scholarly journals Survival analysis and mortality predictors of hospitalized severe burn victims in a Malaysian burns intensive care unit

2019 ◽  
Vol 7 ◽  
Author(s):  
Henry Tan Chor Lip ◽  
Jih Huei Tan ◽  
Mathew Thomas ◽  
Farrah-Hani Imran ◽  
Tuan Nur’ Azmah Tuan Mat
Keyword(s):  
Risk Factors ◽  
Mechanical Ventilation ◽  
Survival Analysis ◽  
Burn Injury ◽  
Survival Curve ◽  
Inhalation Injury ◽  
Burn Victims ◽  
Kaplan Meier ◽  
Simple Logistic ◽  
Meier Survival Curve

Abstract Background Prognostic measures to determine burn mortality are essential in evaluating the severity of individual burn victims. This is an important process of triaging patients with high risk of mortality that may be nursed in the acute care setting. Malaysian burn research is lacking with only one publication identified which describes the epidemiology of burn victims. Therefore, the objective of this study was to go one step further and identify the predictors of burn mortality from a Malaysian burns intensive care unit (BICU) which may be used to triage patients at higher risk of death. Methods This is a retrospective cohort study of all admissions to Hospital Sultan Ismail’s BICU from January 2010 till October 2015. Admission criteria were in accordance with the American Burn Association guidelines, and risk factors of interest were recorded. Data was analyzed using simple logistic regression to determine significant predictors of mortality. Survival analysis with time to death event was performed using the Kaplan-Meier survival curve with log-rank test. Results Through the 6-year period, 393 patients were admitted with a male preponderance of 73.8%. The mean age and length of stay were 35.6 (±15.72) years and 15.3 (±18.91) days. There were 48 mortalities with an overall mortality rate of 12.2%. Significant risk factors identified on simple logistic regression were total body surface area (TBSA) > 20% (p < 0.001), inhalation injury (p < 0.001) and presence of early systemic inflammatory response syndrome (SIRS) (p < 0.001). Survival analysis using Kaplan-Meier survival curve showed similar results with TBSA > 20%, presence of SIRS, mechanical ventilation and inhalation injury which were associated with poorer survival (p < 0.001). Conclusion The predictors of mortality identified in a Malaysian BICU were TBSA > 20%, early SIRS, mechanical ventilation and inhalation injury which were associated with poorer survival outcome. The immunological response differs from individual patients and influenced by the severity of burn injury. Early SIRS on admission is an important predictor of death and may represent the severity of burn injury. Patients who required mechanical ventilation were associated with mortality and it is likely related to the severity of pulmonary insults sustained by individual patients. This data is important for outcome prognostication and mortality risk counselling in severely burned patients.

The Incidence Prognosis and Risk Factors of Cognitive Impairment in Maintenance Haemodialysis Patients

2018 ◽  
Vol 47 (1-3) ◽  
pp. 101-108 ◽  
Author(s):  
Renhua Lu ◽  
Chenqi Xu ◽  
Yan Li ◽  
Ling Yu ◽  
Xinghua Shao ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cognitive Impairment ◽  
Diastolic Pressure ◽  
Survival Curve ◽  
Maintenance Haemodialysis ◽  
Kaplan Meier ◽  
Education Status ◽  
Independent Risk Factors ◽  
Meier Survival Curve

Objective: To investigate the incidence and the prognosis of cognitive impairment (CI) and to find out the risk factors associated with the outcome in maintenance haemodialysis (MHD) patients. Methods: Enrolled the patients who met the criteria as below: MHD (≥3 months) patients before July 2014, ≥18 years old and could carry on the cognitive function test (Montreal Cognitive Assessment [MoCA]). All enrolled patients were divided into 2 groups: CI group (MoCA < 26) and non-CI group (MoCA ≥26). All patients were followed up for 36 months. The incidence, demography data, medical history, haemodialysis data, laboratory examination and prognosis of CI in haemodialysis patients were prospectively compared and analyzed. Multivariate logistic regression analysis was used to investigate the risk factors of CI. Kaplan-Meier survival curve was used for survival analysis. Results: In the present study, 219 patients were enrolled. The ratio of male to female was 1.46: 1. Age was 60.07 ± 12.44 and dialysis vintage was 100.79 ± 70.23 months. One hundred thirteen patients’ MoCA scores were lower than 26 were divided into CI group. Education status (OR 3.428), post-dialysis diastolic pressure (OR 2.234) and spKt/V (OR 1.982) were independent risk factors for CI in MHD patients. During the follow-up period, 15 patients died (13.2%) in the CI group and 5 died (4.72%) in the non-CI group (p < 0.05). The Kaplan-Meier survival curve analysis showed that the survival rate of patients with CI was lower than that of non-CI group in MHD patients during 3 years follow-up (p = 0.046). Conclusion: CI is one of the most common complications in MHD patients. The mortality is high in patients who had CI. Education status, post-dialysis diastolic pressure and spKt/V are independent risk factors for CI in MHD patients.

