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  1. Škalamera D, Dahmer-Heath M, Stevenson AJ, Pinto C, Shah ET, Daignault SM, et al.
    Oncotarget, 2016 Sep 20;7(38):61000-61020.
    PMID: 27876705 DOI: 10.18632/oncotarget.11314
    Epithelial to mesenchymal transition (EMT) is a developmental program that has been implicated in progression, metastasis and therapeutic resistance of some carcinomas. To identify genes whose overexpression drives EMT, we screened a lentiviral expression library of 17000 human open reading frames (ORFs) using high-content imaging to quantitate cytoplasmic vimentin. Hits capable of increasing vimentin in the mammary carcinoma-derived cell line MDA-MB-468 were confirmed in the non-tumorigenic breast-epithelial cell line MCF10A. When overexpressed in this model, they increased the rate of cell invasion through Matrigel™, induced mesenchymal marker expression and reduced expression of the epithelial marker E-cadherin. In gene-expression datasets derived from breast cancer patients, the expression of several novel genes correlated with expression of known EMT marker genes, indicating their in vivo relevance. As EMT-associated properties are thought to contribute in several ways to cancer progression, genes identified in this study may represent novel targets for anti-cancer therapy.
    Matched MeSH terms: Disease Progression
  2. Özgüroğlu M, Kilickap S, Sezer A, Gümüş M, Bondarenko I, Gogishvili M, et al.
    Lancet Oncol, 2023 Sep;24(9):989-1001.
    PMID: 37591293 DOI: 10.1016/S1470-2045(23)00329-7
    BACKGROUND: Cemiplimab provided significant survival benefit to patients with advanced non-small-cell lung cancer with PD-L1 tumour expression of at least 50% and no actionable biomarkers at 1-year follow-up. In this exploratory analysis, we provide outcomes after 35 months' follow-up and the effect of adding chemotherapy to cemiplimab at the time of disease progression.

    METHODS: EMPOWER-Lung 1 was a multicentre, open-label, randomised, phase 3 trial. We enrolled patients (aged ≥18 years) with histologically confirmed squamous or non-squamous advanced non-small-cell lung cancer with PD-L1 tumour expression of 50% or more. We randomly assigned (1:1) patients to intravenous cemiplimab 350 mg every 3 weeks for up to 108 weeks, or until disease progression, or investigator's choice of chemotherapy. Central randomisation scheme generated by an interactive web response system governed the randomisation process that was stratified by histology and geographical region. Primary endpoints were overall survival and progression free survival, as assessed by a blinded independent central review (BICR) per Response Evaluation Criteria in Solid Tumours version 1.1. Patients with disease progression on cemiplimab could continue cemiplimab with the addition of up to four cycles of chemotherapy. We assessed response in these patients by BICR against a new baseline, defined as the last scan before chemotherapy initiation. The primary endpoints were assessed in all randomly assigned participants (ie, intention-to-treat population) and in those with a PD-L1 expression of at least 50%. We assessed adverse events in all patients who received at least one dose of their assigned treatment. This trial is registered with ClinicalTrials.gov, NCT03088540.

    FINDINGS: Between May 29, 2017, and March 4, 2020, we recruited 712 patients (607 [85%] were male and 105 [15%] were female). We randomly assigned 357 (50%) to cemiplimab and 355 (50%) to chemotherapy. 284 (50%) patients assigned to cemiplimab and 281 (50%) assigned to chemotherapy had verified PD-L1 expression of at least 50%. At 35 months' follow-up, among those with a verified PD-L1 expression of at least 50% median overall survival in the cemiplimab group was 26·1 months (95% CI 22·1-31·8; 149 [52%] of 284 died) versus 13·3 months (10·5-16·2; 188 [67%] of 281 died) in the chemotherapy group (hazard ratio [HR] 0·57, 95% CI 0·46-0·71; p<0·0001), median progression-free survival was 8·1 months (95% CI 6·2-8·8; 214 events occurred) in the cemiplimab group versus 5·3 months (4·3-6·1; 236 events occurred) in the chemotherapy group (HR 0·51, 95% CI 0·42-0·62; p<0·0001). Continued cemiplimab plus chemotherapy as second-line therapy (n=64) resulted in a median progression-free survival of 6·6 months (6·1-9·3) and overall survival of 15·1 months (11·3-18·7). The most common grade 3-4 treatment-emergent adverse events were anaemia (15 [4%] of 356 patients in the cemiplimab group vs 60 [17%] of 343 in the control group), neutropenia (three [1%] vs 35 [10%]), and pneumonia (18 [5%] vs 13 [4%]). Treatment-related deaths occurred in ten (3%) of 356 patients treated with cemiplimab (due to autoimmune myocarditis, cardiac failure, cardio-respiratory arrest, cardiopulmonary failure, septic shock, tumour hyperprogression, nephritis, respiratory failure, [n=1 each] and general disorders or unknown [n=2]) and in seven (2%) of 343 patients treated with chemotherapy (due to pneumonia and pulmonary embolism [n=2 each], and cardiac arrest, lung abscess, and myocardial infarction [n=1 each]). The safety profile of cemiplimab at 35 months, and of continued cemiplimab plus chemotherapy, was generally consistent with that previously observed for these treatments, with no new safety signals INTERPRETATION: At 35 months' follow-up, the survival benefit of cemiplimab for patients with advanced non-small-cell lung cancer was at least as pronounced as at 1 year, affirming its use as first-line monotherapy for this population. Adding chemotherapy to cemiplimab at progression might provide a new second-line treatment for patients with advanced non-small-cell lung cancer.

