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Rong Lin

Publications and source records attributed to Rong Lin.

At least 19 recordsLinked to original sources
PubMed2026

Integrated Bulk and Single-Cell RNA-Seq Analysis Reveals Transcriptional Activation of PTGS2 by FOS in Progression From T2DM to T2DM-Associated NAFLD.

Type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) frequently coexist, exacerbating disease burden. However, the molecular mechanisms underlying the progression from T2DM to T2DM-associated NAFLD remain unclear. This study investigated the regulatory function of FOS-mediated PTGS2 activation in this transition. We integrated bulk RNA-seq data from GEO, single-cell transcriptomic data and transcriptomes from patients with T2DM-associated NAFLD. Differentially expressed genes were identified using the limma package, and T2DM-related gene modules were defined by weighted gene co-expression network analysis. LASSO regression and random forest identified 14 candidate genes, with PTGS2 and FOS prioritised. Single-cell analysis showed increased FOS and PTGS2 expression in monocytes, CD8+ T cells and Kupffer cells. Transcription factor prediction and dual-luciferase assays confirmed that FOS directly binds the PTGS2 promoter and drives its transcription. In vitro, FOS silencing decreased PTGS2 expression, cytokine secretion and apoptosis under high-glucose and free fatty acid conditions, whereas PTGS2 overexpression exacerbated inflammation and apoptosis independently of FOS expression. These findings demonstrate that FOS transcriptionally activates PTGS2, contributing to hepatic inflammation and apoptosis during the progression from T2DM to NAFLD. PTGS2 may serve as a promising biomarker and therapeutic target for T2DM-associated NAFLD.

Single-Cell Gene Expression Analysis↗
PubMed2006

Prognosis of medullary thyroid carcinoma: demographic, clinical, and pathologic predictors of survival in 1252 cases.

BACKGROUND: Medullary thyroid cancer (MTC) is a rare cancer. There is a relative paucity of data over the last decade with regard to the prognosis of these patients. Therefore, the authors used the population-based Surveillance, Epidemiology, and End Results (SEER) registry to update what to their knowledge is one of the largest series of patients with MTC reported to date. METHODS: All patients with a diagnosis of MTC with active follow-up in the SEER database from 1973 to 2002 were included. Univariate and multivariate regression analyses were used to assess the associations between demographic, clinical, and pathologic characteristics of patients and survival. RESULTS: A total of 1252 patients with MTC were identified over 29 years of follow-up. In all, 87% of patients were white and 60% were female, with a mean age of 50 years. Although many variables were significant on univariate analysis, SEER stage and age at diagnosis were found to be the strongest predictors of survival in the multivariate analysis. Prognosis was poor in patients with advanced disease (hazards ratio [HR], 4.47), or those age >65 years (HR, 6.55). Patients who underwent surgery fared better than those who did not. Overall, 51% of patients had less than the currently recommended treatment guidelines for MTC. Adjuvant radiation therapy was found to be independently associated with a decreased survival (HR, 1.65). CONCLUSIONS: Stage of disease and age at diagnosis were found to be the strongest predictors of survival for patients with MTC. To the authors' knowledge there has been no change in stage at diagnosis or a significant improvement in survival noted over the last 30 years. Many patients underwent surgery that was deemed less than optimal for stage of disease.

Age of Onset↗
PubMed2006

Angiotensin II-induced C-reactive protein generation: inflammatory role of vascular smooth muscle cells in atherosclerosis.

BACKGROUND: As the major target of Angiotensin II (Ang II) in the vessel wall, vascular smooth muscle cells (VSMCs) are a tentative source to produce C-reactive protein (CRP). However, it is largely unknown if Ang II is capable of inducing CRP production in VSMCs. METHODS AND RESULTS: Ang II induced a concentration-dependent release of CRP in cultured rat VSMCs as measured by sandwich ELISA. Real-time PCR revealed that Ang II significantly upregulated CRP mRNA level in vitro. Ang II-induced CRP generation in aortic VSMCs was also investigated using double-labeled fluorescent immunohistochemistry and in situ hybridization in subchronic Ang II administration in rats. Losartan but not PD123319 markedly blocked the Ang II-induced CRP production in cultured VSMCs, suggesting that such effect was mediated via Ang II type 1 receptor. Further, Western blotting analysis showed that mitogen-activated protein kinase (MAPK) activation was obligatory in Ang II-induced CRP production, since specific MAPK inhibitor PD098059 almost abolished the action. CONCLUSIONS: We identified that Ang II is capable of inducing CRP generation in VSMCs, in which Ang II type 1 receptor followed by MAPK signal pathway is involved. It strengthened the role of Ang II-induced CRP production by VSMCs in the inflammatory process in atherosclerosis.

