Cell Cycle Alterations in a Xenografted Human Hypopharynx Carcinoma after Treatment with Carboplatin: Influence of Acquired Resistance to Cisplatin

1992 ◽  
pp. 428-438 ◽  
Author(s):  
M. Jackel ◽  
P. Köpf-Maier
Keyword(s):  
Cell Cycle ◽  
Acquired Resistance ◽  
Cell Cycle Alterations

scholarly journals Resistance to CDK4/6 Inhibitors in Estrogen Receptor-Positive Breast Cancer

2021 ◽  
Vol 22 (22) ◽  
pp. 12292
Author(s):  
Erin R. Scheidemann ◽  
Ayesha N. Shajahan-Haq
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Estrogen Receptor ◽  
Cell Cycle Progression ◽  
Acquired Resistance ◽  
Alternative Methods ◽  
Cycle Progression ◽  
Estrogen Receptor Positive ◽  
New Treatment ◽  
Methods Of Treatment

Estrogen receptor-positive (ER+) breast cancer is the most common form of breast cancer. Antiestrogens were the first therapy aimed at treating this subtype, but resistance to these warranted the development of a new treatment option. CDK4/6 inhibitors address this problem by halting cell cycle progression in ER+ cells, and have proven to be successful in the clinic. Unfortunately, both intrinsic and acquired resistance to CDK4/6 inhibitors are common. Numerous mechanisms of how resistance occurs have been identified to date, including the activation of prominent growth signaling pathways, the loss of tumor-suppressive genes, and noncanonical cell cycle function. Many of these have been successfully targeted and demonstrate the ability to overcome resistance to CDK4/6 inhibitors in preclinical and clinical trials. Future studies should focus on the development of biomarkers so that patients likely to be resistant to CDK4/6 inhibition can initially be given alternative methods of treatment.

scholarly journals Infection of cells with replication deficient adenovirus induces cell cycle alterations and leads to downregulation of E2F-1

2002 ◽  
Vol 1542 (1-3) ◽  
pp. 106-115 ◽  
Author(s):  
Hartmut Kuhn ◽  
Uta Liebers ◽  
Christian Gessner ◽  
Leonid Karawajew ◽  
Velia Ruppert ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Alterations

Abstract B62: Cell cycle alterations in paired diagnosis-relapse childhood acute lymphoblastic leukemia.

2013 ◽  
Author(s):  
Roberta Bortolozzi ◽  
Giampietro Viola ◽  
Maddalena Paganin ◽  
Silvia Bresolin ◽  
Silvia Disarò ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia ◽  
Childhood Acute Lymphoblastic Leukemia ◽  
Cell Cycle Alterations

scholarly journals Unravelling the Potential Cytotoxic Effects of Metal Oxide Nanoparticles and Metal(Loid) Mixtures on A549 Human Cell Line

Nanomaterials ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 447
Author(s):  
Fernanda Rosário ◽  
Maria João Bessa ◽  
Fátima Brandão ◽  
Carla Costa ◽  
Cláudia B. Lopes ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Prolonged Exposure ◽  
Titanium Dioxide Nanoparticles ◽  
Metal Oxide Nanoparticles ◽  
A549 Cells ◽  
Water Soluble ◽  
Oxide Nanoparticles ◽  
Dependent Manner ◽  
Thiazolyl Blue Tetrazolium Bromide ◽  
Cell Cycle Alterations

Humans are typically exposed to environmental contaminants’ mixtures that result in different toxicity than exposure to the individual counterparts. Yet, the toxicology of chemical mixtures has been overlooked. This work aims at assessing and comparing viability and cell cycle of A549 cells after exposure to single and binary mixtures of: titanium dioxide nanoparticles (TiO2NP) 0.75–75 mg/L; cerium oxide nanoparticles (CeO2NP) 0.75–10 μg/L; arsenic (As) 0.75–2.5 mg/L; and mercury (Hg) 5–100 mg/L. Viability was assessed through water-soluble tetrazolium (WST-1) and thiazolyl blue tetrazolium bromide (MTT) (24 h exposure) and clonogenic (seven-day exposure) assays. Cell cycle alterations were explored by flow cytometry. Viability was affected in a dose- and time-dependent manner. Prolonged exposure caused inhibition of cell proliferation even at low concentrations. Cell-cycle progression was affected by TiO2NP 75 mg/L, and As 0.75 and 2.5 μg/L, increasing the cell proportion at G0/G1 phase. Combined exposure of TiO2NP or CeO2NP mitigated As adverse effects, increasing the cell surviving factor, but cell cycle alterations were still observed. Only CeO2NP co-exposure reduced Hg toxicity, translated in a decrease of cells in Sub-G1. Toxicity was diminished for both NPs co-exposure compared to its toxicity alone, but a marked toxicity for the highest concentrations was observed for longer exposures. These findings prove that joint toxicity of contaminants must not be disregarded.