    FUNDING: Regeneron Pharmaceuticals and Sanofi.

    Matched MeSH terms: Disease Progression
  3. Zhou X, Li Y, Wang W, Wang S, Hou J, Zhang A, et al.
    Theranostics, 2020;10(21):9443-9457.
    PMID: 32863938 DOI: 10.7150/thno.46078
    Objective: Esophageal squamous cell carcinoma (ESCC) is one of the most commonly diagnosed cancer types in China. Recent genomic sequencing analysis indicated the over-activation of Hippo/YAP signaling might play important roles for the carcinogenic process and progression for ESCC patients. However, little is known about the molecular mechanisms that controls Hippo signaling activity in ESCC. Our previous studies indicated that PLCE1-an important risk factor for ESCC-linked to ESCC progression through snail signaling, during this period, we found PARK2 was an important downstream target of PLCE1-snail axis. PARK2 was decreased in ESCC human samples, and correlated with good prognosis in ESCC patients. Further research showed that PARK2 could inhibit YAP, which functions as key downstream effectors of the Hippo pathway. Here, we aim to reveal the molecular mechanisms of PARK2 modulated Hippo pathway in ESCC. Methods: To evaluate the function of PARK2 in ESCC, we used a tissue microarray (TMA) of 223 human ESCC patients and immunohistochemistry to analyze the correlation between PARK2 expression and clinicopathologic variables. Depletion of endogenous PARK2 and YAP from ESCC cells using CRISPR/Cas9 technologies. Flow cytometry and EdU cell proliferation assay were used to detect proliferation of ESCC cells. Nude mice subcutaneous injection and Ki-67 staining were used to evaluate tumor growth in vivo. Migration and invasion assays were performed. In addition, lung metastasis models in mice were used to validate the function of PARK2 in vivo. Identification of PARK2 involved in hippo pathway was achieved by expression microarray screening, double immunofluorescence staining and co-immunoprecipitation assays. The RNA-seq analysis results were validated through quantitative real-time PCR (qRT-PCR) analysis. The protein half-life of YAP was analyzed by Cycloheximide assay, and the TEAD activity was detected by Luciferase reporter assays. Results: Clinical sample of ESCC revealed that low PARK2 expression correlated with late tumor stage (P < 0.001), poor differentiation (P < 0.04), lymph node (P < 0.001) and distant metastasis (P = 0.0087). Multivariate Cox proportional regression analysis further revealed that PARK2 expression (P = 0.032) is an independent prognostic factor for the overall survival of ESCC patients. Besides, the immunohistochemistry results showed that PARK2 negatively correlated with YAP protein level (P < 0.001). PARK2 depletion promotes ESCC progression both through Hippo/YAP axis, while PARK2 overexpression suppresses ESCC tumor progression by Hippo signaling. Co-IP and ubiquitination assays revealed that PARK2 could interact with YAP in the cytosol and promotes YAP K48-linked ubiquitination at K90 sites. Conclusion: Clinical sample analysis and mechanistic study have validated PARK2 as a tumor suppressor for ESCC. Multivariate Cox proportional regression analysis further revealed that PARK2 is an independent prognostic factor for the overall survival of ESCC patients. Cellular and molecular mechanisms in this study showed that PARK2 associated with YAP protein in the cytosol, promoted YAP ubiquitination and proteasome-dependent degradation in ESCC cells. Therefore, as a novel modulator for Hippo signaling, modulation of PARK2 activity or gene expression level could be an appealing strategy to treat esophageal.
    Matched MeSH terms: Disease Progression
  4. Zhou J, Shaikh LH, Neogi SG, McFarlane I, Zhao W, Figg N, et al.
    Hypertension, 2015 May;65(5):1103-10.
    PMID: 25776071 DOI: 10.1161/HYP.0000000000000025
    Common somatic mutations in CACNAID and ATP1A1 may define a subgroup of smaller, zona glomerulosa (ZG)-like aldosterone-producing adenomas. We have therefore sought signature ZG genes, which may provide insight into the frequency and pathogenesis of ZG-like aldosterone-producing adenomas. Twenty-one pairs of zona fasciculata and ZG and 14 paired aldosterone-producing adenomas from 14 patients with Conn's syndrome and 7 patients with pheochromocytoma were assayed by the Affymetrix Human Genome U133 Plus 2.0 Array. Validation by quantitative real-time polymerase chain reaction was performed on genes >10-fold upregulated in ZG (compared with zona fasciculata) and >10-fold upregulated in aldosterone-producing adenomas (compared with ZG). DACH1, a gene associated with tumor progression, was further analyzed. The role of DACH1 on steroidogenesis, transforming growth factor-β, and Wnt signaling activity was assessed in the human adrenocortical cell line, H295R. Immunohistochemistry confirmed selective expression of DACH1 in human ZG. Silencing of DACH1 in H295R cells increased CYP11B2 mRNA levels and aldosterone production, whereas overexpression of DACH1 decreased aldosterone production. Overexpression of DACH1 in H295R cells activated the transforming growth factor-β and canonical Wnt signaling pathways but inhibited the noncanonical Wnt signaling pathway. Stimulation of primary human adrenal cells with angiotensin II decreased DACH1 mRNA expression. Interestingly, there was little overlap between our top ZG genes and those in rodent ZG. In conclusion, (1) the transcriptome profile of human ZG differs from rodent ZG, (2) DACH1 inhibits aldosterone secretion in human adrenals, and (3) transforming growth factor-β signaling pathway is activated in DACH1 overexpressed cells and may mediate inhibition of aldosterone secretion in human adrenals.
    Matched MeSH terms: Disease Progression
  5. Zhou C, Tang KJ, Cho BC, Liu B, Paz-Ares L, Cheng S, et al.
    N Engl J Med, 2023 Nov 30;389(22):2039-2051.
    PMID: 37870976 DOI: 10.1056/NEJMoa2306441
    BACKGROUND: Amivantamab has been approved for the treatment of patients with advanced non-small-cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 20 insertions who have had disease progression during or after platinum-based chemotherapy. Phase 1 data showed the safety and antitumor activity of amivantamab plus carboplatin-pemetrexed (chemotherapy). Additional data on this combination therapy are needed.

