Aclarubicin
Topoisomerase II Inhibitors
Amsacrine
Drug Antagonism
Daunorubicin
Antibiotics, Antineoplastic
DNA Topoisomerases, Type II
Carcinoma, Small Cell
Evidence of the role of protein kinase C during aclacinomycin induction of erythroid differentiation in K562 cells. (1/93)
At subtoxic concentrations, aclacinomycin is effective in controlling erythroid differentiation of K562, a human erythroleukemic cell line. To better understand early events implicated in this process, we have used bisindolylmaleimide (GF109203X), an inhibitor with a high selectivity for protein kinase C (PKC). Our data show that GF109203X inhibits aclacinomycin effects on K562, evidenced by a strong reduction of hemoglobinized cells and a marked decrease of mRNA rates of erythroid genes. To establish firmly PKC involvement, we also verified that aclacinomycin stimulates its rapid translocation, from the cytosolic to the membrane compartment. By Western blot analysis, we also show that after short induction times, PKCalpha was the most implicated. (+info)Modifications of aclacinomycin T by aclacinomycin methyl esterase (RdmC) and aclacinomycin-10-hydroxylase (RdmB) from Streptomyces purpurascens. (2/93)
The genes rdmB and rdmC of Streptomyces purpurascens encoding aclacinomycin modifying enzymes RdmB and RdmC were expressed in Streptomyces lividans TK24. In contrast to the earlier suggestion that RdmC may be an esterase that causes the removal of the carbomethoxy group from the 10 position of aclacinomycins, RdmC functions as an aclacinomycin methyl esterase and catalyzes the removal of the methoxy group from the C-15 position of aclacinomycin T producing 15-demethoxyaclacinomycin T. RdmB acts upon C-10 of 15-demethoxyaclacinomycin T and is able to remove the carboxylic group from the C-10 position. It functions also as an aclacinomycin-10-hydroxylase being able to add a hydroxyl group at the same, C-10 position in vitro. Aclacinomycin methyl esterase was purified to apparent homogeneity from S. lividans carrying the rdmC and aclacinomycin-10-hydroxylase as a glutathione S-transferase fusion construct from Escherichia coli carrying the rdmB gene, respectively. Aclacinomycin methyl esterase functions as a monomer and aclacinomycin-10-hydroxylase as a tetramer. Aclacinomycin methyl esterase has an exceptionally high temperature stability and has an apparent K(m) for aclacinomycin T of 15.5 microM. The introduction of rdmC and rdmB in a Streptomyces galilaeus mutant HO38 produced the same modifications of aclacinomycin T in vivo as aclacinomycin methyl esterase and aclacinomycin-10-hydroxylase in vitro. (+info)Molecular cloning and disruption of a novel gene encoding UDP-glucose: tetrahydrobiopterin alpha-glucosyltransferase in the cyanobacterium Synechococcus sp. PCC 7942. (3/93)
The gene encoding UDP-glucose:tetrahydrobiopterin alpha-glucosyltransferase (BGluT) was cloned from the genomic DNA of Synechococcus sp. PCC 7942. The encoded protein consisting of 359 amino acid residues was verified in vitro and in vivo to be responsible for the synthesis of tetrahydrobiopterin (BH4)-glucoside produced in the organism. The BGluT gene is the first cloned in pteridine glycosyltransferases and also a novel one cloned so far in UDP-glycosyltransferases. The mutant cells disrupted in the BGluT gene produced only aglycosidic BH4 at a level of 8.3% of the BH4-glucoside in wild type cells and exhibited half of the wild type growth in normal photoautotrophic conditions. These results suggest that the glucosylation of BH4 is required for the maintenance of the high cellular concentration of the compound, thereby supporting the normal growth of Synechococcus sp. PCC 7942. (+info)Keratin attenuates tumor necrosis factor-induced cytotoxicity through association with TRADD. (4/93)
Keratin 8 and 18 (K8/18) are the major components of intermediate filament (IF) proteins of simple or single-layered epithelia. Recent data show that normal and malignant epithelial cells deficient in K8/18 are nearly 100 times more sensitive to tumor necrosis factor (TNF)-induced cell death. We have now identified human TNF receptor type 1 (TNFR1)-associated death domain protein (TRADD) to be the K18-interacting protein. Among IF proteins tested in two-hybrid systems, TRADD specifically bound K18 and K14, type I (acidic) keratins. The COOH-terminal region of TRADD interacted with the coil Ia of the rod domain of K18. Endogenous TRADD coimmunoprecipitated with K18, and colocalized with K8/18 filaments in human mammary epithelial cells. Overexpression of the NH2 terminus (amino acids 1-270) of K18 containing the TRADD-binding domain as well as overexpression of K8/18 in SW13 cells, which are devoid of keratins, rendered the cells more resistant to killing by TNF. We also showed that overexpressed NH2 termini of K18 and K8/18 were associated with endogenous TRADD in SW13 cells, resulting in the inhibition of caspase-8 activation. These results indicate that K18 may sequester TRADD to attenuate interactions between TRADD and activated TNFR1 and moderate TNF-induced apoptosis in simple epithelial cells. (+info)Aclarubicin treatment restores SMN levels to cells derived from type I spinal muscular atrophy patients. (5/93)