scholarly journals A Prognostic Autophagy-Related Long Non-coding RNA (ARlncRNA) Signature in Acute Myeloid Leukemia (AML)

2021 ◽  
Vol 12 ◽  
Author(s):  
Chunxia Zhao ◽  
Yulu Wang ◽  
Famei Tu ◽  
Shuai Zhao ◽  
Xiaoying Ye ◽  
...  
Keyword(s):  
Cox Regression ◽  
Survival Curve ◽  
Pearson Correlation ◽  
Enrichment Analysis ◽  
Risk Groups ◽  
Gene Set Enrichment Analysis ◽  
Kaplan Meier ◽  
Non Coding Rna ◽  
Novel Biomarkers ◽  
Meier Survival Curve

BackgroundSome studies have proven that autophagy and lncRNA play important roles in AML. Several autophagy related lncRNA signatures have been shown to affect the survival of patients in some other cancers. However, the role of autophagy related lncRNA in AML has not been explored yet. Hence, this study aims to find an autophagy related lncRNA signature that can affect survival for AML patients.MethodA Pearson correlation analysis, a Kaplan–Meier survival curve, a univariate cox regression, and a multivariate cox regression were performed to establish an autophagy related lncRNA signature. A univariate cox regression, a multivariate cox regression, a Kaplan–Meier survival curve, and a ROC curve were applied to confirm if the signature is an independent prognosis for AML patients. The relationship between the signature and the clinical features was explored by using a T test. Gene Set Enrichment Analysis (GSEA) was used to investigate the potential tumor related pathways.ResultsA four-autophagy related lncRNA (MIR133A1HG, AL359715.1, MIRLET7BHG, and AL356752.1) signature was established. The high risk score based on signature was related to the short survival time of AML patients. The signature was an independent factor for the prognosis for AML patients (HR = 1.684, 95% CI = 1.324–2.142, P &lt; 0.001). The signature was correlated with age, leukocyte numbers, and FAB (M3 or non-M3). The P53, IL6/JAK/STAT3, TNF-α, INF-γ, and IL2/STAT5 pathways might contribute to the differences between the risk groups based on signature in AML.ConclusionThe four autophagy related lncRNAs and their signature might be novel biomarkers for predicting the survival of AML patients. Some biological pathways might be the potential mechanisms of the signature for the survival of AML patients.

scholarly journals Diagnostic and Prognostic Value of Presepsin in Patients with Non-Infectious Organ Failure, Sepsis, and Septic Shock: A Prospective Observational Study According to the Sepsis-3 Definitions

2021 ◽  
Author(s):  
Sukyo Lee ◽  
Juhyun Song ◽  
Dae Won Park ◽  
Hyeri Seok ◽  
Jae-hyung Cha ◽  
...  
Keyword(s):  
Septic Shock ◽  
Observational Study ◽  
Organ Failure ◽  
Prospective Observational Study ◽  
Survival Curve ◽  
Curve Analysis ◽  
Roc Curve Analysis ◽  
Kaplan Meier ◽  
Sepsis And Septic Shock ◽  
Meier Survival Curve

