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Journal articles on the topic 'Destruction of cancer cells'

Author: Grafiati

Published: 28 May 2022

Last updated: 31 July 2025

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1

Harada, Takeshi, Masahiro Hiasa, Jumpei Teramachi, and Masahiro Abe. "Myeloma–Bone Interaction: A Vicious Cycle via TAK1–PIM2 Signaling." Cancers 13, no. 17 (2021): 4441. http://dx.doi.org/10.3390/cancers13174441.

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Multiple myeloma (MM) has a propensity to develop preferentially in bone and form bone-destructive lesions. MM cells enhance osteoclastogenesis and bone resorption through activation of the RANKL–NF-κB signaling pathway while suppressing bone formation by inhibiting osteoblastogenesis from bone marrow stromal cells (BMSCs) by factors elaborated in the bone marrow and bone in MM, including the soluble Wnt inhibitors DKK-1 and sclerostin, activin A, and TGF-β, resulting in systemic bone destruction with loss of bone. Osteocytes have been drawn attention as multifunctional regulators in bone meta

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2

Weiss, Leonard. "The hemodynamic destruction of circulating cancer cells." Biorheology 24, no. 2 (1987): 105–15. http://dx.doi.org/10.3233/bir-1987-24204.

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Vacarro, Kyle, Juliet Allen, Asaf Maoz, Sarah Reeves, Aaron Hata, and Kipp Weiskopf. "Abstract 1300: Targeted therapies prime lung cancer cells for macrophage-mediated destruction." Cancer Research 82, no. 12_Supplement (2022): 1300. http://dx.doi.org/10.1158/1538-7445.am2022-1300.

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Abstract The CD47/SIRPa axis is an immune checkpoint that regulates macrophage anti-tumor function. Therapies that block CD47 on cancer cells show promise in clinical trials for solid and hematologic malignancies, particularly when combined with other anticancer agents. However, the best combination strategies for using CD47-blocking therapies remain unknown. In this study, we developed a novel in vitro screening platform to identify drugs that render cancer cells more vulnerable to macrophage attack. We performed an unbiased screen of 800 FDA-approved drugs using primary human macrophages and

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Roodman, G. David. "Biology of Osteoclast Activation in Cancer." Journal of Clinical Oncology 19, no. 15 (2001): 3562–71. http://dx.doi.org/10.1200/jco.2001.19.15.3562.

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ABSTRACT: Bone is a frequent site of cancer metastasis. Bone metastases can result in bone destruction or new bone formation. Bone destruction is mediated by factors produced or induced by tumor cells that stimulate formation and activation of osteoclasts, the normal bone-resorbing cells. Local bone destruction also occurs in patients with osteoblastic metastases and may precede or occur simultaneously with increased bone formation. Several factors, including interleukin (IL)-1, IL-6, receptor activator of NF-kappaB (RANK) ligand, parathyroid hormone-related protein (PTHrP), and macrophage inf

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Hampton, Tracy. "Bacteria Protect Colorectal Cancer Cells From Immune Destruction." JAMA 313, no. 13 (2015): 1305. http://dx.doi.org/10.1001/jama.2015.2854.

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6

Chonghaile, Tríona Ní. "BH3 mimetics: Weapons of cancer cell destruction." Science Translational Medicine 11, no. 475 (2019): eaaw5311. http://dx.doi.org/10.1126/scitranslmed.aaw5311.

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7

Visochek, Leonid, Asher Castiel, Leonid Mittelman, et al. "Exclusive destruction of mitotic spindles in human cancer cells." Oncotarget 8, no. 13 (2017): 20813–24. http://dx.doi.org/10.18632/oncotarget.15343.

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8

Weiss, Leonard. "Deformation-driven destruction of cancer cells in the microvasculature." Clinical & Experimental Metastasis 11, no. 5 (1993): 430–33. http://dx.doi.org/10.1007/bf00132986.

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9

Qiao, Fangfang, Ryan Gordon, Abhinandan Pattanayak, et al. "Abstract 321: BTE-EN1, a novel acting heterobifunctional compound inhibiting bone destruction by established prostate cancer bone metastasis." Cancer Research 85, no. 8_Supplement_1 (2025): 321. https://doi.org/10.1158/1538-7445.am2025-321.

