Noncoding miRNAs as novel prognostic factor for 5-fluorouracil adjuvant therapy in colorectal cancer

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 3609-3609
Author(s):  
Y. Xi ◽  
A. Formentini ◽  
M. Kornmann ◽  
J. Ju
Keyword(s):  
Colorectal Cancer ◽  
Prognostic Factor ◽  
Median Survival ◽  
Survival Curve ◽  
Statistical Significance ◽  
Clinical Samples ◽  
Pcr Analysis ◽  
Transcriptional Level ◽  
Translation Efficiency ◽  
Kaplan Meier

3609 Background: The roles of non-coding miRNAs in tumorgenesis are just emerging. miRNAs regulate gene expression at post-transcriptional level by influencing translation efficiency of their target mRNAs. Previous studies from our laboratory have identified a number of miRNAs that were dis-regulated in colon cancer cell lines related to the loss of p53 tumor suppressor gene. In this study, the in vivo significance of some of these miRNAs was further evaluated using clinical samples. Ten miRNAs (hsa-let-7b, hsa-let-7g, hsa-miR-15b, hsa-miR-181b, hsa-miR-191, hsa-miR-200c, hsa-miR-26a, hsa-miR-27a, hsa-miR-30a-5p and hsa-miR-30c) were evaluated for their potential prognostic value in colorectal cancer patients receiving 5-fluorouracil (5-FU) based therapy. Methods: Forty eight snap frozen clinical colorectal samples (24 normal and 24 paired colorectal cancer patient samples) were selected with detailed clinical follow-up information. RNAs were isolated from these samples using TRIzol reagent. After cDNA synthesis with miRNA specific primers, the expression levels of 10 miRNAs were quantified via qRT-PCR analysis. The statistical significance of these markers for disease prognosis was evaluated using two tailed paired T-test. Kaplan-Meier survival curve was generated and followed by Logrank test. Result: Among the ten miRNAs, hsa-miR-15b (p=0.02), hsa-miR-181b (p=0.01), hsa-miR-191 (p=0.03) and hsa-miR-200c (p=0.005) were significantly over-expressed in tumors compared to normal colorectal samples. Kaplan-Meier survival analysis indicates that hsa-miR-200c was a significant prognostic marker for predicting patient’s survival (p=0.01). The patients (n=15) with higher hsa-miR-200c expression had shorter survival interval (median survival = 26 months) compared to patients (n=9) with lower expression (median survival = 38 months). Conclusions: Some of these miRNAs may function as oncogenes due to their over-expression in tumors. Hsa-miR-200c may be a potential novel prognostic factor for 5-FU based chemotherapy in colorectal cancer. No significant financial relationships to disclose.

scholarly journals NDRG3 overexpression is associated with a poor prognosis in patients with hepatocellular carcinoma

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Ji-sheng Jing ◽  
Hongbo Li ◽  
Shun-cai Wang ◽  
Jiu-ming Ma ◽  
La-qing Yu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cox Regression ◽  
Survival Curve ◽  
Disease Free Survival ◽  
Prognostic Indicator ◽  
Clinicopathological Characteristics ◽  
Pcr Analysis ◽  
Kaplan Meier ◽  
Tumor Tissues ◽  
The Relationship

N-myc downstream-regulated gene 3 (NDRG3), an important member of the NDRG family, is involved in cell proliferation, differentiation, and other biological processes. The present study analyzed NDRG3 expression in hepatocellular carcinoma (HCC) and explored the relationship between expression of NDRG3 in HCC patients and their clinicopathological characteristics. We performed quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR) analysis and immunohistochemistry (IHC) analyses on HCC tissues to elucidate NDRG3 expression characteristics in HCC patients. Kaplan–Meier survival curve and Cox regression analyses were used to evaluate the prognoses of 102 patients with HCC. The results revealed that compared with non-tumor tissues, HCC tissues showed significantly higher NDRG3 expression. In addition, our analyses showed that NDRG3 expression was statistically associated with tumor size (P=0.048) and pathological grade (P=0.001). Survival analysis and Kaplan–Meier curves revealed that NDRG3 expression is an independent prognostic indicator for disease-free survival (P=0.002) and overall survival (P=0.005) in HCC patients. The data indicate that NDRG3 expression may be considered as a oncogenic biomarker and a novel predictor for HCC prognosis.

scholarly journals Clinicopathological Variables and Outcome in Chronic Myeloid Leukemia Associated With BCR-ABL1 Transcript Type and Body Weight: An Outcome of European LeukemiaNet Project

