Publications by authors named "Virginia Turati"
Kinase signaling fuels growth of B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Yet its role in leukemia initiation is unclear and has not been shown in primary human hematopoietic cells. We previously described activating mutations in interleukin-7 receptor alpha (IL7RA) in poor-prognosis "ph-like" BCP-ALL.
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- - The study examines genetic differences within childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL) during and after chemotherapy, suggesting that rather than significantly reducing genetic diversity, chemotherapy mainly affects cell behavior and characteristics.
- - Researchers transplanted individual leukemias into multiple hosts to analyze how chemotherapy impacts these tumors at a single-cell level, finding that the treatment decreases the variety of cell states without greatly altering the genetic makeup of the cancer cells.
- - The findings indicate that the reduction of different cell states during chemotherapy leads to a more uniform population of cancer cells, suggesting that this "canalization" of cell states is a key factor in how certain cell types dominate after treatment and may influence outcomes in cancer relapse. *
Article Synopsis
- Checkpoint inhibitors (CPIs) enhance the body's immune response against tumors by analyzing both tumor characteristics and surrounding tissue features, which can help identify how well patients may respond to treatment.
- In a study involving over 1,000 patients with different tumor types, researchers found that clonal tumor mutation burden (TMB) was the strongest predictor of response to CPIs, followed by total TMB and specific gene expressions like CXCL9.
- Additional factors influencing CPI responses were identified, including genetic alterations such as TRAF2 loss linked to better outcomes and CCND1 amplification associated with resistance, as well as specific immune markers found in tumor-infiltrating lymphocytes.
Article Synopsis
- - Tumour mutational burden (TMB) can predict how well patients with non-small cell lung cancer (NSCLC) will respond to immunotherapy, but persistent exposure to antigens can harm T cell function.
- - Research found that higher TMB led to changes in T cell differentiation in untreated NSCLC, such as fewer progenitor-like CD4 T cells and more dysfunctional CD8 and CD4 T cells that resemble those activated by neoantigens.
- - A gene signature indicating the shift from healthy to dysfunctional T cell states was linked to poorer survival rates, highlighting the need for new therapeutic strategies to improve outcomes in NSCLC patients.
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Umbilical cord blood (UCB) has had considerable impact in pediatric stem cell transplantation, but its wider use is limited in part by unit size. Long-term ex vivo culture offers one approach to increase engraftment capacity by seeking to expand stem and progenitor cells. Here, we show brief incubation (8 h) of UCB CD34+ cells with the matricellular regulator Nov (CCN3) increases the frequency of serially transplantable hematopoietic stem cells (HSCs) 6-fold.
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- Somatic mutations and immunoediting contribute to significant diversity within non-small-cell lung cancer (NSCLC), particularly in the T cell antigen receptor (TCR) repertoire.
- The study finds that the number of expanded TCR sequences in tumors varies among and within tumors, correlating with nonsynonymous mutations, and categorizes these TCRs as either ubiquitous (found in all tumor regions) or regional (found in specific areas).
- Ubiquitous TCRs, which show functional impairment in CD8 lymphocytes and are more frequently detected in the blood during tumor resection, offer a promising noninvasive approach to track tumor-reactive TCRs for immunotherapy applications.
Article Synopsis
- * Researchers found a specific type of early B cell progenitor in first-trimester embryos that transitions from myeloid to lymphoid development, suggesting the mutation's origin is tied to embryonic development.
- * Using genome-engineered human pluripotent stem cells, they demonstrated that expressing ETV6-RUNX1 creates a pre-leukemic state, evidenced by abnormal B cell development and myeloid gene expression patterns.
Tumor relapse is associated with dismal prognosis, but responsible biological principles remain incompletely understood. To isolate and characterize relapse-inducing cells, we used genetic engineering and proliferation-sensitive dyes in patient-derived xenografts of acute lymphoblastic leukemia (ALL). We identified a rare subpopulation that resembled relapse-inducing cells with combined properties of long-term dormancy, treatment resistance, and stemness.
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