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1

Ciaiolo, Carlo, Dario Ferrero, Agostino Pugliese, et al. "Enhancement of Methotrexate Cytotoxicity by Modulation of Proliferative Activity in Normal and Neoplastic t Lymphocytes and in a Myeloid Leukemia Cell Line." Tumori Journal 74, no. 5 (1988): 537–42. http://dx.doi.org/10.1177/030089168807400507.

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Recent advances in the modulation of cell kinetics with growth factors suggest that the effect of cyclespecific cytostatic drugs can be enhanced by combination with such factors. The truth of this hypothesis was investigated by studying the effect of phytohemoagglutinin and/or interlenkin 2 on the sensitivity to methotrexate (MTX) of normal T lymphocytes and of lymphoblastis of a patient with acute T-cell lymphoid leukemia. In both cases, inhibition of proliferation by MTX was increased from less than 30% in resting cells or those sub-optimally stimulated, in the case of leukemic blasts, to 68
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2

Miyashita, T., and JC Reed. "Bcl-2 oncoprotein blocks chemotherapy-induced apoptosis in a human leukemia cell line." Blood 81, no. 1 (1993): 151–57. http://dx.doi.org/10.1182/blood.v81.1.151.151.

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Abstract Previous studies have shown that the bcl-2 gene encodes a mitochondrial protein that contributes to neoplastic cell expansion primarily by promoting cell survival through interference with “programmed cell death” (PCD), also termed “apoptosis.” Because many chemotherapeutic drugs are capable of initiating pathways leading to apoptosis, we determined whether deregulated bcl-2 expression could render cells resistant to several drugs commonly used in the treatment of non- Hodgkin's lymphomas, including dexamethasone (DEX), methotrexate (MTX), 1-beta-D-arabinofuranosyl-cytosine (Ara-C), e
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3

Miyashita, T., and JC Reed. "Bcl-2 oncoprotein blocks chemotherapy-induced apoptosis in a human leukemia cell line." Blood 81, no. 1 (1993): 151–57. http://dx.doi.org/10.1182/blood.v81.1.151.bloodjournal811151.

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Previous studies have shown that the bcl-2 gene encodes a mitochondrial protein that contributes to neoplastic cell expansion primarily by promoting cell survival through interference with “programmed cell death” (PCD), also termed “apoptosis.” Because many chemotherapeutic drugs are capable of initiating pathways leading to apoptosis, we determined whether deregulated bcl-2 expression could render cells resistant to several drugs commonly used in the treatment of non- Hodgkin's lymphomas, including dexamethasone (DEX), methotrexate (MTX), 1-beta-D-arabinofuranosyl-cytosine (Ara-C), etoposide
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4

Kothari, Shalin, Daniel Gustafson, Keith Killian, et al. "COXEN prediction of antineoplastic drug sensitivity in bladder cancer patients." Journal of Clinical Oncology 34, no. 2_suppl (2016): 365. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.365.

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365 Background: COXEN (Co-eXpression ExtrapolatioN) uses molecular profiles as a “rosetta stone” for translating drug sensitivities of one set of cancers into predictions for another completely independent set of cell lines or human tumors. The ability of COXEN to predict drug effectiveness in pts using tumor samples from in vitro assays is unique. Methods: We tested the predictive value of COXEN for standard chemotherapies in a cohort of bladder cancer pts. Total RNA was extracted from formalin fixed paraffin embedded (FFPE) tissue and converted to cDNA, amplified with Ovation FFPE WTA, and h
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5

Eischen, Christine M., Timothy J. Kottke, Luis M. Martins, et al. "Comparison of Apoptosis in Wild-Type and Fas-Resistant Cells: Chemotherapy-Induced Apoptosis Is Not Dependent on Fas/Fas Ligand Interactions." Blood 90, no. 3 (1997): 935–43. http://dx.doi.org/10.1182/blood.v90.3.935.

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Abstract The Fas/Fas ligand (FasL) pathway is widely involved in apoptotic cell death in lymphoid and nonlymphoid cells. It has recently been postulated that many chemotherapeutic agents also induce cell death by activating the Fas/FasL pathway. In the present study we compared apoptotic pathways induced by anti-Fas or chemotherapeutic agents in the Jurkat human T-cell leukemia line. Immunoblotting showed that treatment of wild-type Jurkat cells with anti-Fas or the topoisomerase II-directed agent etoposide resulted in proteolytic cleavage of precursors for the cysteine-dependent aspartate-dir
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6

Eischen, Christine M., Timothy J. Kottke, Luis M. Martins, et al. "Comparison of Apoptosis in Wild-Type and Fas-Resistant Cells: Chemotherapy-Induced Apoptosis Is Not Dependent on Fas/Fas Ligand Interactions." Blood 90, no. 3 (1997): 935–43. http://dx.doi.org/10.1182/blood.v90.3.935.935_935_943.

