Efficacy and safety of Weichang' an pill combined with Western Medicine on gastrointestinal diseases: a systematic review and Meta-analysis.

OBJECTIVE: To systematically evaluate the efficacy and safety of Weichang'an pill (, WCA) combined with Western Medicine (WM) for the treatment of gastrointestinal diseases. METHODS: Eight databases, including China National Knowledge Infrastructure Database, Wanfang Data, China Science and Technology Journal Database, SinoMed, PubMed, Web of Science, Cochrane Library, and Embase, were searched for randomized controlled trials (RCTs) of WCA from inception to 30 September 2021. We independently screened the literature, extracted data, and then evaluated the bias risk, effectiveness, safety, and other indicators of the included articles. RESULTS: A total of 33 RCTs were included in this study with 3368 patients. After analysis, it was found that WCA combined with WM could effectively prevent and treat antibiotic-associated gastrointestinal reaction, functional dyspepsia (FD), irritable bowel syndrome, rotavirus diarrhea (RVD), and ulcerative colitis (UC); no serious adverse reactions occurred. Moreover, compared with the control group, the experimental group showed significantly improved symptoms and some biochemical parameters. CONCLUSIONS: WCA combined with WM for the treatment of gastrointestinal diseases had better clinical efficacy than the control group, without serious adverse reactions. Notably, in the treatment of FD, RVD, and UC, WCA improved clinical symptoms and biochemical indicator expression. Nevertheless, owing to the restricted quality and quantity of the literature, the results need to be further studied using high-quality RCTs.

Study of the Subfamily Anabropsinae (Orthoptera: Anostostomatidae) in China V: Two new species of Anabropsis (Apteranabropsis) from Guangxi and phylogenetic analysis of the genus Anabropsis.

This paper is the fifth study of the subfamily Anabropsinae in China and contributes two new species from Guangxi, China, viz. Anabropsis (Apteranabropsis) multispinula sp. nov. (Chinese name: ) and Anabropsis (Apteranabropsis) shii sp. nov. (Chinese name: ). The paraproctal processes and male genitalia of Anabropsis (Apteranabropsis) tonkinensis Rehn, 1906 are illustrated. The entire mitochondrial genomes (mitogenomes) of three species of Anabropsis were sequenced. The complete mitochondrial genomes of A. (Apteranabropsis) multispinula sp. nov., A. (Apteranabropsis) shii sp. nov. and A. (Apteranabropsis) guangxiensis were 16023 bp, 16087 bp and 16148 bp in length, respectively. Entire mitogenome and all protein-coding genes (PCGs) displayed high AT-content values. Besides A. (Pteranabropsis) carnarius and A. (Apteranabropsis) guangxiensis, other species of Anabropsis were not found repeated elements in the A+T-rich region. The phylogenetic relationships were constructed among nine samples of eight species of Anabropsis and two outgroups based on 13 PCGs using both Bayesian Inference (BI) and Maximum Likelihood (ML). The phylogenetic analysis did not support for the monophyly of subgenus Apteranabropsis. It's important to obtain more samples to derive accurate phylogenetic relationships.

Sensitive measurement of quantity dynamics of FLT3 internal tandem duplication at early time points provides prognostic information.

BACKGROUND: The level of minimal residual disease (MRD) in acute myeloid leukemia (AML) at early time points (TPs) may be an important prognostic factor. Although internal tandem duplication of FLT3 (FLT3-ITD) as an MRD marker has been questioned for its instability based on semi-quantitative methods, we hypothesized that FLT3-ITD dynamics measured by sensitive quantitative real-time PCR at early TPs before appearance of instability may provide prognostic information. PATIENTS AND METHODS: We measured mutant quantity in 493 serial samples from 55 patients with a median follow-up time of 64.8 months. The FLT3-ITD quantities after induction (TP1) and after the first post-induction chemotherapy (TP2) were analyzed. RESULTS: We found that lower FLT3-ITD levels at TP2 predicted longer overall survival (OS) and disease-free survival (DFS) regardless of cytogenetic risk. Multivariate analysis showed that ≥3 log reduction of FLT3-ITD at TP2 independently predicted better DFS and a trend toward better OS. FLT3-ITD disappeared at relapse in 16.7% of patients and none in those harboring mutant NPM1 compared with 29.4% in those with wild-type NPM1 (P = 0.032). CONCLUSIONS: Though the mutation may disappear at relapse in a few patients, FLT3-ITD levels at early TPs after chemotherapy provide prognostic information. FLT3-ITD is significantly more stable in those with mutant NPM1.