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Bone destruction by prostate cancer (PCa) metastasis is a major cause of morbidity and mortality. In order to destroy bone, PCa and bone cells stimulate each other in a process that requires their coordinated movement within bone itself. To therapeutically inhibit this process, we synthesized the first-in-class heterobifunctional compound, BTE-EN1. One group is a selective inhibitor of cancer cell motility, discovered by us (Nature Communications 2018). It is chemically coupled to a bisphosphonate group, which binds to bone mineral and enables targeted delivery of the therapeutic to bone-destr

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Singh, S., S. R. Ross, M. Acena, D. A. Rowley, and H. Schreiber. "Stroma is critical for preventing or permitting immunological destruction of antigenic cancer cells." Journal of Experimental Medicine 175, no. 1 (1992): 139–46. http://dx.doi.org/10.1084/jem.175.1.139.

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Inoculated immunogenic cancer cells after initial growth are potentially rejected by specific host immunity; however, the outcome of the interaction between host and inoculated cancer cells is a function of multiple factors including the route of inoculation, the number of cells, the density of antigens on the injected cancer cells, and the state of the immune system of the host. In the present study, we have examined a different kind of variable: the stroma that inoculated tumor cells initially reside in. The impetus to examine this factor arises from observations that cancer cells from sever

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Ismail, Thamir M., Rachel G. Crick, Min Du, et al. "Targeted Destruction of S100A4 Inhibits Metastasis of Triple Negative Breast Cancer Cells." Biomolecules 13, no. 7 (2023): 1099. http://dx.doi.org/10.3390/biom13071099.

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Most patients who die of cancer do so from its metastasis to other organs. The calcium-binding protein S100A4 can induce cell migration/invasion and metastasis in experimental animals and is overexpressed in most human metastatic cancers. Here, we report that a novel inhibitor of S100A4 can specifically block its increase in cell migration in rat (IC50, 46 µM) and human (56 µM) triple negative breast cancer (TNBC) cells without affecting Western-blotted levels of S100A4. The moderately-weak S100A4-inhibitory compound, US-10113 has been chemically attached to thalidomide to stimulate the protea

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Visochek, Leonid, Asher Castiel, Leonid Mittelman, et al. "Correction: Exclusive destruction of mitotic spindles in human cancer cells." Oncotarget 11, no. 14 (2020): 1290–91. http://dx.doi.org/10.18632/oncotarget.27499.

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13

Muniraj, Nethaji, Sumit Siddharth, and Dipali Sharma. "Bioactive Compounds: Multi-Targeting Silver Bullets for Preventing and Treating Breast Cancer." Cancers 11, no. 10 (2019): 1563. http://dx.doi.org/10.3390/cancers11101563.

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Each cell in our body is designed with a self-destructive trigger, and if damaged, can happily sacrifice itself for the sake of the body. This process of self-destruction to safeguard the adjacent normal cells is known as programmed cell death or apoptosis. Cancer cells outsmart normal cells and evade apoptosis and it is one of the major hallmarks of cancer. The cardinal quest for anti-cancer drug discovery (bioactive or synthetic compounds) is to be able to re-induce the so called “programmed cell death” in cancer cells. The importance of bioactive compounds as the linchpin of cancer therapeu

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14

Laptev, R., M. Nisnevitch, G. Siboni, Z. Malik, and M. A. Firer. "Intracellular chemiluminescence activates targeted photodynamic destruction of leukaemic cells." British Journal of Cancer 95, no. 2 (2006): 189–96. http://dx.doi.org/10.1038/sj.bjc.6603241.

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15

Shityakov, Sergey, Viacheslav Kravtsov, Ekaterina V. Skorb, and Michael Nosonovsky. "Ergodicity Breaking and Self-Destruction of Cancer Cells by Induced Genome Chaos." Entropy 26, no. 1 (2023): 37. http://dx.doi.org/10.3390/e26010037.