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The Fas/Fas ligand (FasL) pathway is widely involved in apoptotic cell death in lymphoid and nonlymphoid cells. It has recently been postulated that many chemotherapeutic agents also induce cell death by activating the Fas/FasL pathway. In the present study we compared apoptotic pathways induced by anti-Fas or chemotherapeutic agents in the Jurkat human T-cell leukemia line. Immunoblotting showed that treatment of wild-type Jurkat cells with anti-Fas or the topoisomerase II-directed agent etoposide resulted in proteolytic cleavage of precursors for the cysteine-dependent aspartate-directed pro
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7

Bayraktar, Ulas D., Roberto Ochoa, Soley Bayraktar, Maria Matsangou, and Juan Carlos Ramos. "High-Dose Methotrexate and Azidothymidine in Combination with Alternating DA-EPOCH Is An Effective Regimen for the Treatment of EBV-Related Plasmablastic Lymphoma." Blood 114, no. 22 (2009): 4753. http://dx.doi.org/10.1182/blood.v114.22.4753.4753.

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Abstract Abstract 4753 Introduction Plasmablastic lymphoma (PBL) is an aggressive and generally fatal, rare type of B-cell non-Hodgkin's lymphoma (NHL) with predilection to sino-oral mucosa. PBL is usually associated with human immunodeficiency virus (HIV) and displays an unusual phenotype lacking the expression of B-cell surface antigens. PBLs are infected by Epstein Barr virus (EBV) in approximately 80% of cases and exhibit a restricted pattern of EBV gene expression as they do not typically express latent membrane proteins (LMPs), which enforce viral latency. Azidothymidine (AZT), a thymidi
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8

Melguizo, C., J. Prados, J. Aneiros, J. E. Fernandez, C. Velez, and A. Aranega. "Differentiation of a human rhabdomyosarcoma cell line after antineoplastic drug treatment." Journal of Pathology 175, no. 1 (1995): 23–29. http://dx.doi.org/10.1002/path.1711750105.

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9

Caldito, Elena G., Jay M. Pescatore, and Maha Elsebaie. "Severe multiorgan toxicity after first dose of Capizzi methotrexate in a young adult patient with acute lymphocytic leukaemia." BMJ Case Reports 14, no. 7 (2021): e243153. http://dx.doi.org/10.1136/bcr-2021-243153.

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Methotrexate is a versatile antineoplastic and immunosuppressive agent. We report a case of a young adult on the Cancer and Leukaemia Group B 10403 treatment protocol for B-cell acute lymphoblastic leukaemia. She has previously completed the induction and consolidation phases with good tolerance then started on Capizzi methotrexate during the interim maintenance phase. Few days after receiving one intermediate dose of methotrexate, she developed severe multiorgan toxicities including pancytopaenia and several dermatologic toxicities. The patient underwent extensive diagnostic workup, with all
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10

Virdis, Patrizia, Rossana Migheli, Grazia Galleri, et al. "Antiproliferative and proapoptotic effects of Inula viscosa extract on Burkitt lymphoma cell line." Tumor Biology 42, no. 2 (2020): 101042831990106. http://dx.doi.org/10.1177/1010428319901061.

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Burkitt lymphoma is a very aggressive B-cell non-Hodgkin lymphoma. Although remarkable progress has been made in the therapeutic scenario for patients with Burkitt lymphoma, search and development of new effective anticancer agents to improve patient outcome and minimize toxicity has become an urgent issue. In this study, the antitumoral activity of Inula viscosa, a traditional herb obtained from plants collected on the Asinara Island, Italy, was evaluated in order to explore potential antineoplastic effects of its metabolites on Burkitt lymphoma. Raji human cell line was treated with increasi
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11

Khan, Muhammad Saad, Fred L. Hardwicke, Henry Palangdao Igid, Hassan Kaleem, Sanjay Awasthi, and Daniel Armstrong. "Screening for antineoplastic ionic liquids by targeting RLIP76." Journal of Clinical Oncology 35, no. 15_suppl (2017): e13033-e13033. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e13033.