Angiotensin II↗
PubMed2006

Protective effect of tanshinone IIA on human umbilical vein endothelial cell injured by hydrogen peroxide and its mechanism.

Tanshinone IIA (Tan IIA) is isolated from Salvia miltiorrhiza, the root of which is widely used as a traditional Chinese medicine to treat atherosclerosis. The aim of the present study was to evaluate the putative protective effect of Tan IIA in a human umbilical vein endothelial cell line (ECV-304) injured by hydrogen peroxide in vitro and the mechanism of its protection. The percentage of cell viability was evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. The endothelial cell apoptosis and expression of cluster of differentiation 40 (CD40) were detected by flow cytometric analysis. Preincubation with Tan IIA significantly increased the viability of ECV-304 cell injured by hydrogen peroxide, which was accompanied with the increased nitric oxide level and superoxide dismutase activity in a dose-dependent manner. Moreover, cell apoptosis and CD40 expression were decreased in a dose-dependent manner. In conclusion, our data suggests that Tan IIA protects ECV-304 cell damage induced by hydrogen peroxide through its anti-oxidant effect and CD40 anti-inflammatory approach.

Abietanes↗
PubMed2006

Differentiation potential of bone marrow stromal cells to enteric neurons in vitro.

OBJECTIVE: To investigate whether bone marrow stromal cells (BMSC) can be induced to differentiate into enteric neurons and to produce more nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF). METHODS: Bone marrow stromal cells were harvested from male Sprague-Dawley rats and cultured in Dulbecco's modified eagle medium supplemented with 20% fetal bovine serum. The BMSC were passaged six times and characterized by flow cytometry. The BMSC were pre-induced by basic fibroblast growth factor (10 ng/mL) for 24 h, then induced with GDNF in fetal gut condition medium (FGCM) for 10 days. The expressions of neuronal markers neural specific enolase (NSE), neurofilament (NF), glial cell marker, glial fibrillary acedic protein (GFAP), and enteric neuronal marker protein gene product 9.5 (PGP9.5), neural nitric oxide synthase (nNOS), and enteric neural transmitter vasoactive intestinal polypeptide (VIP) were detected by fluorescent immunohistochemistry. Expression levels of GDNF and NGF mRNA were determined by RT-PCR. RESULTS: The cultured BMSC were CD90 (99.7%) positive and CD45 negative on flow cytometry. At day 10 of induction, 58.5 +/- 10.8% cells adopted neuron-like morphological changes and showed expression of NSE (47.6 +/- 7.5%), NF (75.6 +/- 8.4%), GFAP (negative), PGP9.5 (57.7 +/- 6.5%), nNOS (46.6 +/- 5.4%) and VIP (72.3 +/- 6.7%) by immunofluorescence. The BMSC expressed low levels of NGF and GDNF mRNA; however, after induction of GDNF in FGCM, the expression levels of NGF and GDNF mRNA were significantly increased. CONCLUSION: Bone marrow stromal cells have the potential to be induced to differentiate into enteric neurons, express enteric neural transmitters, and produce more NGF and GDNF. Therefore, BMSC could be used as new method to treat gastrointestinal motility disorders associated with enteric neural lesions.

Animals↗
PubMed2006

Lovastatin reduces apoptosis and downregulates the CD40 expression induced by TNF-alpha in cerebral vascular endothelial cells.