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During the progression of some cancer cells, the degree of genome instability may increase, leading to genome chaos in populations of malignant cells. While normally chaos is associated with ergodicity, i.e., the state when the time averages of relevant parameters are equal to their phase space averages, the situation with cancer propagation is more complex. Chromothripsis, a catastrophic massive genomic rearrangement, is observed in many types of cancer, leading to increased mutation rates. We present an entropic model of genome chaos and ergodicity and experimental evidence that increasing t

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Zhong, Zhisheng, Robert A. Kazmierczak, Alison Dino, Rula Khreis, Abraham Eisenstark, and Heide Schatten. "Salmonella–Host Cell Interactions, Changes in Host Cell Architecture, and Destruction of Prostate Tumor Cells with Genetically AlteredSalmonella." Microscopy and Microanalysis 13, no. 5 (2007): 372–83. http://dx.doi.org/10.1017/s1431927607070833.

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Increasingly, genetically modifiedSalmonellaare being explored as a novel treatment for cancer becauseSalmonellapreferentially replicate within tumors and destroy cancer cells without causing the septic shock that is typically associated with wild-typeS. typhimuriuminfections. However, the mechanisms by which genetically modifiedSalmonellastrains preferentially invade cancer cells have not yet been addressed in cellular detail. Here we present data that showS. typhimuriumstrains VNP20009, LT2, and CRC1674 invasion of PC-3M prostate cancer cells.S. typhimurium-infected PC-3M human prostate canc

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V, Surya, Mohammed Manaz, Preethi Sharon, and Kirubanandan Shanmugam. "Ultrasound-Targeted Microbubble Destruction (UTMD): Targeted Nanodrug Delivery in Cancer." BOHR International Journal of Cancer Research 1, no. 1 (2022): 13–15. http://dx.doi.org/10.54646/bijcr.003.

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Cavitation is a process of formation of microbubbles in the ultrasound method. These microbubbles have the potential to interact with either the normal cells or cancerous cells through developing drug delivery mechanism and targeting. This letter deals with the role and application of microbubbles formed via the cavitation process in the ultrasound method for the treatment of cancer.

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Shanmugam, Kirubanandan, Surya V, Mohammed Manaz, and Preethi Sharon. "Ultrasound-Targeted Microbubble Destruction (UTMD): Targeted Nanodrug Delivery in Cancer." BOHR Journal of Cancer Research 1, no. 1 (2023): 14–16. http://dx.doi.org/10.54646/bjcr.2023.03.

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Cavitation is a process of formation of microbubbles in the ultrasound method. These microbubbles have the potential to interact with either the normal cells or cancerous cells through developing drug delivery mechanism and targeting. This letter deals with the role and application of microbubbles formed via the cavitation process in the ultrasound method for the treatment of cancer.

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19

Hou, Jin, Yong Du, Tao Zhang, Chandra Mohan, and Oomman K. Varghese. "PEGylated (NH4)xWO3 nanorod mediated rapid photonecrosis of breast cancer cells." Nanoscale 11, no. 21 (2019): 10209–19. http://dx.doi.org/10.1039/c9nr01077g.

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Altevogt, Peter, Marei Sammar, Laura Hüser, Viktor Umansky, and Jochen Utikal. "Perspective – Escape from destruction: how cancer-derived EVs are protected from phagocytosis." Extracellular vesicles as biomarkers – in pathophysiology, physical education and home office? 2, no. 1 (2020): 60–64. http://dx.doi.org/10.47184/tev.2020.01.08.

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There is evidence that cancer-derived extracellular vesicles (EVs) have nearby and distant effects in the body. In order to reach distant sites, EVs need to travel through the blood stream and organs where they encounter a hostile environment in the form or phagocytic cells. However, the stability and homeostasis in the blood circulation and in the tumor microenvironment are not well understood. Phagocytosis is an important mechanism for the clearance of apoptotic and necrotic cells. As exosomes (small EV) express “eat-me” signals such as phosphatidyl-serine, it is likely that they are cleared

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Frayssinet, Patrick, Daniel Ciocca, and Nicole Rouquet. "Calcium Phosphate Powder for Cancer Vaccination." Key Engineering Materials 361-363 (November 2007): 1207–10. http://dx.doi.org/10.4028/www.scientific.net/kem.361-363.1207.