Cell type-specific protein-DNA interactions in the human zeta-globin upstream promoter region: displacement of Sp1 by the erythroid cell-specific factor NF-E1.

The protein-DNA interactions of the upstream promoter region of the human embryonic zeta-globin gene in nuclear extracts of erythroid K562 cells and nonerythroid HeLa cells were analyzed by DNase I footprinting, gel mobility shift assay, methylation interference, and oligonucleotide competition experiments. There are mainly two clusters of nuclear factor-binding sites in the zeta promoter. The proximal cluster spans the DNA sequence from -110 to -60 and consists of binding sites for CP2, Sp1, and NF-E1. NF-E1 binding is K562 specific, whereas CP2 binding is common to both types of cells. Overlapping the NF-E1- and CP2-binding sites is a hidden Sp1-binding site or CAC box, as demonstrated by binding studies of affinity-purified Sp1. In the distal promoter region at -250 to -220, another NF-E1-binding site overlaps a CAC box or Sp1-binding site. Extract-mixing experiments demonstrated that the higher affinity of NF-E1 binding excluded the binding of Sp1 in the K562 extract. NF-E1 factors could also displace prebound Sp1 molecules. Between the two clusters of multiple-factor-binding sites are sequences recognized by other factors, including zeta-globin factors 1 and 2, that are present in both HeLa and K562 extracts. We discuss the cell type-specific, competitive binding of multiple nuclear factors in terms of functional implications in transcriptional regulation of the zeta-globin gene.

Overexpression of SOX4 correlates with poor prognosis of acute myeloid leukemia and is leukemogenic in zebrafish.

The SOX4 transcription factor is a key regulator of embryonic development, cell-fate decision, cellular differentiation and oncogenesis. Abnormal expression of SOX4 is related to malignant tumor transformation and cancer metastasis. However, no reports are available regarding the clinical significance of SOX4 in acute myeloid leukemia (AML) and the role of SOX4 in leukemogenesis. In the current study, we found that AML patients with low bone marrow (BM) SOX4 expression had higher remission rates and longer overall survival than those with high SOX4 expression, regardless of age, white blood cell count at diagnosis, karyotype profile and NPM1/FLT3-ITD status. To elucidate the role of SOX4 in leukemogenesis, we generated a transgenic zebrafish model that overexpressed human SOX4 in the myeloid lineage Tg(spi1-SOX4-EGFP). These transgenic zebrafish showed, at 5 months of age, increased myelopoiesis with dedifferentiation in kidney marrow. At 9 months of age, their kidney structure was significantly effaced and distorted by increased infiltration of myeloid progenitor cells. These results suggest that SOX4 is not only an independent prognostic factor of AML, but also an important molecular factor in leukemogenesis.

Clinico-biological significance of suppressor of cytokine signaling 1 expression in acute myeloid leukemia.

Suppressor of cytokine signaling 1 (SOCS1) protein, which encodes a member of signal transducers and activators of transcription-induced inhibitors, takes part in a negative regulation of cytokine signaling. The mechanism of SOCS1 in tumor carcinogenesis is complex and there have been no studies concerning the clinic-biologic implication of SOCS1 expression in acute myeloid leukemia (AML). Here, we first identified that higher bone marrow (BM) SOCS1 expression was closely associated with older age, FLT3-ITD, NPM1 and DNMT3A mutations, but negatively correlated with CEBPA mutation in patients with de novo AML. Compared to patients with lower SOCS1 expression, those with higher expression had lower complete remission rates and shorter overall survival. Further, higher expression of SOCS1 in the BM was an independent unfavorable prognostic factor irrespective of age, white blood cell, cytogenetics and gene mutations. Next, we generated zebrafish model overexpressing SOCS1 by spi1 promoter, which showed kidney marrow from adult SOCS1 zebrafish had increased myelopoiesis, myeloid progenitors and the kidney or spleen structure were effaced and distorted, mimicking leukemia phenotype. The SOCS1/FLT3-ITD double transgenic fish could further facilitate the leukemic process. The results indicate SOCS1 plays an important role in AML and its higher expression serves as a new biomarker to risk-stratify AML patients.

