Publications by authors named "A G Lomakin"

Article Synopsis
  • The study analyzed the structural organization of the extracellular matrix in rectal adenocarcinoma tissue, comparing samples before and after neoadjuvant radiation therapy using advanced techniques like immunohistochemistry and electron microscopy.
  • Significant differences were found in the expression of collagen types I and III, as well as in the ultrastructural characteristics of the extracellular matrix based on the differentiation level of the tumors and the impact of radiation therapy.
  • High levels of collagen I and broader channels in the matrix were linked to better differentiation in adenocarcinomas without radiation therapy, but to poor differentiation in those after radiation, suggesting a connection to metastasis and worse patient outcomes.
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Cells migrating through complex three-dimensional environments experience considerable physical challenges, including tensile stress and compression. To move, cells need to resist these forces while also squeezing the large nucleus through confined spaces. This requires highly coordinated cortical contractility.

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Spontaneous locomotion is a common feature of most metazoan cells, generally attributed to the properties of actomyosin networks. This force-producing machinery has been studied down to the most minute molecular details, especially in lamellipodium-driven migration. Nevertheless, how actomyosin networks work inside contraction-driven amoeboid cells still lacks unifying principles.

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High levels of autophagy can increase the viability of tumor cells as well as their resistance to chemotherapy. Evaluation of the dynamics of autophagy processes at different stages of carcinogenesis can extend our understanding of melanoma pathogenesis to develop new therapeutic approaches. We performed a comparative study of tumor cell autophagy in stages II and III human skin melanoma.

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Enlarged or irregularly shaped nuclei are frequently observed in tissue cells undergoing senescence. However, it remained unclear whether this peculiar morphology is a cause or a consequence of senescence and how informative it is in distinguishing between proliferative and senescent cells. Recent research reveals that nuclear morphology can act as a predictive biomarker of senescence, suggesting an active role for the nucleus in driving senescence phenotypes.

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