scholarly journals Proteomic Analysis of Breast Cancer Resistance to the Anticancer Drug RH1 Reveals the Importance of Cancer Stem Cells

Cancers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 972
Author(s):  
Dalius Kuciauskas ◽  
Nadezda Dreize ◽  
Marija Ger ◽  
Algirdas Kaupinis ◽  
Kristijonas Zemaitis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Proteomic Analysis ◽  
Acquired Resistance ◽  
Cancer Resistance ◽  
Resistant Cells

Antitumor drug resistance remains a major challenge in cancer chemotherapy. Here we investigated the mechanism of acquired resistance to a novel anticancer agent RH1 designed to be activated in cancer cells by the NQO1 enzyme. Data show that in some cancer cells RH1 may act in an NQO1-independent way. Differential proteomic analysis of breast cancer cells with acquired resistance to RH1 revealed changes in cell energy, amino acid metabolism and G2/M cell cycle transition regulation. Analysis of phosphoproteomics and protein kinase activity by multiplexed kinase inhibitor beads showed an increase in the activity of protein kinases involved in the cell cycle and stemness regulation and downregulation of proapoptotic kinases such as JNK in RH1-resistant cells. Suppression of JNK leads to the increase of cancer cell resistance to RH1. Moreover, resistant cells have enhanced expression of stem cell factor (SCF) and stem cell markers. Inhibition of SCF receptor c-KIT resulted in the attenuation of cancer stem cell enrichment and decreased amounts of tumor-initiating cells. RH1-resistant cells also acquire resistance to conventional therapeutics while remaining susceptible to c-KIT-targeted therapy. Data show that RH1 can be useful to treat cancers in the NQO1-independent way, and targeting of the cancer stem cells might be an effective approach for combating resistance to RH1 therapy.

scholarly journals The Integrins Involved in Soybean Agglutinin-Induced Cell Cycle Alterations in IPEC-J2

2017 ◽  
Vol 40 (2) ◽  
pp. 109-116 ◽  
Author(s):  
Li Pan ◽  
Yuan Zhao ◽  
Zhijie Yuan ◽  
Mohammed Hamdy Farouk ◽  
Shiyao Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Soybean Agglutinin ◽  
Cell Cycle Alterations

scholarly journals Targeting Cell Cycle in Breast Cancer: CDK4/6 Inhibitors

2020 ◽  
Vol 21 (18) ◽  
pp. 6479 ◽  
Author(s):  
Michela Piezzo ◽  
Stefania Cocco ◽  
Roberta Caputo ◽  
Daniela Cianniello ◽  
Germira Di Gioia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Clinical Outcomes ◽  
Cell Cycle Control ◽  
Acquired Resistance ◽  
Metastatic Breast ◽  
New Combination ◽  
Hormone Receptor Positive ◽  
Combination Strategies ◽  
New Biomarkers

Deregulation of cell cycle, via cyclin D/CDK/pRb pathway, is frequently observed in breast cancer lending support to the development of drugs targeting the cell cycle control machinery, like the inhibitors of the cycline-dependent kinases (CDK) 4 and 6. Up to now, three CDK4/6 inhibitors have been approved by FDA for the treatment of hormone receptor-positive (HR+), HER2-negative metastatic breast cancer. These agents have been effective in improving the clinical outcomes, but the development of intrinsic or acquired resistance can limit the efficacy of these treatments. Clinical and translational research is now focused on investigation of the mechanism of sensitivity/resistance to CDK4/6 inhibition and novel therapeutic strategies aimed to improve clinical outcomes. This review summarizes the available knowledge regarding CDK4/6 inhibitor, the discovery of new biomarkers of response, and the biological rationale for new combination strategies of treatment.

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