Inflammation may be one of the independent risk factors contributing to many neurological diseases. Moreover, there is an emerging body of data indicating that statins may have neuroprotective action. Recent studies suggest that CD40-CD40 ligand (CD40L) system is proven to be an important mediator of several auto-immune and chronic inflammation diseases. To address whether lovastatin produces neuroprotection as a potential novel anti-inflammatory pathway through the inhibition of CD40 expression, we examined the possible effects of lovastatin on expression of CD40, apoptosis, level of nitric oxide (NO) and nitric oxide synthase (NOS) activity induced by tumor necrosis factor alpha (TNF-alpha) in the cerebral vascular endothelial cells (CVECs) involved in cerebrovascular diseases. Preincubation with lovastatin (10(-7), 10(-6) and 10(-5) mol/l) for 24 hours (h) protected CVECs from TNF-alpha-induced decrease of cellular viability. Further, lovastatin inhibited the TNF-alpha-induced increases of NO level, NOS activity, apoptotic cells and CD40 expression in a dose-dependent manner, and anti-CD40 antibody also inhibited the cellular apoptosis induced by TNF-alpha. In conclusion, our data provide evidence to support a direct pro-inflammatory effect of CD40-CD40L signaling pathway in CVECs, and lovastatin possesses an anti-inflammatory effect independent of its lipid-lowering action involved in the cerebrovascular diseases.

Animals↗
PubMed2006

[Effects of quercetin on angiotensin II induced interleukin-6 in vascular smooth muscle cells].

OBJECTIVE: To observe the effects of quercetin on angiotensin (Ang II) induced interleukin-6 (IL-6) in vascular smooth muscle cells (VSMCs). METHODS: VSMCs were isolated from the thoracic aorta of Sprague-Dawley rats and were stimulated with different doses of Ang II. The production of IL-6 in supernatant of quercetin treated cultures was detected by ELISA. In parallel, IL-6 mRNA level was measured by RT-PCR. RESULTS: Ang II induced a marked increase of IL-6 in a dose- and time-dependent manner in the culture of VSMCs. Quercetin inhibited the production of Ang II -induced IL-6 in the culture in a dose-dependent manner. Similarly, the result with RT-PCR indicated that the expression of IL-6 mRNA induced by Ang II for 24h was down-regulated by quercetin. CONCLUSION: It demonstrates that quercetin possesses a inhibition of Ang II-induced production of IL-6 in VSMCs. Moreover, quercetin also down regulates the expression of IL-6 mRNA, suggesting the action of quercetin on IL-6 release induced by Ang II in VSMCs may underlie its anti-inflammatory properties.

Angiotensin II↗
PubMed2006

Fenofibrate inhibits tumor necrosis factor-alpha-induced expression of CD40 and matrix metalloproteinase in human vascular endothelial cells.

OBJECTIVE: To investigate the regulatory effects of fenofibrate on TNF-alpha-induced CD40 expression and matrix metalloproteinase (MMP) activity in human vascular endothelial cells (HUVECs). METHODS: Quantitative RT-PCR and flow cytometry were employed to evaluate the effect of fenofibrate on TNF-alpha-induced CD40 mRNA and cell surface CD40 expression in HUVECs, and gelatin zymography was used to determine the effect of fenofibrate on the gelatinolytic activities of MMP-2 and MMP-9 in TNF-alpha-stimulated HUVECs. RESULTS: Fenofibrate at the concentrations of 5x10(-5), 1x10(-4) and 2x10(-4) mol/L significantly reduced TNF-alpha-induced increment of CD40 mRNA and cell surface CD40 expressions (P<0.01), with the maximal inhibition achieved at the concentration of 1x10(-4) mol/L. Fenofibrate at 2x10(-4) mol/L did not further decrease CD40 expression induced by TNF-alpha. Fenofibrate significantly inhibited the stimulatory effect of TNF-alpha on MMP-2 and MMP-9 activities in HUVECs. CONCLUSION: Fenofibrate reduces TNF-alpha-induced increment of CD40 expression and MMP-2 and MMP-9 activities in HUVECs.

CD40 Antigens↗
PubMed2005

Parathyroidectomy improves neurocognitive deficits in patients with primary hyperparathyroidism.