Efficacy of cetuximab-based chemotherapy in metastatic colorectal cancer according to RAS and BRAF mutation subgroups: A meta-analysis.

The epidermal growth factor receptor (EGFR)-targeting monoclonal antibody, cetuximab, has been added to standard chemotherapy regimens for treating metastatic colorectal cancer (mCRC). However, the efficacy of adding cetuximab to chemotherapy regimens for patients of differing genetic backgrounds remains controversial. The present study aimed to investigate the efficacy of adding cetuximab to chemotherapeutic regimens in subgroups of patients defined according to the RAS and BRAF mutation status in the first-line treatment of patients with mCRC. A systematic literature search was performed in databases (including PubMed, Embase, the Cochrane library, the American Society of Clinical Oncology and the European Society For Medical Oncology) up to August 2015. Randomized controlled trials analyzing overall survival (OS) and progression-free survival (PFS) in mCRC treated with cetuximab, and grouped by RAS and BRAF mutation status, were identified. The major outcome measures were hazard ratios (HRs). Pooled HRs were calculated using fixed- or random-effects models, according to the magnitude of the heterogeneity. A total of nine studies met the inclusion criteria. Use of cetuximab was significantly associated with longer OS in KRAS exon 2 wild-type tumors [HR=0.87, 95% confidence interval (CI)=0.79-0.96, Z=2.91, P=0.004] and wild-type KRAS/RAS (in exons 2, 3 and 4 of KRAS and exons 2, 3 and 4 of an associated gene, NRAS; HR=0.72, 95% CI=0.60-0.85, Z=3.74, P=0.0002). No significant differences in OS and PFS were identified between KRAS exon 2 mutations and tumors with the other RAS mutations (in exons 3 and 4 of KRAS and exons 2, 3 and 4 of an associated gene, NRAS). The meta-analysis demonstrated that cetuximab-based chemotherapeutic regimens led to a marked improvement in OS in patients with mCRC who lacked any RAS mutations (either KRAS exon 2 or any other RAS mutation). By contrast, the subgroup analyses revealed no evident PFS or OS benefit in using cetuximab for patients with any RAS mutation. Taken together, the evidence indicates that cetuximab should only be used for mCRC patients with the wild-type RAS gene. Some benefits were observed in patients with wild-type KRAS/BRAF who received cetuximab-based chemotherapy, even though there were insufficient data to perform meta-analysis with the BRAF mutation status.

Clinicopathological observation of primary lung enteric adenocarcinoma and its response to chemotherapy: A case report and review of the literature.

Primary lung enteric adenocarcinoma is a rare type of invasive lung carcinoma. Its morphology and immunohistochemistry are those of colorectal carcinoma, but there is no associated primary colorectal carcinoma. The present study describes the case of a 53-year-old female who presented with an irritating cough and a mass around the right sternoclavicular joint. Comprehensive evaluation revealed involvement of the mediastinum, lungs, right sternoclavicular joint and right kidney. Biopsies from the mediastinal and right sternoclavicular joint tumors showed features of adenocarcinoma. Immunohistochemistry was positive for cytokeratin (CK)20 and caudal type homeobox transcription factor 2, and negative for CK7, thyroid transcription factor-1 and napsin A. Genotypic analysis identified the expression of wild-type epidermal growth factor receptor, Kirsten rat sarcoma viral oncogene homolog, serine/threonine-protein kinase B-Raf and UDP-glucuronosyltransferase 1-1. There was no expression of echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase and a moderate expression of excision repair cross-complementation group 1, ribonucleoside-diphosphate reductase large subunit and tubulin ß-3 chain. A strong expression of thymidylate synthase and 677TC genotype expression of methylenetetrahydrofolate reductase was observed. Gastroscopy, enteroscopy, colorectal colonoscopy and positron emission tomography-computed tomography failed to find evidence of a gastrointestinal malignancy and primary lung enteric adenocarcinoma was diagnosed. The presence of multiple metastases did not permit curative surgery. The patient was treated with 3 monthly cycles of the XELOX chemotherapy regimen; the response was poor with progression of supraclavicular lesions. Treatment was switched to the TP regimen for 4 monthly cycles, which resulted in a significant reduction in the size of the lung lesions; however, the supraclavicular lesion responded poorly to the treatment. The patient then received 2 cycles of the FOLFIRI regimen; however, the lung and right supraclavicular lesions progressed, causing increased right upper limb pain. The pain was alleviated by palliative surgery. Following surgery, the DP regimen was employed. Follow-up of the patient remains ongoing. The present findings suggest that the early diagnosis and treatment of primary lung enteric adenocarcinoma is likely to improve patient outcome.

