demonstrated that TNFα stimulation in vitro induces cell lines. Here, we explored mechanism TNFα-induced and therapeutic strategies to overcome it.Trastuzumab-sensitive cells, genetically engineered stably overexpress TNFα, de novo trastuzumab-resistant tumors, were used evaluate response TNFα-blocking antibodies effectiveness respectively....

10.1158/1078-0432.ccr-16-0970 article EN Clinical Cancer Research 2016-10-04

Abstract Increased regulatory T cells (Treg) after radiotherapy have been reported, but the mechanisms of their induction remain incompletely understood. TGFβ is known to foster Treg differentiation within tumors and activated following radiotherapy. Thus, we hypothesized that blockade would result in decreased Tregs irradiated tumor microenvironment. We found increased mice treated with focal blockade. This increase was mediated by upregulation another family member, activin A. In vitro, A...

10.1158/2326-6066.cir-19-0305 article EN Cancer Immunology Research 2020-10-22

Abstract Cytosolic DNA promotes inflammatory responses upon detection by the cyclic GMP‐AMP (cGAMP) synthase (cGAS). It has been suggested that cGAS downregulation is an immune escape strategy harnessed tumor cells. Here, we used glioblastoma cells show undetectable levels to address if alternative pathways can promote pro‐inflammatory signaling. We DNA‐PK repair complex (i) drives cGAS‐independent IRF3‐mediated type I Interferon and (ii) its catalytic activity required for cGAS‐dependent...

10.15252/embj.2022111961 article EN cc-by The EMBO Journal 2022-12-27

Invasive micropapillary carcinoma of the breast (IMPC) is a histological tumor variant that occurs with low frequency characterized by an inside-out formation clusters pseudopapillary arrangement. IMPC aggressive poor clinical outcome. In addition, this subtype usually expresses human epidermal growth factor receptor 2 (HER2) which also correlates more tumor. work we studied significance in HER2-positive cancer patients treated adjuvant trastuzumab. We analyzed mucin 4 (MUC4) expression as...

10.1186/s12885-017-3897-x article EN cc-by BMC Cancer 2017-12-01

Stat3 is constitutively activated in several tumor types and plays an essential role maintaining their malignant phenotype immunosupression. To take advantage of the promising antitumor activity targeting, it vital to understand mechanism by which regulates both cell autonomous non-autonomous processes. Here, we demonstrated that turning off constitutive activation different cancer induces senescence, thus revealing addiction. Taking senescence-associated secretory (SASP) induced silencing...

10.1080/2162402x.2020.1715767 article EN cc-by-nc OncoImmunology 2020-01-01

Triple-negative breast cancer (TNBC) is clinically defined by the absence of estrogen and progesterone receptors lack membrane overexpression or gene amplification receptor tyrosine kinase ErbB-2/HER2. Due to TNBC heterogeneity, clinical biomarkers targeted therapies for this disease remain elusive. We demonstrated that ErbB-2 localized in nucleus (NErbB-2) cells primary tumors, from where it drives growth. also discovered expresses both wild-type (WTErbB-2) alternative isoform c (ErbB-2c)....

10.1038/s41419-022-04855-0 article EN cc-by Cell Death and Disease 2022-05-09

Abstract Accumulated findings have demonstrated the presence of bidirectional interactions between progesterone receptor (PR) and ErbB family tyrosine kinases signaling pathways in breast cancer. We previously revealed signal transducer activator transcription 3 (Stat3) as a nodal convergence point said proving that Stat3 is activated by one ErbBs' ligands, heregulin (HRG)β1 via ErbB2 through co-option PR molecule. Here, we found HRGβ1 induced recruitment to promoters progestin-regulated...

10.1210/me.2015-1170 article EN Molecular Endocrinology 2015-09-04

Abstract Background: Novel strategies aimed to overcome trastuzumab (Tz) resistance of HER2+ breast cancer (BC) are needed. Recently, we demonstrated a novel immune evasion strategy used by BC where tumor necrosis factor alpha (TNF) induces upregulation the transmembrane glycoprotein mucin 4 (MUC4) via NF-kB activation impair Tz binding that prevents antibody mediated killing cells. Etanercept, non-selective inhibitor soluble and TNF (sTNF, tmTNF), downregulated MUC4 expression sensitized de...

10.1158/1538-7445.sabcs18-p6-20-14 article EN Cancer Research 2019-02-15

<h3>Background</h3> Radiation therapy (RT) induces nucleic acid sensing followed by cancer cell-intrinsic interferon (IFN-I) responses in various cancers. However, combining RT with immunotherapy glioblastoma has failed to improve patient survival, suggesting robust immunosuppression. Our previous findings showed that a metabolic shift towards fatty synthase (FASN)-mediated lipid synthesis, supporting survival. Since metabolism hampers IFN-I viral immunity, we hypothesized FASN might...

10.1136/jitc-2024-sitc2024.1358 article EN cc-by-nc Regular and Young Investigator Award Abstracts 2024-11-01

<h3>Background</h3> Radiation therapy (RT) is the standard of care for glioblastoma. While RT can trigger abscopal responses in some cancers by stimulating immune system against tumor, glioblastoma inevitably recurs after RT, indicating that does not generate a long-lasting response. Our recent work shows drives resistance creating lipid-enriched environment tolerant to survival. This metabolic shift, mediated fatty acid synthase (FASN), enhances production prostaglandin E2, known promote...

10.1136/jitc-2024-sitc2024.0843 article EN cc-by-nc Regular and Young Investigator Award Abstracts 2024-11-01
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