2021 ◽  
Vol 28 ◽  
pp. 107327482110384
Author(s):  
Mohammad A. J. Abdulla ◽  
Prem Chandra ◽  
Susanna El Akiki ◽  
Mahmood B. Aldapt ◽  
Sundus Sardar ◽  
...  
Keyword(s):  
Body Weight ◽  
Survival Curve ◽  
Statistical Significance ◽  
Response Assessment ◽  
Test Methods ◽  
Response To Treatment ◽  
Molecular Response ◽  
Kaplan Meier ◽  
Significant Difference ◽  
Transcript Type

Objective It is debatable whether BCR-ABL1 transcript type has an impact on outcome of treatment of patients with CML, and it is not widely studied whether body weight influences response to treatment. In this study, we tried to find out if any of these factors has an impact on response to treatment and outcome. Methodology We conducted a retrospective analysis of the files of 79 patients being treated in our center for CML with known BCR-ABL1 breakpoints, and patients’ management and response assessment was done based on ELN 2013 guidelines. The analysis was performed based on two main groups, obese vs. normal BMI, and then based on BCR-ABL1 transcripts: e13a2 vs. e14a2. Cumulative incidence of MMR, CCyR, and DMR were estimated using the Kaplan–Meier survival curve method, and comparisons between groups were performed by the Log-rank/Gray test methods. Results/conclusion In the patient-cohort studied, there was no statistically significant difference in molecular response between patients with CML based on body weight or transcript type although patients in the obesity group achieved higher and faster MMR with no statistical significance.

scholarly journals The prognostic role of tissue TLR2 and TLR4 in colorectal cancer

2020 ◽  
Vol 477 (5) ◽  
pp. 705-715
Author(s):  
Ines Beilmann-Lehtonen ◽  
Camilla Böckelman ◽  
Harri Mustonen ◽  
Selja Koskensalo ◽  
Jaana Hagström ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Prognostic Factor ◽  
Distant Metastases ◽  
University Hospital ◽  
Rank Test ◽  
Pathogen Invasion ◽  
Kaplan Meier ◽  
Node Positive Disease ◽  
Colorectal Cancer Patients ◽  
Dukes C

Abstract Colorectal cancer (CRC), the second most common cancer globally, resulted in 881,000 deaths in 2018. Toll-like receptors (TLRs) are crucial to detecting pathogen invasion and inducing the host’s immune response. This study aimed to explore the prognostic value of TLR2 and TLR4 tumor expressions in colorectal cancer patients. We studied the immunohistochemical expressions of TLR2 and TLR4 using tissue microarray specimens from 825 patients undergoing surgery in the Department of Surgery, Helsinki University Hospital, between 1982 and 2002. We assessed the relationships between TLR2 and TLR4 expressions and clinicopathological variables and patient survival. We generated survival curves using the Kaplan-Meier method, determining significance with the log-rank test. Among patients with lymph node–positive disease and no distant metastases (Dukes C), a strong TLR2 immunoactivity associated with a better prognosis (p < 0.001). Among patients with local Dukes B disease, a strong TLR4 immunoactivity associated with a worse disease-specific survival (DSS; p = 0.017). In the multivariate survival analysis, moderate TLR4 immunoactivity compared with strong TLR4 immunoactivity (hazard ratio (HR) 0.66, 95% confidence interval (CI) 0.49–0.89, p = 0.007) served as an independent prognostic factor. In the multivariate analysis for the Dukes subgroups, moderate TLR2 immunoactivity (HR 2.63, 95% CI 1.56–4.44, p < 0.001) compared with strong TLR2 immunoactivity served as an independent negative prognostic factor in the Dukes C subgroup. TLR2 and TLR4 might be new prognostic factors to indicate which CRC patients require adjuvant therapy and which could spare from an unnecessary follow-up, but further investigations are needed.

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.

Retrospective analysis of resected primary colorectal cancer revealed

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e15137-e15137
Author(s):  
K. H. Khan
Keyword(s):  
Colorectal Cancer ◽  
Lymph Nodes ◽  
Histological Examination ◽  
Survival Curve ◽  
Statistical Significance ◽  
Prognostic Significance ◽  
Disease Free Survival ◽  
National Audit ◽  
Primary Colorectal Cancer ◽  
Rectal Cancers