BACKGROUND: Clinical guidelines for the treatment of primary hyperparathyroidism (pHPT) often suggest parathyroidectomy, but generally fail to consider neurocognitive and psychiatric symptoms because of the relative paucity of evidence. METHODS: In this prospective study, patients with pHPT (PTX) and benign euthyroid thyroid disease (THY) referred for operation were evaluated pre- and postoperatively with validated psychometric and neurocognitive instruments to determine whether learning, memory, or concentration improved with after parathyroidectomy. Statistical comparisons between groups were performed with univariate analysis and repeated measures of analysis of variance. RESULTS: Fifty-five subjects, mean age of 54 years, were evaluated preoperatively; 41 returned postoperatively. There were no significant differences between groups by age and gender. PTXs reported more depression symptoms preoperatively (P = .04) that improved postoperatively. There were no differences between the 2 groups on verbal memory and trait anxiety. For PTXs, average preoperative serum calcium concentration (11.3 mg/dL) and serum PTH level (100 pg/mL) normalized postoperatively. Preoperatively PTXs showed greater delays in their spatial learning (P = .03). All subjects learned across the 5 trials, but PTXs were more delayed (P = .03). After operation, PTXs improved and functioned at a level equivalent to the THYs. There was an interaction between trial (neurocognitive testing), visit (pre- vs postoperative), status (PTX vs THY), and change in PTH level (P = .06), suggesting that individuals with greater change in PTH were more likely to improve in their learning efficiency postparathyroidectomy. CONCLUSIONS: PHPT may be associated with a spatial learning deficit and processing that improves after parathyroidectomy. While longer-term follow-up is necessary, neurocognitive symptoms perhaps should be considered as criteria for parathyroidectomy.

Adult↗
PubMed2005

Critical role for Kalirin in nerve growth factor signaling through TrkA.

Kalirin is a multidomain guanine nucleotide exchange factor (GEF) that activates Rho proteins, inducing cytoskeletal rearrangement in neurons. Although much is known about the effects of Kalirin on Rho GTPases and neuronal morphology, little is known about the association of Kalirin with the receptor/signaling systems that affect neuronal morphology. Our experiments demonstrate that Kalirin binds to and colocalizes with the TrkA neurotrophin receptor in neurons. In PC12 cells, inhibition of Kalirin expression using antisense RNA decreased nerve growth factor (NGF)-induced TrkA autophosphorylation and process extension. Kalirin overexpression potentiated neurotrophin-stimulated TrkA autophosphorylation and neurite outgrowth in PC12 cells at a low concentration of NGF. Furthermore, elevated Kalirin expression resulted in catalytic activation of TrkA, as demonstrated by in vitro kinase assays and increased NGF-stimulated cellular activation of Rac, Mek, and CREB. Domain mapping demonstrated that the N-terminal Kalirin pleckstrin homology domain mediates the interaction with TrkA. The effects of Kalirin on TrkA provide a molecular basis for the requirement of Kalirin in process extension from PC12 cells and for previously observed effects on axonal extension and dendritic maintenance. The interaction of TrkA with the pleckstrin homology domain of Kalirin may be one example of a general mechanism whereby receptor/Rho GEF pairings play an important role in receptor tyrosine kinase activation and signal transduction.

Animals↗
PubMed2005

Lovastatin reduces nuclear factor kappaB activation induced by C-reactive protein in human vascular endothelial cells.

The role of C-reactive protein (CRP) in atherogenesis has been supported by more recent data. Some studies have demonstrated marked up-regulation inflammatory responses in endothelial cells subjected to CRP. The nuclear factor-kappaB (NF-kappaB) signal transduction is known to play a key role in the expression of these proatherogenic entities. Statins have anti-inflammatory properties independent of their cholesterol-lowering effects. Therefore, we studied the effects of CRP and lovastatin on NF-kappaB activation in human umbilical vein endothelial cells (HUVECs). By using an electrophoretic mobility shift assays (EMSA), we found that CRP (50 microg/ml) increased activation of NF-kappaB and degradation of inhibitory kappa B (IkappaB) in HUVECs, reaching a maximal effect after the incubation with CRP for 1 h. Lovastatin (10(-5) mol/l) diminished NF-kappaB activation induced by CRP. Furthermore, lovastatin may block NF-kappaB activation by causing a stabilization of the IkappaB-alpha in cellular cytoplasm with western blotting analysis. Preincubation of HUVECs with pyrrolidinethiocarbamate (PDTC, NF-kappaB inhibitor) diminished CD40 expression induced by CRP with flow cytometry. Our results suggest that CRP increases activation of NF-kappaB and induces CD40 expression in HUVECs partly via activation of NF-kappaB. Lovastatin, through the inhibition of NF-kappaB activation, reduces the inflammation involved in the pathogenesis of atherosclerosis.

Blotting, Western↗
PubMed2005

[Liposome-mediated human CD40 gene transfection and human umbilical vein endothelial ECV-304 cells].