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Cancer cells synthesize abnormal proteins and peptides which are associated to heat shock proteins being overproduced by these cells due to the stress induced by the particular biology of cancer tissue. We have purified on hydroxylapatite powder heat shock proteins using the HAparticles as purification bed, vectors for the proteins and vaccination adjuvant. The powder make possible that the purified HSPs and their associated peptides are transfected to the antigen presenting cells and presented to the T cells for the destruction of the cancer cells bearing the antigens.

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22

Kang, Eun Ji, Sun Kyoung Lee, Kwang-Kyun Park, Seung Hwa Son, Ki Rim Kim, and Won-Yoon Chung. "Liensinine and Nuciferine, Bioactive Components of Nelumbo nucifera, Inhibit the Growth of Breast Cancer Cells and Breast Cancer-Associated Bone Loss." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/1583185.

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Once breast cancer cells grow aggressively and become lodged in the skeleton through migration and invasion, they interact with bone microenvironment and accelerate much more tumor growth and bone destruction. We investigated whether liensinine and nuciferine, major active components in Nelumbo nucifera (lotus), could prevent breast cancer cell-mediated bone destruction. Liensinine and nuciferine inhibited the growth of MDA-MB-231 and MCF-7 human breast cancer cells by inducing apoptosis and inhibiting proliferation via cell cycle arrest. Liensinine treatment led to the increased Bax/Bcl-2 rat

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23

Zhang, Bin, Natalie A. Bowerman, Joseph K. Salama, et al. "Induced sensitization of tumor stroma leads to eradication of established cancer by T cells." Journal of Experimental Medicine 204, no. 1 (2007): 49–55. http://dx.doi.org/10.1084/jem.20062056.

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Targeting cancer cells, as well as the nonmalignant stromal cells cross-presenting the tumor antigen (Ag), can lead to the complete destruction of well-established solid tumors by adoptively transferred Ag-specific cytotoxic T lymphocytes (CTLs). If, however, cancer cells express only low levels of the Ag, then stromal cells are not destroyed, and the tumor escapes as Ag loss variants. We show that treating well-established tumors expressing low levels of Ag with local irradiation or a chemotherapeutic drug causes sufficient release of Ag to sensitize stromal cells for destruction by CTLs. Thi

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24

Na, Di, Fu-Nan Liu, Zhi-Feng Miao, Zong-Min Du, and Hui-Mian Xu. "Astragalus extract inhibits destruction of gastric cancer cells to mesothelial cells by anti-apoptosis." World Journal of Gastroenterology 15, no. 5 (2009): 570. http://dx.doi.org/10.3748/wjg.15.570.

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25

Hwang, Kuo Chu, Po Dong Lai, Chi-Shiun Chiang, Pei-Jen Wang, and Chiun-Jye Yuan. "Neutron capture nuclei-containing carbon nanoparticles for destruction of cancer cells." Biomaterials 31, no. 32 (2010): 8419–25. http://dx.doi.org/10.1016/j.biomaterials.2010.07.057.

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26

Wang, Jun-Feng, Jia-Bei Wang, Hua Chen, et al. "Ultrasound-mediated microbubble destruction enhances gene transfection in pancreatic cancer cells." Advances in Therapy 25, no. 5 (2008): 412–21. http://dx.doi.org/10.1007/s12325-008-0051-9.

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27

Xu, C. S., A. W. N. Leung, L. Liu, and X. S. Xia. "LED-activated pheophorbide a induces cellular destruction of colon cancer cells." Laser Physics Letters 7, no. 7 (2010): 544–48. http://dx.doi.org/10.1002/lapl.201010008.

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28

Roberts, David M., Mira I. Pronobis, John S. Poulton, Eric G. Kane, and Mark Peifer. "Regulation of Wnt signaling by the tumor suppressor adenomatous polyposis coli does not require the ability to enter the nucleus or a particular cytoplasmic localization." Molecular Biology of the Cell 23, no. 11 (2012): 2041–56. http://dx.doi.org/10.1091/mbc.e11-11-0965.