Proximal spinal muscular atrophy (SMA) is a common motor neuron disorder caused by mutation of the telomeric survival of motor neuron gene SMN1. The centromeric survival of motor neuron SMN2 gene is retained in all SMA patients but does not produce sufficient SMN protein to prevent the development of clinical symptoms. The SMN1 and SMN2 genes differ functionally by a single nucleotide change. This change affects the efficiency with which exon 7 is incorporated into the mRNA transcript. Thus, SMN2 produces less full-length mRNA and protein than SMN1. We have screened a library of compounds in order to identify ones that can alter the splicing pattern of the SMN2 gene. Here, we report that the compound aclarubicin increases the retention of exon 7 into the SMN2 transcript. We show that aclarubicin effectively induces incorporation of exon 7 into SMN2 transcripts from the endogenous gene in type I SMA fibroblasts as well as into transcripts from a SMN2 minigene in the motor neuron cell line NSC34. In type I fibroblasts, treatment resulted in an increase in SMN protein and gems to normal levels. Our results suggest that alteration of splicing pattern represents a new approach to modification of gene expression in disease treatment and demonstrate the feasibility of high throughput screens to detect compounds that affect the splicing pattern of a gene. (+info)Superior outcome of infant acute myeloid leukemia with intensive chemotherapy: results of the Japan Infant Leukemia Study Group. (6/93)
This study analyzed data on 35 infants with acute myeloid leukemia (AML) who were treated with intensive chemotherapy between 1995 and 1998 in Japan. The incidence of boys, younger age (< 6 months old), and hyperleukocytosis at onset was high in patients with the M4/M5 subtype (n = 23) in the French-American-British classification, compared with the non-M4/M5 subtype (n = 12). Thirteen (56%) and 16 (70%) patients with the M4/M5 subtype also showed 11q23 translocations and MLL gene rearrangements, respectively, whereas only one patient with the non-M4/M5 subtype had this rearrangement. All 35 patients were treated with the ANLL91 protocol consisting of etoposide, high-dose cytarabine, and anthracyclines. Overall survival and the event-free survival (EFS) rates at 3 years of all patients were 76% (95% confidence interval [CI], 61.3%-90.7%) and 72% (95% CI, 56.4%-87.9%), respectively. EFS showed no significant difference between 2 subgroups divided by age, gender, presence of the MLL gene rearrangements, and white blood cell count at onset; EFS in patients with the M4/M5 subtype tended to be better than those with the non-M4/M5 subtype. Although all 6 patients who underwent allogeneic stem cell transplantation (SCT) have been in complete remission, no benefit of SCT was confirmed. These findings suggest that the intensive chemotherapy with the ANLL91 protocol might have been responsible for the observed good outcome of infant AML, even without SCT. The presence of the MLL gene rearrangements or the age at onset had no impact on the outcome of infant AML. (+info)Induction of p16INK4a transcription and of cellular senescence by aclacinomycin-derivatives and cardiac glycosides. (7/93)
Stable transformants of Saos-2 cells that contain the luciferase reporter gene under the control of the human p16INK4a transcriptional regulatory region were established, and were used to identify growth-inhibiting substances from culture broths of actinomycetes and extracts of plants. Among the active substances so far identified were an aclacinomycin-derivative, cenerubin B, and a cardiac glycoside, periplocin. These substances inhibited growth of normal human fibroblasts, and induced senescent phenotypes including a flattened morphology and increased acidic beta-galactosidase activity, although the activities of their derivatives to induce p16CDKN2 and beta-galactosidase did not coincided with each other. These results suggest that the reporter system using the p16CDKN2 transcriptional regulatory region is a useful means for screening growth inhibiting substances that are potential anti-tumor agents. (+info)Characterization of mutations in aclacinomycin A-non-producing Streptomyces galilaeus strains with altered glycosylation patterns. (8/93)