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e13033 Background: RLIP76 is a stress-responsive multispecific transporter which functions as an anti-apoptotic protein in cancer cells. The targeting of RLIP76 by antibodies, antisense, or siRNA modalities causes complete regression of cancers such as melanoma, colon cancer and lung cancer. We carried out studies to determine whether the ATPase activity of purified recombinant human RLIP76 protein (encoded by RALBP1, chromosome 18p11.22) can be used to screen for novel ionic liquid compounds with antineoplastic activity. Methods: A series of ionic liquid compounds were tested for their abilit
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12

Mini, E., G. Pizzorno, M. Coronnello, et al. "Impaired methotrexate polyglutamylation in a human leukemia cell line resistant to short-term, high-dose methotrexate." Pharmacological Research Communications 20, no. 5 (1988): 445–46. http://dx.doi.org/10.1016/s0031-6989(88)80035-3.

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13

Sur, Pratima, Yoshinobu Matsuo, Takeshi Otanl, and Jun Minowada. "Reversal of Methotrexate-Induced Folate Pool Depletion by Thymidine in a Human Leukemia Cell Line in Vitro." Tumori Journal 79, no. 6 (1993): 433–38. http://dx.doi.org/10.1177/030089169307900613.

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In an In vitro study using a human monocytic leukemia cell line, U-937, the effects of interferon-γ (IFN-γ) in combination with the antifolate methotrexate and the role of thymidine introduced as a biochemical modulator were investigated. Methotrexate alone or in combination with INF-γ was found to enhance the induction of morphologic and functional monocytic differentiation in the U-937 cell line. Various cellular effects with the addition of thymidine to the medium with methotrexate and IFN-γ were studied. Enhanced inhibition of cell growth and perturbation of the cell cycle were noted when
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14

Mendoza-Santiago, Alma, Edgardo Becerra, Edith Garay, et al. "Glutamic Acid Increased Methotrexate Polyglutamation and Cytotoxicity in a CCRF-SB Acute Lymphoblastic Leukemia Cell Line." Medicina 55, no. 12 (2019): 758. http://dx.doi.org/10.3390/medicina55120758.

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Background and Objectives: Acute lymphoblastic leukemia (ALL) is the most common type of cancer in childhood. The majority of patients respond to treatment, but those with resistant phenotypes suffer relapse or death. The antifolate methotrexate (MTX) is the most commonly used drug against ALL due to its efficacy. Once inside leukemic cells, MTX is metabolized into methotrexate polyglutamates (MTX-PG) by action of the enzyme folylpolyglutamate synthetase (FPGS), leading to a longer action compared to that of MTX alone. Materials and Methods: In this work, we demonstrated that the combination t
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15

Hill, Anna B., Jeffrey M. Trent, Floyd H. Thompson, Mary K. Danks, and William T. Beck. "Loss of tumorigenicity in a methotrexate-resistant human leukemia cell line." Cancer Genetics and Cytogenetics 70, no. 1 (1993): 48–55. http://dx.doi.org/10.1016/0165-4608(93)90130-e.

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16

Kawami, Masashi, Mioka Miyamoto, Ryoko Yumoto, and Mikihisa Takano. "Methotrexate influx via folate transporters into alveolar epithelial cell line A549." Drug Metabolism and Pharmacokinetics 30, no. 4 (2015): 276–81. http://dx.doi.org/10.1016/j.dmpk.2015.04.005.

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17

Atassi, Bassel, Khaled Alsibai, George H. Yoo, et al. "Methotrexate and cetuximab for metastatic advanced head and neck squamous cell carcinoma: A retrospective study." Journal of Clinical Oncology 30, no. 15_suppl (2012): e16019-e16019. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e16019.

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e16019 Background: After the failure of first line palliative chemotherapy in recurrent non-resectable or metastatic head and neck squamous-cell carcinoma (HNSCC), there is no standard of care treatment that improves survival or quality of life. Both, methotrexate and cetuximab have single agent activity in metastatic HNSCC. We are presenting our institutional experience in using unique combination chemotherapy with methotrexate plus cetuximab (MC). Methods: Retrospectively, single institution’s charts were reviewed from 2004-2010, all patients have documented recurrent non-resectable or metas
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18

M. Franco, Yollanda E., Marcia Y. Okubo, Adriana D. Torre, et al. "Coronarin D Induces Apoptotic Cell Death and Cell Cycle Arrest in Human Glioblastoma Cell Line." Molecules 24, no. 24 (2019): 4498. http://dx.doi.org/10.3390/molecules24244498.