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Wnt signaling plays key roles in development and disease. The tumor suppressor adenomatous polyposis coli (APC) is an essential negative regulator of Wnt signaling. Its best-characterized role is as part of the destruction complex, targeting the Wnt effector β-catenin (βcat) for phosphorylation and ultimate destruction, but several studies suggested APC also may act in the nucleus at promoters of Wnt-responsive genes or to shuttle βcat out for destruction. Even in its role in the destruction complex, APC's mechanism of action remains mysterious. We have suggested APC positions the destruction

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Azuma, Takeshi, Sheng Yao, Gefeng Zhu, Andrew S. Flies, Sarah J. Flies, and Lieping Chen. "B7-H1 is a ubiquitous antiapoptotic receptor on cancer cells." Blood 111, no. 7 (2008): 3635–43. http://dx.doi.org/10.1182/blood-2007-11-123141.

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Abstract B7-H1 is an immunoglobulin-like immune suppressive molecule broadly detectable on the majority of human and rodent cancers, and its functions have been attributed to delivering an inhibitory signal to its counter-receptor programmed death-1 (PD-1) on T cells. Here we report that B7-H1 on cancer cells receives a signal from PD-1 to rapidly induce resistance against T cell–mediated killing because crippling signaling capacity of B7-H1 but not PD-1 ablates this resistance. Importantly, loss of B7-H1 signaling is accompanied by increased susceptibility to immune-mediated tumoricidal activ

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Shariff, Afreen Idris, Sohail Syed, Rebecca A. Shelby, et al. "Novel cancer therapies and their association with diabetes." Journal of Molecular Endocrinology 62, no. 2 (2019): R187—R199. http://dx.doi.org/10.1530/jme-18-0002.

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Over the last decade, there has been a shift in the focus of cancer therapy from conventional cytotoxic drugs to therapies more specifically directed to cancer cells. These novel therapies include immunotherapy, targeted therapy and precision medicine, each developed in great part with a goal of limiting collateral destruction of normal tissues, while enhancing tumor destruction. Although this approach is sound in theory, even new, specific therapies have some undesirable, ‘off target effects’, in great part due to molecular pathways shared by neoplastic and normal cells. One such undesirable

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31

Lin, Jui-Teng, Yueh-Sheng Chiang, Guang-Hong Lin, Hsinyu Lee, and Hsia-Wei Liu. "In Vitro Photothermal Destruction of Cancer Cells Using Gold Nanorods and Pulsed-Train Near-Infrared Laser." Journal of Nanomaterials 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/861385.

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We present a novel pulsed-train near-IR diode laser system with real-time temperature monitoring of the laser-heated cancer cell mixed in gold nanorod solution. Near-IR diode laser at 808 nm matching the gold nanorod absorption peak (with an aspect ratio about 4.0) was used in this study. Both surface and volume temperatures were measured and kept above 43°C, the temperature for cancer cells destruction. The irradiation time needed in our pulsed-train system with higher laser fluence for killing the cancel cells is about 1–3 minutes, much shorter than conventional methods (5–10 minutes). Cell

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32

Schietinger, Andrea, Mary Philip, Rebecca B. Liu, Karin Schreiber, and Hans Schreiber. "Bystander killing of cancer requires the cooperation of CD4+ and CD8+ T cells during the effector phase." Journal of Experimental Medicine 207, no. 11 (2010): 2469–77. http://dx.doi.org/10.1084/jem.20092450.

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Cancers frequently evade cytotoxic T lymphocyte–mediated destruction through loss or down-regulation of tumor antigens and antigen-presenting major histocompatibility complex molecules. Therefore, we have concentrated our efforts on immunological strategies that destroy nonmalignant stromal cells essential for the survival and growth of cancer cells. In this study, we developed a non–T cell receptor transgenic, immunocompetent tumor model to determine whether tumor-bearing hosts’ own immune systems could eliminate cancer cells through stromal targeting and what role CD4+ T cells play alongside

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Tsuneo, Ishida. "Highly Bactericidal Silver () against Bacteria and Anti-Cancer Activity of Ag+ ions for Regulation of Cancer/Tumor Cell Growth." Cancer Medicine Journal 1, no. 1 (2018): 24–36. http://dx.doi.org/10.46619/cmj.2018.1-1004.

