The exponential slope from absolute lymphocyte counts during radiochemotherapy can predict an aggressive course of cervical cancer.
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ABSTRACT:
PROVIDER: PRJEB56159 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR10223908.fastq.gz | Fastqsanger.gz | |||
| ERR10223909.fastq.gz | Fastqsanger.gz | |||
| ERR10223910.fastq.gz | Fastqsanger.gz | |||
| ERR10223911.fastq.gz | Fastqsanger.gz | |||
| ERR10223912.fastq.gz | Fastqsanger.gz |
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Project description:We sequenced plasma exosomal RNA obtained from 24 blood samples from 12 cervical cancer patients treated with concurrent chemoradiotherapy (CCRT) followed by intracavitary brachytherapy. The patients with 2018 International Federation of Gynecology and Obstetrics [FIGO] stage IB-3C2 at diagnosis were included. The 12 cervical cancer patients had two blood samples for each patient drawn before and after CCRT. Next generation sequencing data from plasma exosome included small RNAs, long non-coding RNAs, and mRNAs, of which miRNAs and mRNAs were used for analysis. The log2 fold change values were calculated between the two samples from each patient to detect mRNAs as predictors of slope of function estimated from ALCs and survival. We selected several potential exosomal mRNAs associated with clinical results.
2023-08-13 | E-MTAB-12187 | biostudies-arrayexpress
Project description:This study aimed to investigate whether the exponential slope α from absolute lymphocyte counts during concurrent radio−chemotherapy (CRT) is associated with aggressive and non-aggressive courses of cervical cancer. We analyzed 362 patients with stage IB−IVB cervical cancer treated with CRT in two groups: 323 patients without mRNA data (cohort 1) and 39 with mRNA data (cohort 2) from plasma exosomes. We calculated the α of each patient; 69 patients who died of cancer in cohort 1 were divided into 44 who died within 30 months (aggressive group), and 25 who died after more than 30 months (non-aggressive group). The median follow-up periods of cohorts 1 and 2 were 63 and 28 months, respectively. The log2 fold change (log2FC) between read counts of mRNAs before treatment and after the second week of CRT was calculated. Multivariate analyses from cohort 1 showed that neutrophil-to-lymphocyte ratio (NLR) ≥ 2.43 and α < 0.08 were statistically significant predictors of disease-specific survival (DSS) in the aggressive group (DSS-A), whereas α ≥ 0.08 was the only significant predictor of DSS in the non-aggressive group (DSS-NA). The 2.5-year DSS-A and 8-year DSS-NA rates of patients with α ≥ 0.08 and α < 0.08 were 86.7% and 73%, and 78.5% and 94.8% in the high-NLR group, respectively. In cohort 2, patients with both NLR < 2.7 and α ≥ 0.07 had a higher 2.5-year DSS rate than did those with either NLR ≥ 2.72 or α < 0.07. E2F8 and STX6 significantly correlated with ɑ and survival. The 2.5-year DSS rates in patients with E2F8 + STX6 (log2FC) < 0.2429 and ≥0.2429 were 100% and 77.2%, respectively. The exponential slope α can potentially distinguish between aggressive and non-aggressive courses in cervical cancer patients.
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Project description:In chronic lymphocytic leukemia (CLL) the increment in peripheral blood lymphocytes is slower than the expected increment calculated from the cells’ proliferation rate, suggesting that cellular proliferation and apoptosis are concurrent. Exploring this phenomenon, we found overexpression of caspase3, higher cleaved poly (ADP-ribose) polymerase (PARP) levels (P <0.007), and a higher apoptosis rate in cells from patients with high counts compared with cells from patients with low counts. Although we previously found that signal transducer and activator of transcription 3 (STAT3) protects CLL cells from apoptosis, STAT3 levels were significantly higher in cells from patients with high counts than in cells from patients with low counts. Furthermore, overexpression of STAT3 in MM-1 cells did not protect the cells. Rather, it upregulated caspase3 and induced apoptosis. Remarkably, putative STAT3 binding sites were identified in the caspase3 promoter and a luciferase assay, chromatin immunoprecipitation (ChIP), and an electromobility shift assay (EMSA) revealed that STAT3 activated caspase3. However, caspase3 levels increased only when STAT3 levels were sufficiently high. Using ChIP and EMSA, we found that STAT3 binds with low affinity to the caspase3 promoter, suggesting that at high levels, STAT3 activates a negative proapoptotic feedback mechanism. 4 samples from patients with high-count CLL were compared to 4 samples from patients with low-count CLL
2015-05-12 | E-GEOD-68721 | biostudies-arrayexpress
