Publications by authors named "Ankita Sankar"
Lymphoma growth, progression, and dissemination require tumor cell interaction with supporting vessels and are facilitated through tumor-promoted angiogenesis, lymphangiogenesis, and/or lymphoma vessel co-option. Vessel co-option has been shown to be responsible for tumor initiation, metastasis, and resistance to anti-angiogenic treatment but is largely uncharacterized in the setting of lymphoma. We developed an in vitro model to study lymphoma-vessel interactions and found that mantle cell lymphoma (MCL) cells co-cultured on Matrigel with human umbilical vein (HUVEC) or human lymphatic (HLEC) endothelial cells migrate to and anneal with newly formed capillary-like (CLS) or lymphatic-like (LLS) structures, consistent with lymphoma-vessel co-option.
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- The study investigates a new protein, αEGFR-E-P125A, designed to inhibit blood vessel formation (angiogenesis) and a cancer-associated process called vasculogenic mimicry (VM) in triple-negative breast cancer (TNBC).
- RNA sequencing of TNBC cells showed that VM activation is linked to specific signaling pathways and that treatment with αEGFR-E-P125A effectively downregulates these pathways.
- In laboratory and animal models, αEGFR-E-P125A demonstrated significant reduction in tumor growth and metastasis, highlighting its potential as a therapeutic strategy for targeting aggressive forms of breast cancer.
Article Synopsis
- Triple negative breast cancer (TNBC) is a tough-to-treat cancer subtype that often leads to high mortality due to its aggressive nature and tendency to spread (metastasize).
- A novel anti-EGFR antibody-endostatin fusion protein, αEGFR-E-P125A, was developed to target EGFR-expressing TNBC tumors, showing strong potential in reducing tumor cell motility and disruption of abnormal blood vessel formation (vasculogenic mimicry) in lab tests.
- In animal studies, αEGFR-E-P125A effectively inhibited tumor growth and metastasis, making it a promising approach for preventing the spread of TNBC due to its dual action against angiogenesis and tumor cell behavior