Abstract Background: Sepsis is life-threatening organ dysfunction due to a dysregulated host response to infection. Early diagnosis of sepsis is challenging due to unknown sources of infection, and mortality prediction is usually complex. We aimed to investigate the clinical value of presepsin for discriminating sepsis from non-infectious organ failure and predicting mortality among sepsis patients in the emergency department (ED).Methods: This prospective observational study included 420 patients divided into three groups according to the Sepsis-3 definitions: non-infectious organ failure (n=142), sepsis (n=141), and septic shock (n=137). Blood samples for biomarker measurement of presepsin, procalcitonin, and C-reactive protein were drawn in the ED and biomarker levels were compared between the groups. Optimal cut-off values for presepsin to discriminate between the three clinical diagnoses were evaluated using receiver operating characteristic (ROC) curve analysis. We also performed ROC curve analysis for each biomarker as a predictor of mortality. After excluding non-infectious organ failure, we extracted the optimal cut-off value of presepsin to predict mortality associated with sepsis and septic shock and performed Kaplan–Meier survival curve analysis according to the cut-off value.Results: Presepsin levels (median [IQR]) were significantly higher in sepsis than in non-infectious organ failure (792 [450–1273] vs. 286 [170–417], p <0.001) and significantly higher in septic shock than in sepsis (1287 [589–2365] vs. 792 [450–1273], p=0.002). The optimal cut-off value for presepsin to discriminate between sepsis and non-infectious organ failure was 582 pg/mL (sensitivity, 70.1; specificity, 89.4; AUC, 0.877; p <0.001) and to discriminate between sepsis and septic shock was 1285 pg/mL (sensitivity, 50.4; specificity, 76.6; AUC, 0.618; p <0.001). The optimal cut-off value for presepsin for predicting 30-day mortality was 821 pg/mL (sensitivity, 68.9; specificity, 50.5; AUC, 0.605; p=0.005) in patients with sepsis and septic shock. Kaplan-Meier survival curve analysis showed that patients with higher presepsin levels (≥821 pg/mL) had significantly higher mortality than patients with lower presepsin levels (<821 pg/mL) (log-rank test; p=0.004). Conclusions: Presepsin levels could effectively differentiate sepsis from non-infectious organ failure and septic shock from sepsis. Presepsin levels could help clinicians predict mortality in patients with sepsis and septic shock.

DDRE-26. INHIBITION OF PRMT5 SENSITIZES GLIOBLASTOMA MODELS TO TRAMETINIB TREATMENT

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi79-vi80
Author(s):  
Yesh Banasavadi ◽  
Sriya Namagiri ◽  
yoshihiro Otani ◽  
Shilpa Thammegowda ◽  
Hannah Sur ◽  
...  
Keyword(s):  
Cell Cycle Progression ◽  
Survival Curve ◽  
Oral Gavage ◽  
Cycle Progression ◽  
Arginine Methyltransferase ◽  
Tumor Bearing ◽  
Nsg Mice ◽  
Kaplan Meier ◽  
Meier Survival Curve

Abstract With limited effective therapeutic strategies, the prognosis for glioblastoma (GBM) is very poor. Our previous study shows that the expression of Protein Arginine Methyltransferase 5 (PRMT5) is upregulated in GBM; its inhibition promotes apoptosis and senescence in differentiated and stem-like tumor cells, respectively. MEK inhibitors, including trametinib, are currently under investigation for GBM therapy. In this study, we tested whether inhibition of PRMT5 can enhance the anti-GBM efficacy of trametinib. Patient-derived primary GBM neurospheres (GBMNS) with transient PRMT5 knockdown were treated with trametinib and cell viability, proliferation, cell cycle progression, ELISA, and western blot analysis were conducted. In vivo, PRMT5-intact and -depleted GBMNS were intracranially implanted in NSG mice and treated with trametinib by daily oral gavage, and tumor progression and mice survival rate were analyzed by MRI and Kaplan-Meier survival curve, respectively. Depletion of PRMT5 increased the cytotoxic effect of trametinib in GBMNS. Trametinib treatment increased the activity of ERBB3 and AKT; With PRMT5 knockdown, the activity of both AKT and ERBB3 decreased significantly. But, inhibition of ERBB3 alone failed to block the trametinib-induced AKT activity suggesting that even though PRMT5 regulates the activity of both ERBB3 and AKT, the enhanced antitumor effect imparted by PRMT5 knockdown in trametinib treated GBMNS is because of AKT inhibition alone. In vivo, PRMT5-depletion extended the survival of the tumor-bearing mice that further increased in combination with trametinib treatment. Interestingly, trametinib treatment alone had no survival benefit.

scholarly journals In Vitro Fatigue Resistance of Teeth Restored With Bulk Fill versus Conventional Composite Resin

2016 ◽  
Vol 27 (4) ◽  
pp. 452-457 ◽  
Author(s):  
Gabrielle Branco Rauber ◽  
Jussara Karina Bernardon ◽  
Luiz Clovis Cardoso Vieira ◽  
Hamilton Pires Maia ◽  
Françoá Horn ◽  
...  
Keyword(s):  
Fatigue Resistance ◽  
Composite Resin ◽  
Survival Curve ◽  
Maximum Force ◽  
Lower Percentage ◽  
Rank Test ◽  
Log Rank Test ◽  
Kaplan Meier ◽  
Significant Difference ◽  
Meier Survival Curve