In this study a set of Streptomyces galilaeus ATCC 31615 mutants was characterized, which are incapable of synthesizing some or all of the deoxyhexose sugars of aclacinomycin A. Complementation experiments with the the mutant strains H026, H038, H039, H054, H063, H065 and H075 were carried out with glycosylation genes previously derived from the wild-type S. galilaeus. Mutations in strains H038, H063 and H075 were complemented with single PCR-amplified genes. Furthermore, amplification and sequencing of the corresponding genes from the mutant strains revealed single point mutations in the sequences. First, in H038 a transition mutation in aknQ, encoding a putative dTDP-hexose 3-ketoreductase, causes an amino acid substitution from glycine to aspartate, suppressing the biosynthesis of both 2-deoxyfucose and rhodinose and thus leading to the accumulation of aclacinomycin T with rhodosamine as its only sugar. Second, in H063, which accumulates aklavinone without a sugar moiety, amino acid substitution occurs, with threonine being substituted by isoleucine in dTDP-glucose synthase, the first enzyme participating in deoxyhexose biosynthesis, encoded by aknY. Third, a nonsense mutation in aknP leads to truncated dTDP-hexose 3-dehydratase in H075, which is incapable of synthesizing rhodinose. In addition, mutants H054 and H065, which accumulate aclacinomycins without aminosugars, were complemented by a gene for an aminotransferase, aknZ. Characterization of the nature of the mutations adds to the usefulness and value of the mutants in the analysis of gene function and in the creation of novel compounds by combinatorial biosynthesis. Furthermore, these results strengthen the assignments of akn gene products and enlighten the biosynthetic pathway for deoxyhexoses. (+info)
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Spinal muscular atrophy
Early leads also included sodium orthovanadate and aclarubicin. Morpholino-type antisense oligonucleotides, with the same ... "Aclarubicin treatment restores SMN levels to cells derived from type I spinal muscular atrophy patients". Human Molecular ...
Drug discovery
Anthracyclines (Aclarubicin · Daunorubicin · Doxorubicin · Epirubicin · Idarubicin · Amrubicin · Pirarubicin · Valrubicin · ...
Chemotherapy
This group includes novobiocin, merbarone, and aclarubicin, which also have other significant mechanisms of action. The ... Other clinically used drugs in the anthracycline group are pirarubicin, aclarubicin, and mitoxantrone. The mechanisms of ...
Topoisomerase inhibitor
Dexrazoxane Novobiocin Merbarone Anthrycycline aclarubicin Dexrazoxane also known as ICRF-187 is currently the only clinically ... Common catalytic inhibitors that target TopII are dexrazoxane, novobiocin, merbarone and anthrycycline aclarubicin. ...
Jacques Neefjes
Since 2019, Jacques Neefjes is co-financing the production of a promising cancer drug, Aclarubicin, which disappeared from the ...
Streptomyces isolates
... aclarubicin, tomaymycin, sibiromycin, and mazethramycin. Derivatives of Streptomycetes isolate migrastatin, including ...
List of MeSH codes (D09)
... aclarubicin MeSH D09.408.051.059.200 - daunorubicin MeSH D09.408.051.059.200.150 - carubicin MeSH D09.408.051.059.200.175 - ...
ATC code L01
L01CX01 Trabectedin L01DA01 Dactinomycin L01DB01 Doxorubicin L01DB02 Daunorubicin L01DB03 Epirubicin L01DB04 Aclarubicin ...
List of drugs: Ac
... aclarubicin (INN) aclatonium napadisilate (INN) aclidinium bromide (USAN, INN) Aclovate acolbifene (USAN) acodazole (INN) ...
List of MeSH codes (D04)
... aclarubicin MeSH D04.615.562.050.200 - daunorubicin MeSH D04.615.562.050.200.150 - carubicin MeSH D04.615.562.050.200.175 - ...
Aclarubicin
... (INN) or aclacinomycin A is an anthracycline drug that is used in the treatment of cancer. Soil bacteria ... October 1991). "Antagonistic effect of aclarubicin on daunorubicin-induced cytotoxicity in human small cell lung cancer cells: ... Streptomyces galilaeus can produce aclarubicin. It can induce histone eviction from chromatin upon intercalation. CID 451415 ...
Aclarubicin - Wikipedia
Aclarubicin (INN) or aclacinomycin A is an anthracycline drug that is used in the treatment of cancer. Soil bacteria ... October 1991). "Antagonistic effect of aclarubicin on daunorubicin-induced cytotoxicity in human small cell lung cancer cells: ... Streptomyces galilaeus can produce aclarubicin. It can induce histone eviction from chromatin upon intercalation. CID 451415 ...