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Glioblastoma (GBM) is the most frequent and highest–grade brain tumor in adults. The prognosis is still poor despite the use of combined therapy involving maximal surgical resection, radiotherapy, and chemotherapy. The development of more efficient drugs without noticeable side effects is urgent. Coronarin D is a diterpene obtained from the rhizome extract of Hedychium coronarium, classified as a labdane with several biological activities, principally anticancer potential. The aim of the present study was to determine the anti–cancer properties of Coronarin D in the glioblastoma cell line and
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19

Madeira, Klesia, Murilo Cerri, Renata Daltoé, et al. "In vitro antineoplastic activity in triple-negative breast cancer cell line and in vivo." BMC Proceedings 8, Suppl 4 (2014): P22. http://dx.doi.org/10.1186/1753-6561-8-s4-p22.

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20

Toffoli, Giuseppe, Alessandra Viel, Loretta Tumiotto, Patrizio Buttazzi, Gabriella Biscontin, and Mauro Boiocchi. "Sensitivity Pattern of Normal and Ha-Ras Transformed Nih3T3 Fibroblasts to Antineoplastic Drugs." Tumori Journal 75, no. 5 (1989): 423–28. http://dx.doi.org/10.1177/030089168907500505.

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Ha-ras-transformed NIH3T3 fibroblasts were compared with the parental cell line to investigate the influence of the Ha-ras oncogene on cellular chemosensitivity to antineoplastic drugs. Four NIH3T3 cell clones independently transformed by the Ha-ras oncogene, activated by mutation or overexpression, were analyzed: 3 clones were obtained by transfection of NIH3T3 cells with a mutation-activated Ha-ras gene and 1 clone by transfection of a large copy number of the normal Ha-ras protooncogene. Chemosensitivity of the transformed clones and of the parental cell line was analyzed when cells were in
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21

Samorapoompichit, Puchit, Marianne Steiner, Trevor Lucas, et al. "Induction of Apoptosis in the Human Mast Cell Leukemia Cell Line HMC-1 by Various Antineoplastic Drugs." Leukemia & Lymphoma 44, no. 3 (2003): 509–15. http://dx.doi.org/10.1080/1042819021000046976.

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22

Underhill, T. M., and W. F. Flintoff. "Complementation of a methotrexate uptake defect in Chinese hamster ovary cells by DNA-mediated gene transfer." Molecular and Cellular Biology 9, no. 4 (1989): 1754–58. http://dx.doi.org/10.1128/mcb.9.4.1754-1758.1989.

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A methotrexate-resistant Chinese hamster ovary cell line deficient in methotrexate uptake has been complemented to methotrexate sensitivity by transfection with DNA isolated from either wild-type Chinese hamster ovary or human G2 cells. Primary and secondary transfectants regained the ability to take up methotrexate in a manner similar to that of wild-type cells, and in the case of those transfected with human DNA, to contain human-specific DNA sequences. The complementation by DNA-mediated gene transfer of this methotrexate-resistant phenotype provides a basis for the cloning of a gene involv
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23

Hollingsworth, S. J., N. P. Shankley, E. M. Anderson, and A. Bennett. "Interaction between methotrexate and indomethacin on a human normal haemopoietic cell line." British Journal of Pharmacology 114, no. 3 (1995): 715–19. http://dx.doi.org/10.1111/j.1476-5381.1995.tb17197.x.

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24

Kawami, Masashi, Rika Harabayashi, Mioka Miyamoto, Risako Harada, Ryoko Yumoto, and Mikihisa Takano. "Methotrexate-Induced Epithelial–Mesenchymal Transition in the Alveolar Epithelial Cell Line A549." Lung 194, no. 6 (2016): 923–30. http://dx.doi.org/10.1007/s00408-016-9935-7.

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25

Atassi, Bassel, George H. Yoo, Natasha Robinette, Khaled Sibai, and Ammar Sukari. "Methotrexate and cetuximab for metastatic advanced head and neck squamous cell carcinoma." Journal of Clinical Oncology 31, no. 15_suppl (2013): e17033-e17033. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e17033.