Abstract The aim of this study was to compare the fatigue resistance of restored teeth with bulk fill composite resin, conventional composite resin with incremental insertion and unprepared sound teeth. Twenty-eight extracted maxillary premolars were selected and divided into 4 groups based on composite resin and insertion technique: control (C), conventional composite resin with incremental insertion (I) and bulk fill composite resin with three (BF3) or single increment (BF1). The restored specimens were submitted to fatigue resistance test with a 5 Hz frequency. An initial application of 5,000 sinusoidal load cycles with a minimum force of 50 N and a maximum force of 200 N was used. Next, were applied stages of 30,000 load cycles with the maximum force increasing gradually: 400, 600, 800, 1000, 1200 and 1400 N. The test was concluded when 185,000 load cycles were achieved or the specimen failed. The fatigue resistance data were recorded for comparison, using the Kaplan-Meier survival curve and analyzed by log-rank test at 0.05 significance. Fractures were classified based on the position of the failure - above or below the cementoenamel junction (CEJ). Statistical analysis of the Kaplan-Meier survival curve and log-rank test showed a significant difference between groups (p=0.001). The fracture analysis demonstrated that only 28.58% of failures were below the CEJ in group C, while for groups I, BF1 and BF3 they were 42.85%, 85.71% and 85.71%, respectively. Teeth restored with composite bulk fill in both techniques present similar fatigue resistance values compared with those restored with a conventional incremental insertion of composite, while the fatigue strength values of unprepared sound teeth were higher. Furthermore, unprepared sound teeth showed a lower percentage of fractures below the CEJ.

Incidence of Laryngotracheal Stenosis after Thermal Inhalation Airway Injury

2019 ◽  
Vol 40 (6) ◽  
pp. 961-965 ◽  
Author(s):  
Anne Sun Lowery ◽  
Greg Dion ◽  
Callie Thompson ◽  
Liza Weavind ◽  
Justin Shinn ◽  
...  
Keyword(s):  
Risk Factors ◽  
Burn Injury ◽  
Patient Characteristics ◽  
Inhalation Injury ◽  
Interquartile Range ◽  
Laryngotracheal Stenosis ◽  
Chi Square ◽  
Laryngeal Function ◽  
Airway Injury ◽  
Incidence Risk

Abstract Inhalation injury is independently associated with burn mortality, yet little information is available on the incidence, risk factors, or functional outcomes of thermal injury to the airway. In patients with thermal inhalation injury, we sought to define the incidence of laryngotracheal stenosis (LTS), delineate risk factors associated with LTS development, and assess long-term tracheostomy dependence as a proxy for laryngeal function. Retrospective cohort study of adult patients treated for thermal inhalation injury at a single institution burn critical care unit from 2012 to 2017. Eligible patients’ records were assessed for LTS (laryngeal, subglottic, or tracheal stenosis). Patient characteristics, burn injury characteristics, and treatment-specific covariates were assessed. Descriptive statistics, Mann–Whitney U-tests, odds ratio, and chi-square tests compared LTS versus non-LTS groups. Of 129 patients with thermal inhalation injury during the study period, 8 (6.2%) developed LTS. When compared with the non-LTS group, patients with LTS had greater mean TBSA (mean 30.3, Interquartile Range 7–57.5 vs 10.5, Interquartile Range 0–15.12, P = .01), higher grade of inhalation injury (mean 2.63 vs 1.80, P = .05), longer duration of intubation (12.63 vs 5.44; P &lt; .001), and greater inflammatory response (mean white blood cell count on presentation 25.8 vs 14.9, P = .02, mean hyperglycemia on presentation 176.4 vs 136.9, P = .01). LTS patients had a significantly higher rate of tracheostomy dependence at last follow-up (50 vs 1.7%, P &lt; .001). Six percent of patients with thermal inhalation injury develop LTS. LTS was associated with more severe thermal airway injury, longer duration of intubation, and more severe initial host inflammation. Patients with inhalation injury and LTS are at high risk for tracheostomy dependence. In burn patients with thermal inhalation injury, laryngeal evaluation and directed therapy should be incorporated early into multispecialty pathways of care.

scholarly journals Jaccoud’s arthropathy in SLE: findings from a Latin American multiethnic population