Genetic alterations and their clinical implications in older patients with acute myeloid leukemia.

A number of patient-specific and leukemia-associated factors are related to the poor outcome in older patients with acute myeloid leukemia (AML). However, comprehensive studies regarding the impact of genetic alterations in this group of patients are limited. In this study, we compared relevant mutations in 21 genes between AML patients aged 60 years or older and those younger and exposed their prognostic implications. Compared with the younger patients, the elderly had significantly higher incidences of PTPN11, NPM1, RUNX1, ASXL1, TET2, DNMT3A and TP53 mutations but a lower frequency of WT1 mutations. The older patients more frequently harbored one or more adverse genetic alterations. Multivariate analysis showed that DNMT3A and TP53 mutations were independent poor prognostic factors among the elderly, while NPM1 mutation in the absence of FLT3/ITD was an independent favorable prognostic factor. Furthermore, the status of mutations could well stratify older patients with intermediate-risk cytogenetics into three risk groups. In conclusion, older AML patients showed distinct genetic alterations from the younger group. Integration of cytogenetics and molecular mutations can better risk-stratify older AML patients. Development of novel therapies is needed to improve the outcome of older patients with poor prognosis under current treatment modalities.

microRNA-195 inhibits the proliferation, migration and invasion of cervical cancer cells via the inhibition of CCND2 and MYB expression.

The functions of microRNAs (miRNA/miR) in the development of cervical cancer remain largely undefined. The present study investigated the role of miR-195 in cervical cancer development. The expression of miR-195 mimics in the cervical cancer HeLa cell line significantly decreased the cell proliferation, migration and invasion capacities in vitro. Using miRNA target prediction algorithms and reporter assays, cyclin D2 (CCND2) and v-myb avian myeloblastosis viral oncogene homolog (MYB) were identified as direct targets of miR-195. Moreover, miR-195 repressed the expression of CCND2 and MYB in the HeLa cells at the mRNA and protein levels. Finally, the expression of miR-195 was downregulated in cervical cancer tissues compared with normal tissues. Together, these data suggest that miR-195 is a tumor suppressor in cervical cancer.

Reductions in calcitonin gene-related peptide may be associated with the impairment of the contralateral testis in unilateral cryptorchidism.

The aim of the present study was to investigate the mechanism underlying the impairment of the contralateral testis in unilateral cryptorchidism in experimental rats using a molecular neurophysiological approach. Thirty-six male rats (21 days old) were divided into a cryptorchidism group, a cryptorchidism with division of the genitofemoral nerve (GFN) group and a control group (n=12/group). The distribution of the calcitonin gene-related peptide (CGRP) immunoreactive nerve fibers in the testes was studied using an immunohistochemistry technique. Germ cell apoptosis was detected using the terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling method. The concentration of malondialdehyde (MDA) in the testis tissue was evaluated using a spectrophotometric determination method, and the ultrastructure of Sertoli cells was observed using transmission electron microscopy. It was found that, 100 days after the surgery, the concentration of CGRP in the cryptorchidism group was decreased significantly, whereas the levels of MDA and the number of apoptotic germ cells were increased significantly compared with the control group (P<0.01). Following the division of the GFN, the damaging effects were decreased (P<0.01). The impairment mechanism may therefore be associated with a reduction in the level of CGRP in the contralateral testis. The reflex decrease in CGRP may be caused by germ cell apoptosis, decreased blood flow and oxygen levels, and the increase in reactive oxygen free radicals and lipid peroxidation.

TP53 mutations in de novo acute myeloid leukemia patients: longitudinal follow-ups show the mutation is stable during disease evolution.