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e17033 Background: After the failure of first-line palliative chemotherapy in recurrent non-resectable or metastatic head and neck squamous-cell carcinoma (HNSCC), there is no standard of care second-line treatment that is proven to improve quality of life or prolong survival. Both methotrexate and cetuximab has shown a single-agent activity in advanced HNSCC. We are presenting our institutional experience in using unique combination chemotherapy with methotrexate plus cetuximab (MC). Methods: Retrospectively, single institution’s charts were reviewed from 2004-2010, all patients have document
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26

Pamila, Miss, Ramya Sugumar, and Darling Chellathai David. "Evaluation of Roflumilast (BCRP inhibitor) and Methotrexate (BCRP substrate) on Viability of Primary Squamous Cell Carcinoma – An in vitro Study." Biomedical and Pharmacology Journal 12, no. 2 (2019): 683–87. http://dx.doi.org/10.13005/bpj/1689.

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In this study we evaluated the possible beneficial drug- interaction between Roflumilast (BCRP inhibitor) and Methotrexate (BCRP substrate) on viability of primary squamous cell carcinoma cell line using an in vitro technique. The KB cell line was treated with Roflumilast and Methotrexate to evaluate its anticancer activity using MTT assay. Image analysis under phase contrast microscopy was performed and flow-cytometry was done to see for cell cycle arrest as a result of drug treatment. Cell viability gradually decreased with the increasing concentrations of roflumilast, methotrexate and the c
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27

Heaney, Mark L., Jeffrey R. Gardner, Nicos Karasavvas, et al. "Vitamin C Antagonizes the Cytotoxic Effects of Antineoplastic Drugs." Blood 106, no. 11 (2005): 498. http://dx.doi.org/10.1182/blood.v106.11.498.498.

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Abstract Vitamin C is an antioxidant vitamin that has been hypothesized to antagonize the effects of antineoplastic drugs that generate reactive oxygen species. Leukemia (K562) and lymphoma (RL) cells pre-treated with dehydroascorbic acid, the commonly transported form of vitamin C, demonstrated a dose-dependent attenuation of cytotoxicity after treatment with the widely-used antineoplastic drugs, doxorubicin, cisplatin, vincristine, methotrexate and imatinib that ranged from 30–80% as measured by trypan blue exclusion and colony formation in methylcellulose. While treatment with vitamin C alo
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28

Pantshwa, Jonathan M., Khadija Rhoda, Sarah J. Clift, et al. "Chemotherapeutic Efficacy of Implantable Antineoplastic-Treatment Protocols in an Optimal Mouse Model for Human Ovarian Carcinoma Cell Targeting." International Journal of Molecular Sciences 19, no. 10 (2018): 3030. http://dx.doi.org/10.3390/ijms19103030.

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The present study aimed to design and develop a nanocomposite drug delivery system employing an antineoplastic-loaded antibody functionalized nanomicelle encapsulated within a Chitosan–Poly(vinylpyrrolidone)–Poly(N-isopropylacrylamide) (C–P–N) hydrogel to form an in situ forming implant (ISFI), responsive to temperature and pH for cancer cell-targeting following intraperitoneal implantation. The optimum nanomicelle formulation was surface-functionalized with anti-MUC 16 (antibody) for the targeted delivery of methotrexate to human ovarian carcinoma (NIH:OVCAR-5) cells in Athymic nude mice that
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29

Paulson, Thomas G., Alexandru Almasan, Linnea L. Brody, and Geoffrey M. Wahl. "Gene Amplification in a p53-Deficient Cell Line Requires Cell Cycle Progression under Conditions That Generate DNA Breakage." Molecular and Cellular Biology 18, no. 5 (1998): 3089–100. http://dx.doi.org/10.1128/mcb.18.5.3089.

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ABSTRACT Amplification of genes involved in signal transduction and cell cycle control occurs in a significant fraction of human cancers. Loss of p53 function has been proposed to enable cells with gene amplification to arise spontaneously during growth in vitro. However, this conclusion derives from studies employing the UMP synthesis inhibitor N-phosphonacetyl-l-aspartate (PALA), which, in addition to selecting for cells containing extra copies of the CAD locus, enables p53-deficient cells to enter S phase and acquire the DNA breaks that initiate the amplification process. Thus, it has not b
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30

Grando, Rogério, Marcia A. Antônio, Carlos E. P. Araújo, et al. "Antineoplastic 31-Norcycloartanones from Solanum cernuum Vell." Zeitschrift für Naturforschung C 63, no. 7-8 (2008): 507–14. http://dx.doi.org/10.1515/znc-2008-7-807.

