Publications by authors named "M Lahnalampi"
Background: Targeted therapies exploiting vulnerabilities of cancer cells hold promise for improving patient outcome and reducing side-effects of chemotherapy. However, efficacy of precision therapies is limited in part because of tumor cell heterogeneity. A better mechanistic understanding of how drug effect is linked to cancer cell state diversity is crucial for identifying effective combination therapies that can prevent disease recurrence.
View Article and Find Full Text PDFThe t(1;19) translocation, encoding the oncogenic fusion protein E2A (TCF3)-PBX1, is involved in acute lymphoblastic leukemia (ALL) and associated with a pre-B-cell receptor (preBCR+) phenotype. Relapse in patients with E2A-PBX1+ ALL frequently occurs in the central nervous system (CNS). Therefore, there is a medical need for the identification of CNS active regimens for the treatment of E2A-PBX1+/preBCR+ ALL.
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- Scientists studied how changes in gene regulation, which are not directly about the genes themselves, affect cancer in mice.
- They found that small variations in gene activity can play a big role in how tumors develop and grow.
- Their research helped identify certain non-coding regions linked to cancer and showed how these changes can lead to serious tumors in specific types of cells.
Article Synopsis
- Prostate cancer shows significant variability among patients, making it essential to identify which individuals will benefit most from systemic therapies.
- Through advanced techniques like single-cell ATAC and RNA sequencing, researchers have discovered specific cell subpopulations that respond differently to enzalutamide treatment, including those that can regenerate even after treatment.
- This study highlights the importance of analyzing changes in chromatin and gene expression at the single-cell level to uncover new molecular indicators of treatment response, which could enhance clinical decision-making in prostate cancer care.
Background: Tight regulatory loops orchestrate commitment to B cell fate within bone marrow. Genetic lesions in this gene regulatory network underlie the emergence of the most common childhood cancer, acute lymphoblastic leukemia (ALL). The initial genetic hits, including the common translocation that fuses ETV6 and RUNX1 genes, lead to arrested cell differentiation.
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