The TP53 mutation is frequently detected in acute myeloid leukemia (AML) patients with complex karyotype (CK), but the stability of this mutation during the clinical course remains unclear. In this study, TP53 mutations were identified in 7% of 500 patients with de novo AML and 58.8% of patients with CK. TP53 mutations were closely associated with older age, lower white blood cell (WBC) and platelet counts, FAB M6 subtype, unfavorable-risk cytogenetics and CK, but negatively associated with NPM1 mutation, FLT3/ITD and DNMT3A mutation. Multivariate analysis demonstrated that TP53 mutation was an independent poor prognostic factor for overall survival and disease-free survival among the total cohort and the subgroup of patients with CK. A scoring system incorporating TP53 mutation and nine other prognostic factors, including age, WBC counts, cytogenetics and gene mutations, into survival analysis proved to be very useful to stratify AML patients. Sequential study of 420 samples showed that TP53 mutations were stable during AML evolution, whereas the mutation was acquired only in 1 of the 126 TP53 wild-type patients when therapy-related AML originated from different clone emerged. In conclusion, TP53 mutations are associated with distinct clinic-biological features and poor prognosis in de novo AML patients and are rather stable during disease progression.

Competitive effects of long-chain-triglyceride emulsion on the metabolism of medium-chain-triglyceride emulsions.

This study was conducted to assess the potential metabolic competitive interactions of intravenous medium-chain-triglyceride (MCT) and long-chain-triglyceride (LCT) lipid emulsions. To assess this competition increasing concentrations of LCT emulsion were added to an intravenous dose of MCT emulsion of 3.0 g/kg body wt up to a maximum dose of 3.0 g LCTs/kg body wt. Blood samples were assessed for competitive interactions by analyzing the following metabolites: glucose, insulin, lactate, pyruvate, ketones (acetoacetate, beta-hydroxybutyrate), elimination of triglycerides, and free fatty acids. Evaluation of the data showed a strong competitive interaction between the MCT and LCT emulsions. This competition was evident as soon as LCTs were added to the MCT infusions and appeared to favor LCTs for removal and metabolism over MCTs. This appears to indicate that there is a peripheral, strong affinity site for LCT removal and metabolism and a shared peripheral site and specific visceral site for MCT removal and metabolism.

Significance of nm23 mRNA expression in human hepatocellular carcinoma.

It has been proposed that nm23-H1, a candidate suppressor gene for metastasis, plays an important role in the metastasis of human tumors. In order to investigate its role in the human hepatocellular carcinoma (HCC), 18 matched pairs of tumorous and adjacent nontumorous liver tissues of hepatectomy from patients with HCC were studied by quantitative reverse transcription-PCR. Further analyses of the nm23-H1 gene were also done. The results of these molecular studies were correlated with the clinicopathologic features of the patients. Nm23-H1 transcript was expressed in all neoplastic and adjacent nontumorous liver tissue. The level of expression, however, did not correlate well with the extension or metastatic potential of the tumors. Instead, in 15 (83.3%) of 18 HCC, nm23-H1 expression was higher in the tumorous tissues, compared with the adjacent nontumorous tissues; and significantly higher levels of nm23-H1 mRNA expression was detected in HCC with poor differentiation (Edmonson classification, III and IV) than those with moderate differentiation (I and II). Southern blot analysis of nm23-H1 gene revealed neither amplification nor loss of heterozygosity of all HCC tissues examined. Direct sequencing of the nm23-H1 gene in all HCC tissues detected no mutations. Our findings suggested that increased nm23-H1 mRNA expression is correlated with HCC tumor progression.

Stability of curcumin in buffer solutions and characterization of its degradation products.

The degradation kinetics of curcumin under various pH conditions and the stability of curcumin in physiological matrices were investigated. When curcumin was incubated in 0.1 M phosphate buffer and serum-free medium, pH 7.2 at 37 degrees C, about 90% decomposed within 30 min. A series of pH conditions ranging from 3 to 10 were tested and the result showed that decomposition was pH-dependent and occurred faster at neutral-basic conditions. It is more stable in cell culture medium containing 10% fetal calf serum and in human blood; less than 20% of curcumin decomposed within 1 h, and after incubation for 8 h, about 50% of curcumin is still remained. Trans-6-(4'-hydroxy-3'-methoxyphenyl)-2,4-dioxo-5-hexenal was predicted as major degradation product and vanillin, ferulic acid, feruloyl methane were identified as minor degradation products. The amount of vanillin increased with incubation time.

Analysis of hemoglobin gamma chain in patients with Cooley's anemia in Taiwan.