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Triterpenoids with 31-norcycloartanone structure were isolated for the first time from the Solanum genus. Cycloeucalenone and 24-oxo-31-norcycloartanone were the main constituents of the dichloromethane extract of Solanum cernuum Vell. leaves [7% (w/w) and 1.47% (w/w)]. Both triterpenoids were tested against human tumour cell lines, and 24-oxo-31-norcycloartanone was significantly active and selective against the lung tumour cell line NCI-H460 with total growth inhibition at 1.10 μg/mL, growth inhibition 50 at 0.19 μg/mL and lethal concentration 50 at 8.43 μg/mL, while cycloeucalenone showed p
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31

Barg, Rivka, Jacques S. Beckmann, and Meir Perl. "The Effect of Nicotinamide Dinucleotides on Methotrexate Binding to Proteins in a Methotrexate-Resistant Cell-Line of Petunia hybrida." Journal of Plant Physiology 136, no. 5 (1990): 611–14. http://dx.doi.org/10.1016/s0176-1617(11)80222-1.

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32

Perez-Fidalgo, Jose Alejandro, Paula Montero Magallo, Ines Roger Laparra, et al. "A preclinical model for skin sensitization prediction of antineoplasic drugs." Journal of Clinical Oncology 38, no. 15_suppl (2020): e15643-e15643. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15643.

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e15643 Background: Skin side effects are common manifestations of antineoplastic drugs that are frequently observed in early clinical trials. Therefore, there is a need to identify skin toxic agents before clinical development in order to predict severe skin manifestations. In many cases, skin toxicity is due to sensitization, a key immunologic process mediating redness, swelling and itching that can lead to more severe skin alterations. Methods: We adapted three skin cellular in vitro techniques for cutaneous drug sensitization assessment of the Organization for Economic Cooperation and Devel
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33

Hamkalo, B. A., P. J. Farnham, R. Johnston, and R. T. Schimke. "Ultrastructural features of minute chromosomes in a methotrexate-resistant mouse 3T3 cell line." Proceedings of the National Academy of Sciences 82, no. 4 (1985): 1126–30. http://dx.doi.org/10.1073/pnas.82.4.1126.

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34

Chen, Ya-Xia, Wei-Guo Lv, Huai-Zeng Chen, Feng Ye, and Xing Xie. "Methotrexate induces apoptosis of human choriocarcinoma cell line JAR via a mitochondrial pathway." European Journal of Obstetrics & Gynecology and Reproductive Biology 143, no. 2 (2009): 107–11. http://dx.doi.org/10.1016/j.ejogrb.2008.12.009.

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35

Ozgenc, Emre, Meliha Ekinci, Derya Ilem-Ozdemir, Evren Gundogdu, and Makbule Asikoglu. "Radiolabeling and in vitro evaluation of 99mTc-methotrexate on breast cancer cell line." Journal of Radioanalytical and Nuclear Chemistry 307, no. 1 (2015): 627–33. http://dx.doi.org/10.1007/s10967-015-4210-6.

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36

Jongsma, A. P. M., W. A. L. Duijndam, and P. Borst. "DNA content and structure of (double) minutes of a methotrexate-resistant cell line." Histochemistry 93, no. 1 (1989): 87–92. http://dx.doi.org/10.1007/bf00266852.

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37

Opoku, A. R., M. Geheeb-Keller, J. Lin, et al. "Preliminary screening of some traditional Zulu medicinal plants for antineoplastic activities versus the HepG2 cell line." Phytotherapy Research 14, no. 7 (2000): 534–37. http://dx.doi.org/10.1002/1099-1573(200011)14:7<534::aid-ptr661>3.0.co;2-a.

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38

Neumann, K., K. M. Al-Batayneh, M. J. Kuiper, et al. "A single point mutation in Drosophila dihydrofolate reductase confers methotrexate resistance to a transgenic CHO cell line." Genome 46, no. 4 (2003): 707–15. http://dx.doi.org/10.1139/g03-046.

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Sequence analysis of a cDNA encoding dihydrofolate reductase (DHFR) from a selected methotrexate-resistant Drosophila melanogaster cell line (S3MTX) revealed a substitution of Gln for Leu at position 30. Although the S3MTX cells were ~1000 fold more resistant to methotrexate (MTX), the karyotype was similar to the parental line and did not show elongated chromosomes. Furthermore, kinetic analysis of the recombinant enzyme showed a decreased affinity for MTX by the mutant DHFR. To determine if the resistance phenotype could be attributed to the mutant allele, Drosophila Dhfr cDNAs isolated from
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39

Underhill, T. M., and W. F. Flintoff. "Complementation of a methotrexate uptake defect in Chinese hamster ovary cells by DNA-mediated gene transfer." Molecular and Cellular Biology 9, no. 4 (1989): 1754–58. http://dx.doi.org/10.1128/mcb.9.4.1754.