e15137 Background: Lymphadenectomy in colorectal cancer is believed to be a critical component concerning prognosis and survival of patients.. The aim of this study was to analyze the relationship between the number of lymph nodes harvested (LNH) and the number of lymph nodes involved (LNI), at the histological examination of the specimens of resected primary colorectal cancer (CRC) at our unit. Results: Over the five-year study period, 142 resections for primary CRC were performed on 141 patients (one metachronous). Mean number of resections per annum was 28. There were 86 (60.5%) colonic and 56 (39.5%) rectal cancers (Fig 1). There were 70 (49.3%) anterior resections (Fig 2). M:F ratio was 0.97:1. Median age was 71years for colonic and 69.5years for rectal cancers. Eighty eight percent of resections were elective (OR=2.2 RR=1.14 p=0.003 compared to the national audit)1. Adenocarcinoma NOS constituted 94% of all histology results (5% mucinous and 1% signet ring). Median CRM was 7.5mm (mean=8.8mm) (fig 3). The CRM involvement was 12.7% for all CRC and 16% for rectal cancers. The LRM involvement was 1.5%. Median overall LNH was 12, (mean=13 p=0.08 when compared to the recommended LNH of 12) (Fig 5). Median LNH for rectal cancers=11 and for colonic cancer=13. There were 11 (14%) APRs compared to 70 (86%) sphincter-saving operations from a total of 83 rectal resections. 84%of resections were R0. The 30-day all-cause mortality was 4.3%. Actuarial survival curve demonstrated 17.6% chance of metastasis at presentation, all-stage 3-year disease-free survival (DFS) of 67% and of 82% for stages I-III (Tany Nany M0). CEA relapse as a marker of disease recurrence (available for n=125) revealed 3-year DFS=71%.When correlation was determined between LNH and lymph node involvement, it revealed a low correlation (r=0.159 p=0.06) which was statistically insignificant. When the national audit calculated the same relationship among its much larger sample the results were the same (r=0.152 p=0.001)3 and had achieved statistical significance. Conclusions: LNI as a function of tumour and host behaviour is of prognostic significance whereas LNH may be a marker of ‘pathologist's diligence’ at the histological examination and therefore a quality assurance (QA) tool. No significant financial relationships to disclose.

scholarly journals TXNRD1 Is an Unfavorable Prognostic Factor for Patients with Hepatocellular Carcinoma

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Binsheng Fu ◽  
Wei Meng ◽  
Xiancheng Zeng ◽  
Hui Zhao ◽  
Wei Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Prognostic Factor ◽  
Clinical Stage ◽  
Thioredoxin Reductase ◽  
Immunohistochemical Analysis ◽  
Independent Prognostic Factor ◽  
Clinical Samples ◽  
Kaplan Meier ◽  
Thioredoxin Reductase 1 ◽  
N Classification

Thioredoxin reductase 1 (TXNRD1) which is a selenocysteine-containing protein is overexpressed in many malignancies. Its role in the hepatocellular carcinoma (HCC) prognosis has not been investigated. In this study, we investigated whether TXNRD1 functions as an independent prognostic factor for HCC patients. We found TXNRD1 was overexpressed in HCC tissues and cells, immunohistochemical analysis suggested TXNRD1 was elevated in 57 of 120 (47.5%) clinical samples, and its level was increased with the increasing clinical stage. In addition, TXNRD1 expression was positively correlated with clinical stage (p=3.5e-5), N classification (p=4.4e-4), and M classification (p=0.037) of HCC patients. Kaplan-Meier analysis revealed that patients with high TXNRD1 expression had significantly shorter survival time than patients with low TXNRD1 expression. Multivariate analysis found TXNRD1 was an independent prognostic factor for HCC patients. In conclusion, our data suggested that TXNRD1 was a biomarker for the prognosis of patients with HCC.

Liver metastases of colorectal carcinoma: Prospective study on the use of transarterial chemoembolization (TACE)

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 4062-4062
Author(s):  
T. J. Vogl ◽  
T. Gruber ◽  
S. Zangos ◽  
J. O. Balzer
Keyword(s):  
Colorectal Cancer ◽  
Survival Rate ◽  
Liver Metastases ◽  
Survival Time ◽  
Cancer Patients ◽  
Median Survival ◽  
Local Control ◽  
Median Survival Time ◽  
Kaplan Meier ◽  
Colorectal Cancer Patients

