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Comparison of the subrenal capsule assay and succinate dehydrogenase inhibition test as drug sensitivity tests for cancer.

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The same chemotherapeutic agents were tested against fresh surgical explants of solid tumors obtained from 50 patients using the in vivo subrenal capsule (SRC) assay and the in vitro succinate dehydrogenase inhibition (SDI) test in comparison. Control growth adequate to meet evaluable assay criteria

Succinate Dehydrogenase-Deficient Gastrointestinal Stromal Tumors: Small Steps Toward Personalized Medicine?

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Various molecular triggers define heterogeneous subsets of gastrointestinal stromal tumors (GISTs), differing in clinical behavior and drug sensitivity. KIT/PDGFRA-wild-type GISTs, including those succinate dehydrogenase (SDH)-deficient, are overall unresponsive to the tyrosine kinase

The succinate dehydrogenase inhibition test for evaluating biopsy specimens and resected tumors of advanced gastric cancer.

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An in vitro chemosensitivity study of both biopsy specimens and surgically resected tumors of advanced gastric cancer from 12 patients was evaluated using the succinate dehydrogenase inhibition (SDI) test. A decrease in succinate dehydrogenase (SD) activity as an indicator of chemosensitivity was

Succinate dehydrogenase inhibition test for evaluating head and neck tumors.

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In vitro chemosensitivity was evaluated in human head and neck cancers using the succinate dehydrogenase (SD) test and the results were compared to findings in cases of malignant lymphomas and gastric cancers. Tumor fragments were exposed to several antitumor drugs at ten times the peak plasma

Chemosensitivity testing of human lung cancer tissues using the succinate dehydrogenase inhibition test.

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We examined the chemosensitivity of 57 primary lung cancer specimens to 9 antitumor drugs, using the succinate dehydrogenase inhibition (SDI) test. Average succinate dehydrogenase (SD) activity was reduced to less than 50% by cis-diaminedichloroplatinum (II) (DDP), cyclophosphamide (CPA), carboquone

[The sensitivity of 1,000 human tumors to antitumor drugs using the succinate dehydrogenase inhibition (SDI) test].

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The chemosensitivity was evaluated by the in vitro succinate dehydrogenase inhibition (SDI) test in 1,000 human tumors including 237 gastric cancers, 116 colorectal cancers, 113 hepatoma and 534 others. These tumor cells were exposed to 5 kinds of antitumor drugs, carboquone (CQ), adriamycin (ADM),

[In vitro chemosensitivity of various human tumors evaluated by the succinate dehydrogenase inhibition (SDI) test (2)].

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In vitro chemosensitivity was evaluated by succinate dehydrogenase inhibition (SDI) test in 94 human tumors including 59 gastric cancers, 27 colo-rectal cancers and 8 malignant lymphomas. Tumor fragments were exposed to 12 kinds of antitumor drugs at ten times peak plasma concentration. Evaluable

[In vitro chemosensitivity of various human tumors evaluated by the SDI (succinate dehydrogenase inhibition) test].

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In vitro chemosensitivity was evaluated by SDI test in various human tumors including 1 lymph node metastasis of esophageal cancer, 10 gastric cancers, 4 colo-rectal cancers, 1 hepatoma, 2 lung cancers, 2 breast cancers and 1 gallbladder cancer. Tumor fragments cut with scissors were exposed to

2-Methoxyestradiol Affects Mitochondrial Biogenesis Pathway and Succinate Dehydrogenase Complex Flavoprotein Subunit A in Osteosarcoma Cancer Cells.

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Dysregulation of mitochondrial pathways is implicated in several diseases, including cancer. Notably, mitochondrial respiration and mitochondrial biogenesis are favored in some invasive cancer cells, such as osteosarcoma. Hence, the aim of the current work was to investigate the effects of

The mitochondrial chaperone TRAP1 promotes neoplastic growth by inhibiting succinate dehydrogenase.

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We report that the mitochondrial chaperone TRAP1, which is induced in most tumor types, is required for neoplastic growth and confers transforming potential to noncancerous cells. TRAP1 binds to and inhibits succinate dehydrogenase (SDH), the complex II of the respiratory chain. The respiratory

Succinate dehydrogenase B-deficient cancer cells are highly sensitive to bromodomain and extra-terminal inhibitors.

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Mutations in succinate dehydrogenase B (SDHB) gene are frequently observed in several tumors and associated with poor prognosis in these tumors. Therefore, drugs effective for SDHB-deficient tumors could fulfill an unmet medical need. In addition, such drugs would have an advantage in that selection

Current management of succinate dehydrogenase-deficient gastrointestinal stromal tumors.

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Gastrointestinal stromal tumors (GISTs) are increasingly recognized as having diverse biology. With the development of tyrosine kinase inhibitors molecularly matched to oncogenic KIT and PDGFRA mutations, GISTs have become a quintessential model for precision oncology. However, about 5-10% of GIST

Breast cancer-associated macrophages promote tumorigenesis by suppressing succinate dehydrogenase in tumor cells

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Tumor-associated macrophages (TAMs) can exist in pro- and anti-inflammatory states. Anti-inflammatory TAMs (also referred to as M2-polarized) generally suppress antitumor immune responses and enhance the metastatic progression of cancer. To explore the mechanisms behind this phenomenon, we isolated

Studies of succinate dehydrogenase inhibition (SDI) test with cisplatin encapsulated liposome against cancer cells.

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In the present study, by means of encapsulating into liposome, cisplatin was made a soluble capsule, and augmentation of the antitumor effect through the cell affinity of liposome was investigated by chemosensitivity test for cancer cells. Augmentation of the antitumor effect by collaboration of the

[Study of in vitro cancer sensitivity of anticancer drugs by SDI (succinate dehydrogenase inhibition test)].

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To clarify the effect of fibroblast mixture in in vitro sensitivity test using SDI method. I have investigated the influence of fibroblast on the anticancer sensitivity test in a colon cancer cell line. The anticancer drugs, such as MMC (mitomycin C), CDDP (cisplatin) and 5-FU (5-fluorouracil) were

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