Project description:Purpose: Tumor-infiltrating lymphocytes (TIL) in pretreatment biopsies are associated with improved survival in triple-negative breast cancer (TNBC). We investigated whether higher peripheral lymphocyte counts are associated with lower breast cancer-specific mortality (BCM) and overall mortality (OM) in TNBC.Experimental Design: Data on treatments and diagnostic tests from electronic medical records of two health care systems were linked with demographic, clinical, pathologic, and mortality data from the California Cancer Registry. Multivariable regression models adjusted for age, race/ethnicity, socioeconomic status, cancer stage, grade, neoadjuvant/adjuvant chemotherapy use, radiotherapy use, and germline BRCA1/2 mutations were used to evaluate associations between absolute lymphocyte count (ALC), BCM, and OM. For a subgroup with TIL data available, we explored the relationship between TILs and peripheral lymphocyte counts.Results: A total of 1,463 stage I-III TNBC patients were diagnosed from 2000 to 2014; 1,113 (76%) received neoadjuvant/adjuvant chemotherapy within 1 year of diagnosis. Of 759 patients with available ALC data, 481 (63.4%) were ever lymphopenic (minimum ALC <1.0 K/μL). On multivariable analysis, higher minimum ALC, but not absolute neutrophil count, predicted lower OM [HR = 0.23; 95% confidence interval (CI), 0.16-0.35] and BCM (HR = 0.19; CI, 0.11-0.34). Five-year probability of BCM was 15% for patients who were ever lymphopenic versus 4% for those who were not. An exploratory analysis (n = 70) showed a significant association between TILs and higher peripheral lymphocyte counts during neoadjuvant chemotherapy.Conclusions: Higher peripheral lymphocyte counts predicted lower mortality from early-stage, potentially curable TNBC, suggesting that immune function may enhance the effectiveness of early TNBC treatment. Clin Cancer Res; 24(12); 2851-8. ©2018 AACR.
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Project description:Absolute quantification of miRNAs
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Project description:BackgroundSeveral studies have demonstrated the prognostic utility of absolute lymphocyte count (ALC) during therapy for a range of malignancies, with low ALC associated with adverse outcome. Here we investigated whether ALC retained independent prognostic significance with respect to minimal residual disease (MRD) status in children with acute lymphoblastic leukemia (ALL).ProcedureWe reviewed 171 cases of pediatric ALL treated on the Children's Oncology Group P9900 series of treatment trials. Variables analyzed included ALC at several time points during Induction, age at diagnosis, cytogenetics, initial white blood cell count, and MRD status at Day 29 of Induction (MRD-29).ResultsWe found high ALC at Induction Day 29 (ALC-29) to be an independent, clinically significant predictor of improved relapse-free and overall survival (OS). Patients with ALC-29 >1,500 cells/µl had a superior 6-year relapse-free survival (80 ± 4% vs. 62 ± 8%, P = 0.018) and overall survival (96 ± 2% vs. 74 ± 8%, P = 0.001). Moreover, ALC-29 identified distinct prognostic subgroups within cases stratified by MRD-29. In subjects with >0.01% MRD, ALC-29 > or <1,500 cells/µl had a significant 51% difference in 6-year OS (92 ± 7% vs. 41 ± 16%, P = 0.0001).ConclusionsALC, a readily obtainable test, constitutes a significant and independent prognostic factor in childhood ALL that may refine current MRD-based risk stratification algorithms and provide key prognostic information in settings where MRD determination is not feasible.
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Project description:Unique Molecular Identifiers (UMIs) are random oligonucleotide barcodes sequences? that are critical for the removal of PCR amplification biases within both bulk and single-cell sequencing experiments. However, the impact that PCR and sequencing errors have on the accuracy of generating absolute counts of RNA molecules is underappreciated. We demonstrate that PCR errors and not sequencing errors are the main source of inaccuracy in sequencing data and that the use of UMIs synthesized with homotrimeric nucleoside building blocks provides a solution to pinpoint and remove errors, allowing absolute counting of sequenced molecules.
2023-06-01 | GSE218899 | GEO
Project description:In chronic lymphocytic leukemia (CLL) the increment in peripheral blood lymphocytes is slower than the expected increment calculated from the cells’ proliferation rate, suggesting that cellular proliferation and apoptosis are concurrent. Exploring this phenomenon, we found overexpression of caspase3, higher cleaved poly (ADP-ribose) polymerase (PARP) levels (P <0.007), and a higher apoptosis rate in cells from patients with high counts compared with cells from patients with low counts. Although we previously found that signal transducer and activator of transcription 3 (STAT3) protects CLL cells from apoptosis, STAT3 levels were significantly higher in cells from patients with high counts than in cells from patients with low counts. Furthermore, overexpression of STAT3 in MM-1 cells did not protect the cells. Rather, it upregulated caspase3 and induced apoptosis. Remarkably, putative STAT3 binding sites were identified in the caspase3 promoter and a luciferase assay, chromatin immunoprecipitation (ChIP), and an electromobility shift assay (EMSA) revealed that STAT3 activated caspase3. However, caspase3 levels increased only when STAT3 levels were sufficiently high. Using ChIP and EMSA, we found that STAT3 binds with low affinity to the caspase3 promoter, suggesting that at high levels, STAT3 activates a negative proapoptotic feedback mechanism.
2015-05-12 | GSE68721 | GEO