The beta-like globin gene cluster, consisting of five genes and a pseudogene, is located on chromosome 11 and is arranged in the order 5'-epsilon-G gamma-A gamma-phi beta-delta-beta-3'. With the fast and sensitive method of high-performance liquid chromatography (HPLC) in the gradient mobile system, we studied the G gamma values of fetal hemoglobin in 34 patients with Cooley's anemia, 100 normal adults and 100 newborns. There were 84 newborns with a mean G gamma value of 67.41 +/- 2.37%, 15 newborns with a G gamma value of 83.45 +/- 1.92% and one newborn with a G gamma value of 100%. Because the medium value of 67.41% and 100% is near the value of 83.45%, we speculate that there are different g gene genotypes; that is, the group with a G gamma value of 100% has a genotype of G gamma-G gamma/G gamma-G gamma, the group with a G gamma value of 83.45% has a genotype of G gamma-G gamma/G gamma-A gamma, and the group with a G gamma value of 67.41% has a genotype of G gamma-A gamma/G gamma-A gamma. The G gamma value for normal adults was 41.84 +/- 20.91%. While the G gamma values for patients with Cooley's anemia were divided into two groups, 56.23 +/- 6.55% and 80.60 +/- 3.05%. There was no case having a G gamma value of 100%. Our results suggest that the expression of the gamma gene in Cooley's anemia is similar to that of the newborns.

Detection of enterovirus RNA in patients with idiopathic dilated cardiomyopathy by polymerase chain reaction.

The pathogenic role of enterovirus in patients with idiopathic dilated cardiomyopathy has been determined through a molecular biologic approach. Sensitivity in the detection of viral genomes in tissues varied between conventional nucleic acid hybridization and polymerase chain gene amplification. To improve diagnosis, we developed a strategy for reverse transcription polymerase chain reaction (RT-PCR) to detect viral RNA. We synthesized two sequence-specific oligonucleotides, primer 1 (5'dACCGACGAATACCACTGTTA3') and primer 2 (5'dCCTCCGGCCCCTGAATGCGGCTAAT3'), complementary to the 5' conserved viral genomic fragments. Viral RNA was amplified by double PCR with these two primers and hybridized with a 32-P labeled inter-primer probe (5'dATGAAACCCACAGGCACAAAG3'). Using this strategy, we detected as little as 10(-8) micrograms of coxsackievirus B3 RNA after amplification with RT-PCR, but detected none in the plasma of eight healthy adults. Among 15 patients with idiopathic dilated cardiomyopathy, viral RNA could be detected in one out of 12 plasmas (8%) and three out of four explanted heart tissues (75%). In contrast, no viral RNA could be detected in six samples of myocardial tissue from patients with other heart diseases. The only patient who had viral RNA in his plasma also had viral RNA in his myocardium. Thus, the high incidence of viral RNA in these patients suggests a possible etiologic link between them. Correct selection of specific PCR primers and the application of double PCR can improve chances of diagnosing enteroviral infection.

Integration of cytogenetic and molecular alterations in risk stratification of 318 patients with de novo non-M3 acute myeloid leukemia.

Conventionally, acute myeloid leukemia (AML) patients are categorized into good-, intermediate- and poor-risk groups according to cytogenetic changes. However, patients with intermediate-risk cytogenetics represent a largely heterogeneous population regarding treatment response and clinical outcome. In this study, we integrated cytogenetics and molecular mutations in the analysis of 318 patients with de novo non-M3 AML who received standard chemotherapy. According to the mutation status of eight genes, including NPM1, CEBPA, IDH2, RUNX1, WT1, ASXL1, DNMT3A and FLT3, that had prognostic significance, 229 patients with intermediate-risk cytogenetics could be refinedly stratified into three groups with distinct prognosis (P<0.001); patients with good-risk genotypes had a favorable outcome (overall survival, OS, not reached) similar to those with good-risk cytogenetics, whereas those with poor-risk genotypes had an unfavorable prognosis (OS, 10 months) similar to those with poor-risk cytogenetics (OS, 13.5 months), and the remaining patients with other genotypes had an intermediate outcome (OS, 25 months). Integration of cytogenetic and molecular profiling could thus reduce the number of intermediate-risk AML patients from around three-fourth to one-fourth. In conclusion, integration of cytogenetic and molecular changes improves the prognostic stratification of AML patients, especially those with intermediate-risk cytogenetics, and may lead to better decision on therapeutic strategy.