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A methotrexate-resistant Chinese hamster ovary cell line deficient in methotrexate uptake has been complemented to methotrexate sensitivity by transfection with DNA isolated from either wild-type Chinese hamster ovary or human G2 cells. Primary and secondary transfectants regained the ability to take up methotrexate in a manner similar to that of wild-type cells, and in the case of those transfected with human DNA, to contain human-specific DNA sequences. The complementation by DNA-mediated gene transfer of this methotrexate-resistant phenotype provides a basis for the cloning of a gene involv
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40

Kano, Y., T. Ohnuma, and JF Holland. "Folate requirements of methotrexate-resistant human acute lymphoblastic leukemia cell lines." Blood 68, no. 2 (1986): 586–91. http://dx.doi.org/10.1182/blood.v68.2.586.586.

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Abstract We studied the folate requirements of a human acute lymphoblastic leukemia cell line, MOLT-3, and methotrexate (MTX)-resistant sublines established in vitro. The requirement of pteroylglutamate (PGA) for optimal cell growth was different for each cell line. With increasing MTX resistance, there was progressive increase in PGA requirements, moving the PGA concentration-cell growth curve (dose-response curve) 1 log order of magnitude to the right. The increases in the requirement of 5-methyltetrahydrofolate (5-methyl-THF) by the resistant sublines were more pronounced than PGA requireme
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41

Kano, Y., T. Ohnuma, and JF Holland. "Folate requirements of methotrexate-resistant human acute lymphoblastic leukemia cell lines." Blood 68, no. 2 (1986): 586–91. http://dx.doi.org/10.1182/blood.v68.2.586.bloodjournal682586.

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We studied the folate requirements of a human acute lymphoblastic leukemia cell line, MOLT-3, and methotrexate (MTX)-resistant sublines established in vitro. The requirement of pteroylglutamate (PGA) for optimal cell growth was different for each cell line. With increasing MTX resistance, there was progressive increase in PGA requirements, moving the PGA concentration-cell growth curve (dose-response curve) 1 log order of magnitude to the right. The increases in the requirement of 5-methyltetrahydrofolate (5-methyl-THF) by the resistant sublines were more pronounced than PGA requirement, movin
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42

Tishler, David M., and Corey Raffel. "Development of multidrug resistance in a primitive neuroectodermal tumor cell line." Journal of Neurosurgery 76, no. 3 (1992): 502–6. http://dx.doi.org/10.3171/jns.1992.76.3.0502.

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✓ Drug resistance remains a formidable obstacle to the successful treatment of pediatric primitive neuroectodermal tumors. Resistance to chemotherapeutic agents may be related, in part, to expression of the multidrug resistance gene 1 (MDR1). The protein product of this gene, P-glycoprotein, confers resistance to multiple unrelated antineoplastic drugs. The cell line DAOY, derived from a primitive neuroectodermal tumor, was used as an in vitro model to examine the development of drug resistance. Cell lines resistant to actinomycin D were developed by the growth of DAOY in increasing concentrat
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43

Zhao, Zhuofei, Xiaona Lin, Lulu Zhang, et al. "Lipidated Methotrexate Microbubbles: A Promising Rheumatoid Arthritis Theranostic Medicine Manipulated via Ultrasonic Irradiation." Journal of Biomedical Nanotechnology 17, no. 7 (2021): 1293–304. http://dx.doi.org/10.1166/jbn.2021.3105.

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De novo designed lipidated methotrexate was synthesized and self-assembled into microbubbles for targeted rheumatoid arthritis theranostic treatment. Controlled lipidatedmethotrexate delivery was achieved by ultrasound-targetedmicrobubble destruction technique. Methotrexate was dissociated inflammatory microenvironment of synovial cavity, owing to representive low pH and enriched leucocyte esterase. We first manipulated methotrexate controlled release with RAW 264.7 cell line in vitro and further verified with rheumatoid arthritis rabbits in vivo. Results showed that lipidated methotrexate mic
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Sur, Pratima, Yoshinobu Matsuo, Takeshi Otani, and Jun Minowada. "Modulation of Methotrexate Cytotoxicity with Natural Interferon upon Human Leukemia Cell Line HL-60." Oncology 48, no. 6 (1991): 469–73. http://dx.doi.org/10.1159/000226983.