4062 Background: To evaluate the efficacy of chemoembolization (TACE) in the treatment of liver metastases in colorectal cancer patients concerning local control and survival. Methods: 207 patients with liver metastases of colorectal cancer were treated with repeated TACE in 4-week intervals. In total, 1,307 chemoembolizations were performed with a mean of 6.3 sessions per patient. At the time of first chemoembolization the average age of the patients was 68.8 years (range, 39.4–83.5 years). 158 patients were treated palliatively, 35 symptomatically and 14 patients neoadjuvantly. The chemotherapy consisted of Mitomycin C with/without Gemcitabin; embolization was performed with Lipiodol and starch microspheres for vessel occlusion. Tumor response was evaluated by magnetic resonance imaging (MRI). The change in size was calculated and the response was evaluated according to the RECIST criteria. Survival rates from the first diagnosis and from the first TACE session were both calculated according to the Kaplan-Meier method to obtain the median survival. Results: While 70% of the patients showed multiple metastases, 6% had 1 metastasis, 5.8% had 2 metastases and 18.2% had 3 to 4 metastases. Lesion size and number before, during and after treatment were assessed to deduce the morphological response. Local control results according to the RECIST criteria were as follows: partial response 12% of patients, stable disease in 51% and progressive disease in 37%. The 1-year survival rate after TACE was 62%, but the 2-year survival rate had been reduced to 38%. The median survival time from the date of diagnosis of metastases was 3.4 years (according to Kaplan-Meier), the median survival time from the start of TACE treatment was 1.34 years. The median survival time of the palliative group was 1.4 years, of the symptomatic group 0.8 years and of the neoadjuvant group 1.5 years. Conclusions: TACE is an effective minimal-invasive therapy for neoadjuvant, symptomatic or palliative treatment of liver metastases in colorectal cancer patients. No significant financial relationships to disclose.

Relationship between primary tumor location and prognosis in metastatic colorectal cancer patients treated with irinotecan/5-FU/leucovorin (FOLFIRI).

2017 ◽  
Vol 35 (4_suppl) ◽  
pp. 557-557 ◽  
Author(s):  
Qianqian Yu ◽  
Hong Qiu ◽  
Mingsheng Zhang ◽  
Xianglin Yuan
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Median Survival ◽  
Survival Probability ◽  
Primary Tumor ◽  
Statistical Significance ◽  
Tumor Location ◽  
First Line ◽  
Primary Tumor Location ◽  
The Impact

557 Background: Clinical trials including CALGB/SWOG 80405 and FIRE-3 reveal differences in overall survival (OS) for metastatic colorectal cancer (mCRC) patients treated with targeted therapy based on primary tumor location. We assessed the impact of tumor location on prognosis in a prospective series of patients with mCRC received FOLFIRI in first-line therapy. Methods: Patients treated with FOLFIRI were consecutively recruited between November 2010 and December 2014. Follow-up information was updated in February 2016 when 77.3% of the patients were deceased. We defined the right-sided colon = cecum to transverse colon, left-sided colon = splenic flexure to sigmoid descending colon, rectum = rectosigmoid plus rectal cancer, respectively. We measured median survival using Kaplan-Meier plots and 2-year survival probability using life tables. Associations between tumor locations and treatment outcomes were estimated using a Cox proportional hazards model. Age and gender were included in adjusted Cox models to estimate the hazard ratio (HR) for death of rectal and left-sided tumors relative to right-sided tumors. Results: Right-sided cancer had a shorter median survival (13.5 vs. 20.4 months) and worse 2-year survival probability (28% vs. 39%) than left-sided and rectal cancers, however the difference was of no statistical significance no matter in unadjusted (HR = 1.002, 95% CI 0.635-1.581) or adjusted models (HR = 1.037, 95% CI 0.657-1.639). Conclusions: mCRC patients with right-sided colon got comparative survival benefit from FOLFIRI in first-line treatment to the left-sided colon and rectum. This result needs to be validated in studies with larger sample size. Clinical trial information: NCT01282658.

Impact of income in stage IV prostate cancer.

2017 ◽  
Vol 35 (6_suppl) ◽  
pp. 244-244
Author(s):  
Aabra Ahmed ◽  
Timothy Dean Malouff ◽  
Ryan W Walters ◽  
Sydney Marsh ◽  
Peter T. Silberstein
Keyword(s):  
Prostate Cancer ◽  
Median Survival ◽  
Statistical Significance ◽  
Stage Iv ◽  
Median Income ◽  
High School Degree ◽  
Kaplan Meier ◽  
Survival Differences ◽  
The Impact ◽  
Zip Code

244 Background: There is growing evidence of the impact of socioeconomic status on survival in cancer patients. To our knowledge, this is the largest study to examine demographics and the association between income and survival in patients with stage IV prostate cancer. Methods: Using the National Cancer Database, 50,639 patients diagnosed with stage IV prostate cancer between 2004-2011 were identified. Income was evaluated using the median income of the patient’s zip code. Between-income survival differences were estimated by the Kaplan-Meier method and associated log-rank tests; Tukey-Kramer adjusted p < .05 indicated statistical significance. Results: Survival differences were indicated between all income quartiles. Median survival was highest for patients in zip codes with a median income ≥ $63,000 and lowest for patients in zip codes with an income < $38,000 (46.1 months vs. 31.6 months, respectively; p < .001). As such, 41% of patients in zip codes with a median income ≥ $63,000 were alive five years following diagnosis, compared to 31% of patients in zip codes with median income < $38,000. Additionally, compared to patients in zip codes in which the median income was < $38,000, patients in zip codes with a median income ≥ $63,000 had a higher rate of zero comorbidities (81% vs. 76%), a greater percentage of patients living in an area where >93% people have a high school degree (58% vs 1%), and a lower proportion of African Americans (8% vs 41%). Conclusions: Compared to patients with a median income < $38,000, patients in zip codes with a median income > $63,000 had a median survival nearly 15 months longer, had 10% more patients alive after 5 years, and had fewer comorbidities. [Table: see text]

