Publications by authors named "D O Karpova"
Circulating tumor cells (CTCs) drive metastasis, the leading cause of death in individuals with breast cancer. Due to their low abundance in the circulation, robust CTC expansion protocols are urgently needed to effectively study disease progression and therapy responses. Here we present the establishment of long-term CTC-derived organoids from female individuals with metastatic breast cancer.
View Article and Find Full Text PDFIn this study, we carried out large-scale leaf spot symptom observation on vineyards in the Krasnodar Krai of Russia and determined their distribution. The incidence and severity of leaf spot were higher on the Euro-American grapevine hybrids (Bianka, Levokumskij, Avgustin, Moldova, Pervenets Magaracha, Dunavski lazur). A total of 433 isolates that belonged to the genus were isolated from samples with leaf spot.
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- Chromosomal instability contributes significantly to the diversity within tumors, making it a key factor in tumor growth, particularly in complex karyotype acute myeloid leukemia (CK-AML).
- The study revealed various structural variants, including unique patterns of clonal evolution in CK-AML, with a noteworthy 75% of cases exhibiting multiple subclones that continue to evolve.
- By using patient-derived models, researchers identified potential therapies targeting leukemic stem cells, highlighting the importance of genetic changes and cell adaptability in disease progression.
Article Synopsis
- Somatic mutations in hematopoietic stem cells (HSCs) can give these cells a survival advantage, particularly affecting a crucial chromatin modifier gene involved in blood cell formation.* -
- A study using a conditional loss of function model showed that this gene is vital for normal development of red and monocytic blood cells, revealing that HSCs lacking this gene fail to function properly despite having a normal number.* -
- The absence of this gene leads to increased DNA damage and stress in HSCs, activating the p53 pathway, which emphasizes its critical role in preserving HSC function and genomic stability during blood cell development.*
We have reported the direct repair of the sickle cell mutation in vivo in a disease model using vectorized prime editors after hematopoietic stem cell (HSC) mobilization with granulocyte colony-stimulating factor (G-CSF)/AMD3100. The use of G-CSF for HSC mobilization is a hurdle for the clinical translation of this approach. Here, we tested a G-CSF-free mobilization regimen using WU-106, an inhibitor of integrin α4β1, plus AMD3100 for in vivo HSC prime editing in sickle cell disease (SCD) mice.
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