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Since highly bactericidal silver (I) ions against bacteria have been obtained, as highly accurate results, prospect effects of silver (I) ions for regulation of cancer and tumor cell growth can be expected to occur even at apoptotic conditions. This mini-review article is reported that as an availability for most highly bactericidal effect of Ag+ ions, the regulation of cancer cell growth may be able to be achieved by Ag+ ions-mediated hydrolyzing and degrading functions. Bactericidal effects of silver (I) ions on bacteriolyses of bacterial cell walls by activation of peptidoglycan (PGN) autol

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34

Xie, K., S. Huang, Z. Dong, S. H. Juang, Y. Wang, and I. J. Fidler. "Destruction of Bystander Cells by Tumor Cells Transfected With Inducible Nitric Oxide (NO) Synthase Gene." JNCI Journal of the National Cancer Institute 89, no. 6 (1997): 421–27. http://dx.doi.org/10.1093/jnci/89.6.421.

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Plitas, George, and Alexander Y. Rudensky. "Regulatory T Cells in Cancer." Annual Review of Cancer Biology 4, no. 1 (2020): 459–77. http://dx.doi.org/10.1146/annurev-cancerbio-030419-033428.

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The immune system has evolved complex effector mechanisms to protect the host against a diversity of pathogenic organisms and regulatory adaptations that can curtail pathological sequelae of inflammatory events, prevent autoimmunity, and assist in tissue repair. Cancers, by virtue of their local manifestations of tissue dysfunction and destruction, inflammation, and genomic instability, can evoke these protective mechanisms, which support the progression of tumors and prevent their immune eradication. Central to these processes is a subset of CD4+ T cells, known as regulatory T (Treg) cells, t

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Voros, Andras, Bernadett Kormos, Tibor Valyi-Nagy, and Klara Valyi-Nagy. "Increased Resistance of Breast, Prostate, and Embryonic Carcinoma Cells against Herpes Simplex Virus in Three-Dimensional Cultures." ISRN Oncology 2013 (December 22, 2013): 1–9. http://dx.doi.org/10.1155/2013/104913.

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In previous studies we found that uveal melanoma cells grown in extracellular matrix (ECM)-containing three-dimensional (3D) cultures have increased resistance against herpes simplex virus type 1 (HSV-1)-mediated destruction relative to cells cultured without ECM. Using additional tumor cell types including MB-231 human breast cancer cells, PC-3 human prostate cancer cells, and P19 mouse embryonal carcinoma cells, we show here that tumor cell lines other than melanoma are also more resistant to HSV-1-mediated destruction in 3D cultures than cells grown in 2D. We also demonstrate here that one

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Lopez, Sara, Nicolas Hallali, Yoann Lalatonne, et al. "Magneto-mechanical destruction of cancer-associated fibroblasts using ultra-small iron oxide nanoparticles and low frequency rotating magnetic fields." Nanoscale Advances 4, no. 2 (2022): 421–36. http://dx.doi.org/10.1039/d1na00474c.

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Pavlíčková, Vladimíra, Michal Jurášek, Silvie Rimpelová, et al. "Oxime-based 19-nortestosterone–pheophorbide a conjugate: bimodal controlled release concept for PDT." Journal of Materials Chemistry B 7, no. 36 (2019): 5465–77. http://dx.doi.org/10.1039/c9tb01301f.

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Chu, Binbin, Fei Peng, Houyu Wang, Yuanyuan Su, and Yao He. "Synergistic effects between silicon nanowires and doxorubicin at non-toxic doses lead to high-efficacy destruction of cancer cells." Journal of Materials Chemistry B 6, no. 45 (2018): 7378–82. http://dx.doi.org/10.1039/c8tb02070a.

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Lee, Hui-Ting, Chen-Sung Lin, Chao-Yu Liu, Po Chen, Chang-Youh Tsai, and Yau-Huei Wei. "Mitochondrial Plasticity and Glucose Metabolic Alterations in Human Cancer under Oxidative Stress—From Viewpoints of Chronic Inflammation and Neutrophil Extracellular Traps (NETs)." International Journal of Molecular Sciences 25, no. 17 (2024): 9458. http://dx.doi.org/10.3390/ijms25179458.