OBJECTIVE: To construct an eukaryotic expression vector containing human CD40 gene for its efficient, continuous and stable expression in human umbilical vein endothelial ECV-304 cells. METHODS: The recombinant plasmid pUCD40 was digested with endonucleases to obtain human CD40 gene fragment, which was cloned into pCDNA3.1 vector to construct recombinant eukaryotic expression vector pCDNA3.1(+)/CD40. The recombinant vector was identified by enzyme digestion before introduced into ECV-304 cells via liposome, with the positive cell clones selected with G418. The stable transfection and expression of CD40 in ECV-304 cells were identified by reverse transcription (RT)-PCR, Western blotting and flow cytometry, respectively. RESULTS: Enzyme digestion analysis showed that target gene had been cloned into the recombinant vector. The transfected ECV-304 cells successfully expressed human CD40 as determined by RT-PCR and Western-blotting, and 95% of the cells were CD40-positive as shown by flow cytometry. CONCLUSION: The recombinant eukaryotic expression vector pCDNA3.1(+)/CD40 has been successfully constructed, which is capable of stable transfection and expression of CD40 in ECV-304 cells to facilitate further investigation of the roles of CD40 molecule in antiatherosclerotic drug development.

CD40 Antigens↗
PubMed2004

Deposition of amyloid fibrils promotes cell-surface accumulation of amyloid beta precursor protein.

Amyloid beta protein (Abeta) deposition and neuronal degeneration are characteristic pathological features of Alzheimer's disease (AD). In vitro, Abeta fibrils (fAbeta) induce neuronal degeneration reminiscent to AD, but the mechanism of neurotoxicity is unknown. Here we show that amyloid fibrils increase the level of cell-surface full-length amyloid beta precursor protein (h-AbetaPP) and secreted AbetaPP (s-AbetaPP). Pulse-chase analysis indicated that fAbeta selectively inhibited the turnover of cell-surface AbetaPP, without altering its intracellular levels. FAbeta-induced AbetaPP accumulation was not abrogated by cycloheximide, suggesting that increased protein synthesis is not critically required. Abeta fibrils sequester s-AbetaPP from the culture medium and promote its accumulation at the cell surface, indicating that binding of Abeta fibrils mediates AbetaPP accumulation. A time course analysis of Abeta treatment showed that AbetaPP level is elevated before significant cell death can be detected, while other toxic insults do not augment AbetaPP level, suggesting that AbetaPP may be specifically involved in early stages of Abeta-induced neurodegeneration. Finally, Abeta fibrils promote clustering of h-AbetaPP in abnormal focal adhesion-like (FA-like) structures that mediate neuronal dystrophy, increasing its association with the cytoskeleton. These results indicate that the interaction of Abeta fibrils with AbetaPP is an early event in the mechanism of Abeta-induced neurodegeneration that may play a significant role in AD pathogenesis.

Alzheimer Disease↗
PubMed2004

C-reactive protein-induced expression of CD40-CD40L and the effect of lovastatin and fenofibrate on it in human vascular endothelial cells.

Inflammation plays a pivotal role in the formation of atherosclerosis. In addition to being a risk marker for cardiovascular diseases, the role of C-reactive protein (CRP) in atherogenesis has been supported by more recent data. CD40-CD40L system is proven to be an important mediator of several auto-immune and chronic inflammation diseases. Interruption of CD40-CD40L signaling pathway not only reduces the initiation and progression of atherosclerotic lesions, but also modulates plaque architecture. By using a flow cytometry and western blotting, we found that incubation of human umbilical vein endothelial cells (HUVECs) with CRP resulted in a time- and dose-dependent increase in the cell-surface expression of CD40 and CD40L. In addition, CRP (25 microg/ml) increased gelatinolytic activities of MMP-2 and MMP-9. Anti-CD40 antibody significantly reversed the upregulated activities of MMP-2 and MMP-9 induced by CRP with gelatin zymography. Furthermore, lovastatin (10(-7), 10(-6), 10(-5) mol/l) and fenofibrate (5 x 10(-5), 10(-4), 2 x 10(-4) mol/l) significantly diminished the expression of CD40, CD40L and gelatinase activities (MMP-2, MMP-9) induced by CRP in HUVECs. In conclusion, our data provide evidence to support the direct pro-inflammatory effects of CRP via CD40-CD40L signaling pathway involved in the pathogenesis of atherosclerosis, and lovastatin and fenofibrate possess anti-inflammatory effects independent of their lipid-lowering action.

C-Reactive Protein↗
PubMed2004

[Protection of vascular endothelial cells from TNF-alpha induced injury by quercetin].