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せりみっく副作用リスト
aciclovir, aclarubicin, cefepime, cytarabine, famotidine, fluconazole, granisetron, tazobactam・piperacillin, vancomycin. 80. 上肢 ... aciclovir, aclarubicin, cefepime, cytarabine, famotidine, fluconazole, granisetron, tazobactam・piperacillin, vancomycin. 80. 低 ... aciclovir, aclarubicin, cefepime, cytarabine, famotidine, fluconazole, granisetron, tazobactam・piperacillin, vancomycin. 80. 好中 ... aciclovir, aclarubicin, cefepime, cytarabine, famotidine, fluconazole, granisetron, tazobactam・piperacillin, vancomycin. 80. 脱水 ...
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せりみっく副作用リスト
aciclovir, aclarubicin, cefepime, cytarabine, famotidine, fluconazole, granisetron, tazobactam・piperacillin, vancomycin. 80. 上肢 ... aciclovir, aclarubicin, cefepime, cytarabine, famotidine, fluconazole, granisetron, tazobactam・piperacillin, vancomycin. 80. 低 ... aciclovir, aclarubicin, cefepime, cytarabine, famotidine, fluconazole, granisetron, tazobactam・piperacillin, vancomycin. 80. 好中 ... aciclovir, aclarubicin, cefepime, cytarabine, famotidine, fluconazole, granisetron, tazobactam・piperacillin, vancomycin. 80. 脱水 ...
MiR-7e-5p downregulation promotes transformation of low-grade follicular lymphoma to aggressive lymphoma by modulating an...
Aclarubicin, which belongs to the anthracycline family and inhibits cell proliferation by inhibiting topoisomerase, is widely ... Macrophages were pretreated with DMSO as the negative control for aclarubicin.. Supporting Figure S6. Expression of CD81 and ... For the treatment of FL, aclarubicin inhibits DNA replication in cells and is currently used as a standard chemotherapy for ... With the presence of aclarubicin in cultured medium (2.7 μg/ml), Western blotting revealed obvious higher levels of FasL and ...
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Treosulfan, sold under the brand name Trecondi, is a medication given to people before they have a bone marrow transplant from a donor known as allogeneic hematopoietic stem cell transplantation. It is used as a conditioning treatment to clear the bone marrow and make room for the transplanted bone marrow cells, which can then produce healthy blood cells.[3][4] It is used together with another medicine called fludarabine in adults and children from one month of age with blood cancers as well as in adults with other severe disorders requiring a bone marrow transplant.[3] It belongs to the family of drugs called alkylating agents.[3] In the body, treosulfan is converted into other compounds called epoxides which kill cells, especially cells that develop rapidly such as bone marrow cells, by attaching to their DNA while they are dividing.[3] The most common side effects in adults and children are infections, nausea (feeling sick), stomatitis (inflammation of the lining of the mouth), vomiting, ...
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Treatment1
- Aclarubicin (INN) or aclacinomycin A is an anthracycline drug that is used in the treatment of cancer. (wikipedia.org)
Cytarabine1
- MDS: decitabine, cytarabine, aclarubicin, and granulocyte colony-stimulating factor) with HLA-mismatched donor CD3+ allo-TLI 24 hours after each course. (hematologyadvisor.com)
Daunorubicin1
- Involved in the biosynthesis of aklavinone which is an important precursor common to the formation of the clinically significant anthracyclines such as carminomycin, daunorubicin (daunomycin), rhodomycin, aclacinomycin T (aklavin) and aclacinomycin A (aclarubicin). (icr.ac.uk)
Doxorubicin3
- Positively charged doxorubicin (DOX) and non-positively charged anthracyclines, aclarubicin (ACR) and morpholino-carminomycin (KRN 8602), have been investigated with respect to pharmacological parameters, cytotoxicity, DNA damage and repair in DOX-sensitive and -resistant murine and human cells. (elsevier.com)
- Friend leukemia cells (FLC) resistant to high concentrations of doxorubicin (DOX-RFLC3) or daunorubicin (DNR-RFLC3) (1771 and 1543 fold resistance respectively) express less than 10 fold resistance to aclarubicin (ACR). (elsevier.com)
- Three other compounds, aclarubicin, doxorubicin and mitoxantrone, showed some antifungal activity against C. glabrata and C. neoformans with MIC(50) values in the mid micromolar range. (uea.ac.uk)
Concentrations1
- All of the agents tested were potent in inducing micronuclei in human lymphoblastoid TK6 cells, with significant increases seen at low micromolar, and in the cases of aclarubicin and etoposide, at low nanomolar concentrations. (nih.gov)