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1.
Journal of Experimental Hematology ; (6): 922-926, 2023.
Article Dans Chinois | WPRIM | ID: wpr-982152

Résumé

Acute myeloid leukemia (AML) is a heterogeneous hematopoietic tumor originated from hematopoietic stem cells. FLT3 is an important receptor tyrosine kinase in cell signal transduction pathway and one of the common mutated genes in AML. AML patients with FLT3-ITD mutation have a poor prognosis and tendency to relapse. Therefore, early identification of FLT3 gene mutation and selection of appropriate treatment are particularly important. Currently, the small moleculetargeted drugs have been new treatment methods for AML patients with FLT3-ITD mutation, but accompanied drug resistance need to be solved. This paper reviews the mechanism of FLT3 mutation, the clinical significance of FLT3 mutation in AML, FLT3 inhibitors and drug resistance mechanism.


Sujets)
Humains , Mutation , Inhibiteurs de protéines kinases/usage thérapeutique , Transduction du signal , Récepteurs à activité tyrosine kinase/usage thérapeutique , Leucémie aigüe myéloïde/traitement médicamenteux , Tyrosine kinase-3 de type fms/génétique
2.
Journal of Leukemia & Lymphoma ; (12): 374-377, 2022.
Article Dans Chinois | WPRIM | ID: wpr-953973

Résumé

Chronic myeloid leukemia (CML) is a malignant tumor formed by clonal proliferation of bone marrow hematopoietic stem cells. With the improvement of disease awareness and the introduction of new drugs, more than 90% of CML patients can achieve long-term survival. However, a few patients still show drug resistance. This article reviews the mechanism of drug resistance in CML patients treated with tyrosine kinase inhibitor (TKI) and the characteristics of ABL kinase region mutation.

3.
Acta Pharmaceutica Sinica ; (12): 839-844, 2018.
Article Dans Chinois | WPRIM | ID: wpr-779943

Résumé

Due to the potent bactericidal activity and low incidence of drug resistance, the novel cyclic lipopeptide antibiotic - daptomycin has emerged as one of the first line antimicrobial agents in the treatment of serious infections caused by gram-positive resistant pathogens. This review summarizes the research advances of daptomycin in recent years, mainly including spectrum of antimicrobial activity, biosynthesis, mode of action, mechanism of drug resistance, structure-activity relationships, surotomycin and siderophore-daptomycin conjugate to kill multidrug resistant Acinetobacter baumannii. The findings summarized in this review highlight the directions of next-generation of daptomycin derivatives.

4.
Article Dans Anglais | IMSEAR | ID: sea-136339

Résumé

Among the aetiological agents of treatable sexually transmitted diseases (STDs), Neissseria gonorrhoeae is considered to be most important because of emerging antibiotic resistant strains that compromise the effectiveness of treatment of the disease - gonorrhoea. In most of the developing countries, treatment of gonorrhoea relies mainly on syndromic management rather than the aetiological based therapy. Gonococcal infections are usually treated with single-dose therapy with an agent found to cure > 95 per cent of cases. Unfortunately during the last few decades, N. gonorrhoeae has developed resistance not only to less expensive antimicrobials such as sulphonamides, penicillin and tetracyclines but also to fluoroquinolones. The resistance trend of N. gonorrhoeae towards these antimicrobials can be categorised into pre-quinolone, quinolone and post-quinolone era. Among the antimicrobials available so far, only the third-generation cephalosporins could be safely recommended as first-line therapy for gonorrhoea globally. However, resistance to oral third-generation cephalosporins has also started emerging in some countries. Therefore, it has become imperative to initiate sustained national and international efforts to reduce infection and misuse of antibiotics so as to prevent further emergence and spread of antimicrobial resistance. It is necessary not only to monitor drug resistance and optimise treatment regimens, but also to gain insight into how gonococcus develops drug resistance. Knowledge of mechanism of resistance would help us to devise methods to prevent the occurrence of drug resistance against existing and new drugs. Such studies could also help in finding out new drug targets in N. gonorrhoeae and also a possibility of identification of new drugs for treating gonorrhoea.


Sujets)
Antibactériens/usage thérapeutique , Céphalosporines/métabolisme , Céphalosporines/usage thérapeutique , Résistance bactérienne aux médicaments/génétique , Gonorrhée/traitement médicamenteux , Gonorrhée/épidémiologie , Humains , Neisseria gonorrhoeae/effets des médicaments et des substances chimiques , Neisseria gonorrhoeae/génétique , Quinolinone/métabolisme , Quinolinone/usage thérapeutique , Sulfamides/métabolisme , Sulfamides/usage thérapeutique
5.
Chinese Journal of Nosocomiology ; (24)2006.
Article Dans Chinois | WPRIM | ID: wpr-587965

Résumé

OBJECTIVE To study the differences of quinolones-resistant determining region(QRDR) in DNA gyrase A(gyrA) subunit between drug-resistant Klebsiella pneumoniae induced by fluoroquinolone in vitro and strains isolated from clinical isolates.Furthermore,to reveal the relation between different QRDR gene mutations and drug-resistance. METHODS Ten sensitive K.pneumoniae strains were selected and induced into drug-resistant strains by ciprofloxacin.The QRDR in gyrA by polymerase chain reaction(PCR) was amplified and compared their DNA sequences with clinically isolated quinolone-resistant K.pneumoniae. RESULTS We had found several gene mutations of QRDR in fluoroquinolone-resistant K.pneumoniae induced by ciprofloxacin,including Ser 83(TCC)→Phe(TTC) and Ile(ATC);and Gln106(CAG)→Leu(CTG).And the alteration of Gln106(CAG)→Leu(CTG) was a new discovery. CONCLUSIONS There are gene mutations of QRDR in fluoroquinolone-resistant K.pneumoniae induced by ciprofloxacin.The mutation of Ser 83(TCC) and Gln106(CAG) is probably the molecular basis of inducing drug-resistant strains.

6.
Journal of Medical Postgraduates ; (12)2003.
Article Dans Chinois | WPRIM | ID: wpr-584985

Résumé

Nucleoside analogues are currently the main drug therapy against HBV infection. However, this type of therapy can cause gene mutations in HBV that result in drug resistance. The types of mutations caused by nucleoside analogues and the molecular mechanism of in vitro drug-resistance were reveiwed.

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