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Meltzer, Paul S., Yung-Chi Cheng, and Jeffrey M. Trent. "Analysis of dihydrofolate reductase gene amplification in a methotrexate-resistant human tumor cell line." Cancer Genetics and Cytogenetics 17, no. 4 (1985): 289–300. http://dx.doi.org/10.1016/0165-4608(85)90112-8.

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Frasinyuk, Mykhaylo S., Galyna P. Mrug, Svitlana P. Bondarenko, et al. "Application of Mannich bases to the synthesis of hydroxymethylated isoflavonoids as potential antineoplastic agents." Organic & Biomolecular Chemistry 13, no. 46 (2015): 11292–301. http://dx.doi.org/10.1039/c5ob01828e.

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47

Andrade, Peterson de, Amanda de Fraga Dias, Fabrício Figueiró, et al. "1,2,3-Triazole tethered 2-mercaptobenzimidazole derivatives: design, synthesis and molecular assessment toward C6 glioma cell line." Future Medicinal Chemistry 12, no. 8 (2020): 689–708. http://dx.doi.org/10.4155/fmc-2019-0227.

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Aim: Glioblastoma multiforme (GBM) is an aggressive cancer with very limited clinical therapies. Herein, we have designed novel mercaptobenzimidazole derivatives (1–7) as multitarget antineoplastic drugs and assessed their antiproliferative profiles on an experimental model for GBM, the C6 glioma line. Results: The target compounds were synthesized in few steps with reasonable yields (33–90%). Compounds 1 (∼18 μM) and 4 (∼20 μM) showed dose-dependent antiproliferative effects on C6 glioma and significantly increased early apoptosis, but only 4 disrupted the cell cycle progression and did not i
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48

Gridelli, Cesare, Alma Contegiacomo, Rossella Lauria, et al. "Salvage Chemotherapy with Ccnu and Methotrexate for Small Cell Lung Cancer Resistant to Cav/Pe Alternating Chemotherapy." Tumori Journal 77, no. 6 (1991): 506–10. http://dx.doi.org/10.1177/030089169107700611.

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CCNU and methotrexate were employed as salvage treatment in 34 small cell lung cancer patients resistant to CAV/PE alternating Induction chemotherapy. In the 33 evaluable patients we observed an objective response rate of 21.2 % and 3 % complete response; median survival was 4 months with 2 patients alive 18 months from starting salvage chemotherapy. The treatment was well tolerated. CCNU and methotrexate has shown to be a moderately active and tolerable salvage treatment for small cell lung cancer after CAV/PE alternating first-line chemotherapy.
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Tosi, Patrizia, Filippo Gherlinzoni, Patrizio Mazza, et al. "3′-Azido 3′-Deoxythymidine + Methotrexate as a Novel Antineoplastic Combination in the Treatment of Human Immunodeficiency Virus-Related Non-Hodgkin's Lymphomas." Blood 89, no. 2 (1997): 419–25. http://dx.doi.org/10.1182/blood.v89.2.419.

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Abstract We have previously reported that 3′-azido 3′-deoxythymidine (AZT) can possess a significant antineoplastic activity when combined with drugs that disrupt de novo thymidylate synthesis, such as 5-fluorouracil and methotrexate (MTX). The aim of the present study was to evaluate the efficacy and the tolerance of the combination AZT + MTX in human immunodeficiency virus (HIV)-related non-Hodgkin's lymphoma (NHL). Twenty-nine patients (22 men and 7 women), either newly diagnosed or pretreated, have been enrolled in the trial; the median age was 34 years, 45% had acquired immunodeficiency s
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Pettit, George R., Paul J. Clewlow, Claude Dufresne, Dennis L. Doubek, Ronald L. Cerny, and Klaus Rützler. "Antineoplastic agents. 193. Isolation and structure of the cyclic peptide hymenistatin 1." Canadian Journal of Chemistry 68, no. 5 (1990): 708–11. http://dx.doi.org/10.1139/v90-110.

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The Western Pacific Ocean sponge Hymeniacidon sp. was found to contain a cyclo-octapeptide designated hymenistatin 1 (1) active against the P388 leukemia cell line (ED50 3.5 μg/mL). Structural determination was accomplished utilizing high field NMR (400 MHz) and mass spectral techniques (FAB MS/MS) followed by chiral gas chromatographic analysis to establish the absolute configuration (all S-amino acids). Keywords: cytostatic, Hymeniacidon, hymenistatin, cyclo-octapeptide, P388 leukemia.
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