Gain of 1q as a Potential Adverse Prognostic Marker in Myelodysplastic Syndrome: Comparison with International Prognostic Scoring System Variables

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3640-3640 ◽  
Author(s):  
Hyun-Kyung Park ◽  
Dong Soon Lee ◽  
Hye Ryun Lee ◽  
Han Ik Cho ◽  
Hyun Kyung Kim ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Platelet Count ◽  
Prognostic Marker ◽  
Median Survival ◽  
Survival Curve ◽  
International Prognostic Scoring System ◽  
Chromosomal Anomalies ◽  
Kaplan Meier ◽  
Meier Survival Curve ◽  
1Q Gain

Abstract The gain of the 1q region, which is a recurrent chromosomal aberration in B lymphoproliferative disorder, has been reported one of the most common anomalies in Korean myelodysplastic patients. Recently, risk based application of hypomethylating agents or tailored therapy in MDS rely on the prognostic variables of International Prognostic Scoring System (IPSS). To investigate the possibility of 1q gain as a new prognostic marker, we evaluated the prognostic impact of 1q gain, along with comparison with IPSS variables. A total of 117 patients with newly diagnosed MDS between 1997 and 2007 at the Seoul National University Hospital were investigated. Fluorescence in situ hybridization (FISH) studies with 5 specific probe(EGR1 for 5q31 deletion, D7S522 for 7q31 deletion, CEP8, D20S108 for 20q12 deletion, LSI 1p36/1q25 for 1q gain) and conventional G-banding karyotyping were performed on bone marrow aspirates. Other laboratory findings, such as hemoglobin(Hb), absolute neutrophil count(ANC), platelet count, bone marrow blast percent and IPSS score, and clinical data were collected through the individual medical records. The median age was 54 years and the male-to-female ratio was 1.4. Using WHO classification, refractory anemia(RA) was 27.4% and the other subgroups as follows: RA with ringed sideroblast(RARS), 3.4%; refractory cytopenia with multilineage dysplasia(RCMD), 8.5%; RCMD with ringed sideroblasts(RCMD-RS), 0.9%; RA with excess blasts-1(RAEB-1), 26.5%; RAEB-2, 31.6%; and 5q- syndrome, 1.7%. Cytogenetic abnormalities by FISH and G-banding were detected in 58 patients (49.6%). Most frequent anomaly was trisomy 8 occuring in 28 patients(23.9% of the 117 patients, 48.3% of the 58 patients with clonal cytogenetic abnormalities). Gain of 1q was the second common anomalies seen in 18 patients (15.4%) and other anomalies were −7/del7q (13.7%), −5/del5q (13.7%), and del20q (2.6%). G-banding showed gain of 1q in 7 cases, additional 11 patients with gain of 1q were revealed by FISH only. Patients with 1q gain showed a poor survival (median survival 23 months; n=18) compared to patients without 1q gain (median survival 60 months; p=0.02). EGR1 and D7S522 deletion by FISH also had a shorter median survival (8 months vs. 60 months p=0.0001, 16 months vs. 60 months p=0.005). The initial platelet count and blast count were found to affect overall survival, whereas CEP8 FISH, D20S108 FISH, Hb and ANC did not. Our results show that gain of 1q is associated with an adverse clinical outcome and can be considered as a poor cytogenetic risk factor of IPSS. In the Western study, the prevalence of 1q gain was low because most studies report G-banding result only. But it may be increased up to 2.5 fold higher by using FISH analysis in combination with G-banding. A gain of 1q could be a candidate as an adverse prognostic marker in clinical practice, which could help for risk-adapted therapies. Figure 1. Kaplan-Meier survival curve for chromosomal anomalies and IPSS. (A) gain of 1q. (B) −1/del(7q). (C) del(20q). Figure 1. Kaplan-Meier survival curve for chromosomal anomalies and IPSS. (A) gain of 1q. (B) −1/del(7q). (C) del(20q).

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