2019 ◽  
Vol 6 (1) ◽  
pp. e000343
Author(s):  
Rosana Quintana ◽  
Guillermo Pons-Estel ◽  
Karen Roberts ◽  
Monica Sacnún ◽  
Guillermo Berbotto ◽  
...  
Keyword(s):  
Disease Activity ◽  
Latin American ◽  
Survival Curve ◽  
Damage Index ◽  
Categorical Variables ◽  
Jaccoud’S Arthropathy ◽  
Kaplan Meier ◽  
Damage Accrual ◽  
Jaccoud's Arthropathy ◽  
Meier Survival Curve

ObjectiveTo compare the clinical, laboratory and outcome features of SLE patients with and without Jaccoud’s arthropathy (JA) from the Grupo Latino Americano De Estudio del Lupus (GLADEL) cohort.Methods1480 patients with SLE [(34 centres, 9 Latin American countries with a recent diagnosis (≤2 years)] constitute the GLADEL cohort. JA was defined as reducible deformity of the metacarpophalangeal axis, without radiographic erosions at any time. Within this cohort, a nested case–control study was carried out. Control was matched for age, gender and centre in a 1:3 proportion. The variables included were: sociodemographic, clinical and immunological features, disease activity, damage and mortality. Comparisons were performed with Wilcoxon and χ2 tests for continuous and categorical variables, respectively. ORs and 95% CIs and Kaplan-Meier survival curve were estimated.ResultsOf 1480 patients, 17 (1.1%) JA patients were identified; 16 (94.1%) of them were women, mean age: 31.0 years (SD 12.0). Five (29.4%) patients presented JA at SLE diagnosis and 12 (70.6%) after. The median follow-up time and all disease features were comparable in both groups except for a higher frequency of pneumonitis in the patients with JA [4 (23.5) vs 1 (2.0); p=0.012; (OR: 15.4; 95% CI 1.6 to 149.6)]. The SLE disease activity index, Systemic Lupus International Collaborating Clinics/American College of Rheumatology damage Index and the Kaplan-Meier survival curve were similar in both groups.ConclusionJA may tend to appear early in the course of SLE; it seems not to have an impact on disease activity, damage accrual or in survival.

Cytoplasmic Nucleophosmin (NPMc+) Mutations and FMS-Like Tyrosine Kinase 3 (Flt3) Internal Tandem Duplication (ITD) Mutations Cooperate to Cause Leukemia In a Mouse Model

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 145-145 ◽  
Author(s):  
Rachel E. Rau ◽  
Daniel Magoon ◽  
Emily McIntyre ◽  
Li Li ◽  
Sarah Greenblatt ◽  
...  
Keyword(s):  
T Cell ◽  
Mouse Model ◽  
Median Survival ◽  
Myeloid Leukemia ◽  
Survival Curve ◽  
Erythroid Cells ◽  
Rt Pcr ◽  
Facs Analysis ◽  
Kaplan Meier ◽  
Meier Survival Curve

