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Institution

Hebron University

EducationHebron, Palestinian Territory
About: Hebron University is a education organization based out in Hebron, Palestinian Territory. It is known for research contribution in the topics: Population & Cancer. The organization has 2714 authors who have published 4180 publications receiving 163736 citations.


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Journal ArticleDOI
TL;DR: There is not yet a single approach that can emerge as a standard for the clinical practice, automatically providing an accurate MS lesion evolution quantification, and future trends will focus on combining the lesion detection in single studies with the analysis of the change detection in serial MRI.
Abstract: Multiple sclerosis (MS) is a serious disease typically occurring in the brain whose diagnosis and efficacy of treatment monitoring are vital. Magnetic resonance imaging (MRI) is frequently used in serial brain imaging due to the rich and detailed information provided. Time-series analysis of images is widely used for MS diagnosis and patient follow-up. However, conventional manual methods are time-consuming, subjective, and error-prone. Thus, the development of automated techniques for the detection and quantification of MS lesions is a major challenge. This paper presents an up-to-date review of the approaches which deal with the time-series analysis of brain MRI for detecting active MS lesions and quantifying lesion load change. We provide a comprehensive reference source for researchers in which several approaches to change detection and quantification of MS lesions are investigated and classified. We also analyze the results provided by the approaches, discuss open problems, and point out possible future trends. Lesion detection approaches are required for the detection of static lesions and for diagnostic purposes, while either quantification of detected lesions or change detection algorithms are needed to follow up MS patients. However, there is not yet a single approach that can emerge as a standard for the clinical practice, automatically providing an accurate MS lesion evolution quantification. Future trends will focus on combining the lesion detection in single studies with the analysis of the change detection in serial MRI.

80 citations

Journal ArticleDOI
TL;DR: In this paper, a DNA methylation microarray was used to identify epigenetic differences in oxaliplatin-sensitive and resistant colorectal cancer cells, and the candidate gene SRBC was validated by single-locus DNA methylations and expression techniques.
Abstract: BACKGROUND: A major problem in cancer chemotherapy is the existence of primary resistance and/or the acquisition of secondary resistance. Many cellular defects contribute to chemoresistance, but epigenetic changes can also be a cause. METHODS: A DNA methylation microarray was used to identify epigenetic differences in oxaliplatin-sensitive and -resistant colorectal cancer cells. The candidate gene SRBC was validated by single-locus DNA methylation and expression techniques. Transfection and short hairpin experiments were used to assess oxaliplatin sensitivity. Progression-free survival (PFS) and overall survival (OS) in metastasic colorectal cancer patients were explored with Kaplan-Meier and Cox regression analyses. All statistical tests were two-sided. RESULTS: We found that oxaliplatin resistance in colorectal cancer cells depends on the DNA methylation-associated inactivation of the BRCA1 interactor SRBC gene. SRBC overexpression or depletion gives rise to sensitivity or resistance to oxaliplatin, respectively. SRBC epigenetic inactivation occurred in primary tumors from a discovery cohort of colorectal cancer patients (29.8%; n = 39 of 131), where it predicted shorter PFS (hazard ratio [HR] = 1.83; 95% confidence interval [CI] = 1.15 to 2.92; log-rank P = .01), particularly in oxaliplatin-treated case subjects for which metastasis surgery was not indicated (HR = 1.96; 95% CI = 1.13 to 3.40; log-rank P = .01). In a validation cohort of unresectable colorectal tumors treated with oxaliplatin (n = 58), SRBC hypermethylation was also associated with shorter PFS (HR = 1.90; 95% CI = 1.01 to 3.60; log-rank P = .045). CONCLUSIONS: These results provide a basis for future clinical studies to validate SRBC hypermethylation as a predictive marker for oxaliplatin resistance in colorectal cancer.

79 citations

Journal ArticleDOI
TL;DR: The future development of selective and unselective FGFR inhibitors will rely on a better understanding of the tissue-specific role of FGFR signaling and identification of biomarkers to select those patients who will benefit the most from these drugs.