OBJECTIVE: To investigate the effects of quercetin (Que) on the TNF-alpha injured human umbilical vein endothelial cell line (ECV-304). METHODS: The experiments were performed in culture of TNF-alpha-induced ECV-304 in vitro. Cell viability was assessed with MTT assay. Lipid peroxidation of ECV-304 was monitored as malonaldehyde (MDA) with a fluorometric assay. NO and SOD of ECV-304 were monitored with colorimetry. The expression of NF-kappaB was detected with immunocytochemistry. RESULTS: TNF-alpha inhibited the ECV-304 prolifteration. Preincubation of ECV-304 with Que for 24h before TNF-alpha exposure increased the cell viability. Que significantly decreased the level of NO and MDA and the expression of NF-kappaB, and increased the activity of SOD in TNF-alpha-induced ECV-304. CONCLUSION: These results demonstrate that Que can produce the protective action on TNF-alpha-induced cultured ECV-304 and its mechanism of action may be related to the decrease of NO, antioxidant effect of lipids. However, antioxidant effect might be exerted through NF-kappaB activation pathway.

Cell Line↗
PubMed2004

[Effect of ligustrazine on injury of vascular endothelial cells ECV-304 induced by hypoxia and lack of glucose].

OBJECTIVE: To investigate the effects of ligustrazine on nitric oxide (NO), malonaldehyde (MDA) production, release of intracellular lactate dehydrogenase (LDH) and membrane fluidity of the injured human umbilical vein vascular endothelial cell line (ECV-304) with hypoxia and lack of glucose. METHOD: The experiments were performed in culture of ECV-304 injured with hypoxia and lack of glucose in vitro. The released LDH of ECV-304 was measured with automatic biochemistry analyse. NO content of ECV-304 was monitored with colorimetry. Lipid peroxidation of ECV-304 was monitored as MDA with a fluorometric assay. The membrane fluidity of ECV-304 was measured with the fluorescence polarization method. RESULT: After culture ECV-304 in hypoxia and lack of glucose for 24 h, the LDH release, MDA production and the membrane fluidity increased significantly and NO level was decreased. Preincubation of ECV-304 with ligustrazine for 24 h reduced LDH release, MDA production, membrane fluidity increasing and increased the level of NO in ECV-304 due to hypoxia and lack of glucose. CONCLUSION: Ligustrazine has protective effect on injury of ECV-304 induced by hypoxia and lack of glucose.

Cell Hypoxia↗
PubMed2003

[Detection of core-binding factor in acute leukemia with interphase fluorescence in situ hybridization].

OBJECTIVE: To detect the chromosomal abnormalities involving the core-binding factor (CBF) in acute leukemia at initial diagnosis with interphase in situ hybridization (I-FISH) technique, and monitor the minimal residual disease (MRD) after treatment with I-FISH. This study also aim to compare the sensitivity of I-FISH at initial diagnosis with that of conventional G-banding analysis. METHODS: Based on the diagnosis of bone marrow morphology, 15 acute leukemia patients were examined with conventional G-banding and I-FISH techniques. Seven of these patients were monitored for MRD with I-FISH after treatment. RESULTS: On the basis of the false-positive rate acquired from normal subjects, the normal cutoff values of the 3 probes including AML1/ETO translocation probe, MYH11 breakpoint region probe and ETV6/AML1 translocation probe were 4.13%, 1.95% and 2.12% respectively. With conventional G-banding analysis, 40% (6/15) patients were found with chromosomal abnormality involving CBF, including 5 of the 8 M2 patients with t (8;21) and 1 of the 2 M4EO patients with inv (16). No B-ALL cases were identified with t (12;21). With I-FISH, however, 80% (12/15) of the cases were found with genetic abnormality involving CBF, including all the 8 M2 cases with AML1/ETO fusion gene, both of the M4EO cases with CBFbeta/MYH11 and 2 of the 5 B-ALL cases with ETV6/AML1. In the 7 cases monitored for MRD level with I-FISH, 2 M2 cases and 1 B-ALL case were with positive results. CONCLUSIONS: I-FISH is more sensitive than conventional G-binding analysis in detecting the chromosomal abnormalities involving CBF in acute leukemia. At the time of initial diagnosis, combination of the two techniques may lead to more comprehensive and accurate results.

Adolescent↗