Abstract Abstract 145 NPMc+ mutations occur in up to 60% of adult and 20% of childhood acute myeloid leukemia (AML) with normal karyotype. Flt3 ITD mutations occur in 25% of adult and 15% of childhood AML. Flt3 ITD mutations occur twice as frequently in patients with NPMc+ mutations compared to those who lack a NPMc+ mutation. The presence of Flt3 ITD portends a poor prognosis. NPMc+ is associated with improved outcome, but only in the absence of a concomitant Flt3 ITD mutations. Given the high frequency with which these mutations occur together it is plausible that they cooperate to cause leukemia. However, this has yet to be demonstrated experimentally. To examine this, we crossed mice expressing a knock-in of an 18-bp ITD mutation in the juxtamembrane domain of the murine Flt3 gene (Flt3 wt/ITD) with transgenic mice expressing Flag-tagged type A NPMc+ mutation driven by the myeloid-specific human MRP8 promoter. Flt3wt/ITD mice develop a fatal myeloproliferative disorder (Li L, et al. Blood. 2008;111:3849-58) and NPMc+ transgenic mice develop a non-fatal myeloproliferation (Cheng K, et al. Blood. 2010;115-18), but neither develop leukemia, suggesting that cooperating events are required. Progeny were characterized by: 1) H&E staining of peripheral blood smears, bone marrow (BM) cytospins, and spleen sections; 2) FACS analysis of BM cells, splenocytes and thymocytes to determine the disease phenotype; 3) RT PCR to examine the expression of Flt3 ITD and NPMc+; and 4) immunofluorescence (IF) using an anti-Flag antibody to determine localization of the NPMc+ protein. Mice harboring both mutations develop acute leukemia with a median onset of 285 days (Figure 1). All the leukemic mice exhibit a moribund appearance, leukocytosis (mean WBC 69.3±32.7 vs 11.7±8.3K/μ L in wt/wt mice), splenomegaly (mean weight 0.63±0.3 vs 0.12±0.02g in wt/wt mice), anemia and thrombocytopenia. Four disease phenotypes based on FACS and histologic analysis have been observed (Figure 2). Thirty-three percent develop AML with infiltration of the BM and spleen with Mac1+/Gr1+ myeloblasts. Thiry-three percent develop T cell ALL with infiltration of BM, spleen, thymuses and other organs with abnormal CD3+/CD4+/CD8+ lymphoblasts. An additional 33% develop a mixed phenotype acute T/myeloid leukemia with both Mac1+/Gr1+ myeloblasts and CD3+/CD4+/CD8+ lymphoblasts. One mouse developed an undifferentiated acute leukemia with primitive blasts expressing no markers specific for either lymphoid or myeloid lineage. RT-PCR of bulk leukemia cells demonstrates expression of NPMc+ and Flt3 ITD. IF of BM cells from leukemic mice demonstrates cytoplasmic localization of the NPMc+ protein. In summary, we have utilized a mouse model to demonstrate that NPMc+ and Flt3 ITD mutations cooperate to cause leukemia. Many of the mice with both mutations develop myeloid leukemia with features similar to the human disease. There is also a striking incidence of T cell leukemia, which is particularly interesting as the NPMc+ mutation is driven by the myeloid-specific hMRP8 promotor. It is possible that there is aberrant expression of NPMc+ in lymphoid cells due to position effects of the transgene or the activation of an endogenous leukemogenic retrovirus. Other disease models using this promoter have documented similar phenomenon (Jaiswal, et al. PNAS. 2003;100:10002-7). There is a long latency of disease onset which may be due to a relatively low level of expression of NPMc+ or because additional genetic or epigenetic events are required. Perhaps the Flt3 ITD mutation causes proliferation and NPMc+ impairs DNA repair resulting in the accumulation of additional mutations that contribute to leukemogenesis. This mouse model provides the first in vivo model of NPMc+/Flt3 ITD+ leukemia. The model will allow for the further study of this disease entity, including the examination of involved pathways and the exploration for potential therapeutic targets. Kaplan-Meier Survival Curve. Mice with both NPMc+ and Flt3 ITD mutations have a median survival of 413 days. FACS analysis of leukemic mice BM cells and thymocytes. Mice with AML have cKit+/Mac1+/Gr1+ myelobasts. Mice with T cell ALL have infiltration of the BM, spleen (not shown) and thymus with CD3+/CD4+/CD8+ lymphoblasts. Mice with T/myeloid leukemia have both Mac1+/Gr1+ myeloblasts and CD3+/CD4+/CD8+ lymphoblasts. Leukemic mice have depletion of maturing Ter119+ erythroid cells. Figure 1 Kaplan-Meier Survival Curve. Mice with both NPMc+ and Flt3 ITD mutations have a median survival of 413 days. Figure 1. Kaplan-Meier Survival Curve. Mice with both NPMc+ and Flt3 ITD mutations have a median survival of 413 days. Figure 2 FACS analysis of leukemic mice BM cells and thymocytes. Mice with AML have cKit+/Mac1+/Gr1+ myelobasts. Mice with T cell ALL have infiltration of the BM, spleen (not shown) and thymus with CD3+/CD4+/CD8+ lymphoblasts. Mice with T/myeloid leukemia have both Mac1+/Gr1+ myeloblasts and CD3+/CD4+/CD8+ lymphoblasts. Leukemic mice have depletion of maturing Ter119+ erythroid cells. Figure 2. FACS analysis of leukemic mice BM cells and thymocytes. Mice with AML have cKit+/Mac1+/Gr1+ myelobasts. Mice with T cell ALL have infiltration of the BM, spleen (not shown) and thymus with CD3+/CD4+/CD8+ lymphoblasts. Mice with T/myeloid leukemia have both Mac1+/Gr1+ myeloblasts and CD3+/CD4+/CD8+ lymphoblasts. Leukemic mice have depletion of maturing Ter119+ erythroid cells. Disclosures: No relevant conflicts of interest to declare.

Sign in / Sign up

Export Citation Format

Share Document