79 citations

Journal ArticleDOI
TL;DR: The results suggest that some patients with high-risk, early stage, hormone receptor-positive, HER2-negative breast cancer could achieve molecular downstaging of their disease with CDK4/6 inhibitor and endocrine therapy.
Abstract: Summary Background In hormone receptor-positive, HER2-negative early stage breast cancer, cyclin-dependent kinases 4 and 6 (CDK4/6) inhibition in combination with endocrine therapy could represent an alternative to multiagent chemotherapy. We aimed to evaluate the biological and clinical activity of neoadjuvant ribociclib plus letrozole in the luminal B subtype of early stage breast cancer. Methods CORALLEEN is a parallel-arm, multicentre, randomised, open-label, phase 2 trial completed across 21 hospitals in Spain. We recruited postmenopausal women (≥18 years) with stage I–IIIA hormone receptor-positive, Eastern Cooperative Oncology Group Performance Status 0–1, HER2-negative breast cancer and luminal B by PAM50 with histologically confirmed, operable primary tumour size of at least 2 cm in diameter as measured by MRI. Patients were randomly assigned (1:1) using a web-based system and permuted blocks of 25 to receive either six 28-days cycles of ribociclib (oral 600 mg once daily for 3 weeks on, 1 week off) plus daily letrozole (oral 2·5 mg/day) or four cycles of doxorubicin (intravenous 60 mg/m2) and cyclophosphamide (intravenous 600 mg/m2) every 21 days followed by weekly paclitaxel (intravenous 80 mg/m2) for 12 weeks. The total duration of the neoadjuvant therapy was 24 weeks. Randomisation was stratified by tumour size and nodal involvement. Samples were prospectively collected at baseline (day 0), day 15, and surgery. The primary endpoint was to evaluate the proportion of patients with PAM50 low-risk-of-relapse (ROR) disease at surgery in the modified intention-to-treat population including all randomly assigned patients who received study drug and had a baseline and at least one post-baseline measurement of ROR score. The PAM50 ROR risk class integrated gene expression data, tumour size, and nodal status to define prognosis. This trial was registered at ClinicalTrials.gov , NCT03248427 . Findings Between July 27, 2017 to Dec 7, 2018, 106 patients were enrolled. At baseline, of the 106 patients, 92 (87%) patients had high ROR disease (44 [85%] of 52 in the ribociclib and letrozole group and 48 [89%] of 54 in the chemotherapy group) and 14 (13%) patients had intermediate-ROR disease (eight [15%] and six [11%]). Median follow-up was 200·0 days (IQR 191·2–206·0). At surgery, 23 (46·9%; 95% CI 32·5–61·7) of 49 patients in the ribociclib plus letrozole group and 24 (46·1%; 32·9–61·5) of 52 patients in the chemotherapy group were low-ROR. The most common grade 3–4 adverse events in the ribociclib plus letrozole group were neutropenia (22 [43%] of 51 patients) and elevated alanine aminotransferase concentrations (ten [20%]). The most common grade 3–4 adverse events in the chemotherapy group were neutropenia (31 [60%] of 52 patients) and febrile neutropenia (seven [13%]). No deaths were observed during the study in either group. Interpretation Our results suggest that some patients with high-risk, early stage, hormone receptor-positive, HER2-negative breast cancer could achieve molecular downstaging of their disease with CDK4/6 inhibitor and endocrine therapy. Funding Novartis, Nanostring, Breast Cancer Research Foundation-AACR Career Development Award.

79 citations


Authors

Showing all 2723 results

NameH-indexPapersCitations
José Baselga156707122498
M. I. Martínez134125179885
Josep Tabernero11180368982
Jordi Rello10369435994
Xavier Montalban9576252842
James M. Downey9138129506
Enriqueta Felip8362253364
Joaquim Bellmunt8266041472
Joan Montaner8048922413
Marc Miravitlles7665125671
David H. Salat7524136779
Eduard Gratacós7553120178
Alex Rovira7435619586
Ramon Bataller7228319316
Maria Buti7149326596
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20232
202212
2021568
2020545
2019483
2018385