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Oxidative stress elicited by reactive oxygen species (ROS) and chronic inflammation are involved both in deterring and the generation/progression of human cancers. Exogenous ROS can injure mitochondria and induce them to generate more endogenous mitochondrial ROS to further perpetuate the deteriorating condition in the affected cells. Dysfunction of these cancer mitochondria may possibly be offset by the Warburg effect, which is characterized by amplified glycolysis and metabolic reprogramming. ROS from neutrophil extracellular traps (NETs) are an essential element for neutrophils to defend ag

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Wu, Xiao-Ting, Jun-Quan Liu, Xiao-Ting Lu, et al. "The enhanced effect of lupeol on the destruction of gastric cancer cells by NK cells." International Immunopharmacology 16, no. 2 (2013): 332–40. http://dx.doi.org/10.1016/j.intimp.2013.04.017.

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Na, Di, Funan Liu, Zhifeng Miao, Zongmin Du, and Huimian Xu. "Destruction of gastric cancer cells to mesothelial cells by apoptosis in the early peritoneal metastasis." Journal of Huazhong University of Science and Technology [Medical Sciences] 29, no. 2 (2009): 163–68. http://dx.doi.org/10.1007/s11596-009-0205-2.

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Goncharova, A., and E. Kolpak. "Relapse Modeling Cancer." Bulletin of Science and Practice 10, no. 12 (2024): 22–28. https://doi.org/10.33619/2414-2948/109/02.

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The treatment of oncological diseases is one of the most difficult tasks of clinical medicine. Successful treatment is accompanied in some cases by a relapse followed by a sharp exacerbation of the disease. One of the causes of relapse may be the stimulation of the growth of a pool of dormant cells under the action of drugs. The paper develops a model of tumor cell growth, their destruction due to chemotherapy, and the growth of a pool of cells that are not susceptible to drugs. An assessment of the probability distribution of the moments of initiation of treatment and the moments of recurrenc

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Liu, Dandan, Heng Zou, Wai-Kin Yu, et al. "Microfluidics analysis of cancer cell microenvironments and targeted destruction of cancer stem cells by nanomedicine." Nanomedicine: Nanotechnology, Biology and Medicine 12, no. 2 (2016): 452. http://dx.doi.org/10.1016/j.nano.2015.12.013.

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Sehl, Mary E., Janet S. Sinsheimer, Hua Zhou, and Kenneth L. Lange. "Differential Destruction of Stem Cells: Implications for Targeted Cancer Stem Cell Therapy." Cancer Research 69, no. 24 (2009): 9481–89. http://dx.doi.org/10.1158/0008-5472.can-09-2070.

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Ogiue-Ikeda, M., Y. Sato, and S. Ueno. "Destruction of Targeted Cancer Cells Using Magnetizable Beads and Pulsed Magnetic Forces." IEEE Transactions on Magnetics 40, no. 4 (2004): 3018–20. http://dx.doi.org/10.1109/tmag.2004.830425.

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Weiss, L., D. S. Dimitrov, and M. Angelova. "The hemodynamic destruction of intravascular cancer cells in relation to myocardial metastasis." Proceedings of the National Academy of Sciences 82, no. 17 (1985): 5737–41. http://dx.doi.org/10.1073/pnas.82.17.5737.

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Lu, Jin-Jian, Xiao-Huang Xu, Yu-Chi Chen, et al. "Garcinone E blocks autophagy through lysosomal functional destruction in ovarian cancer cells." World Journal of Traditional Chinese Medicine 7, no. 2 (2021): 209. http://dx.doi.org/10.4103/wjtcm.wjtcm_83_20.

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Yuan, Ahu, Xiaolei Tang, Xuefeng Qiu, Ke Jiang, Jinhui Wu, and Yiqiao Hu. "Activatable photodynamic destruction of cancer cells by NIR dye/photosensitizer loaded liposomes." Chemical Communications 51, no. 16 (2015): 3340–42. http://dx.doi.org/10.1039/c4cc09689d.

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Cobley, Claire M., Leslie Au, Jingyi Chen, and Younan Xia. "Targeting gold nanocages to cancer cells for photothermal destruction and drug delivery." Expert Opinion on Drug Delivery 7, no. 5 (2010): 577–87. http://dx.doi.org/10.1517/17425240903571614.

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