    METHODS: In this phase 3, international, randomized trial, we assigned in a 1:1 ratio patients with advanced NSCLC with EGFR exon 20 insertions who had not received previous systemic therapy to receive intravenous amivantamab plus chemotherapy (amivantamab-chemotherapy) or chemotherapy alone. The primary outcome was progression-free survival according to blinded independent central review. Patients in the chemotherapy group who had disease progression were allowed to cross over to receive amivantamab monotherapy.

    RESULTS: A total of 308 patients underwent randomization (153 to receive amivantamab-chemotherapy and 155 to receive chemotherapy alone). Progression-free survival was significantly longer in the amivantamab-chemotherapy group than in the chemotherapy group (median, 11.4 months and 6.7 months, respectively; hazard ratio for disease progression or death, 0.40; 95% confidence interval [CI], 0.30 to 0.53; P<0.001). At 18 months, progression-free survival was reported in 31% of the patients in the amivantamab-chemotherapy group and in 3% in the chemotherapy group; a complete or partial response at data cutoff was reported in 73% and 47%, respectively (rate ratio, 1.50; 95% CI, 1.32 to 1.68; P<0.001). In the interim overall survival analysis (33% maturity), the hazard ratio for death for amivantamab-chemotherapy as compared with chemotherapy was 0.67 (95% CI, 0.42 to 1.09; P = 0.11). The predominant adverse events associated with amivantamab-chemotherapy were reversible hematologic and EGFR-related toxic effects; 7% of patients discontinued amivantamab owing to adverse reactions.

    CONCLUSIONS: The use of amivantamab-chemotherapy resulted in superior efficacy as compared with chemotherapy alone as first-line treatment of patients with advanced NSCLC with EGFR exon 20 insertions. (Funded by Janssen Research and Development; PAPILLON ClinicalTrials.gov number, NCT04538664.).

    Matched MeSH terms: Disease Progression
  6. Zhao D, Kim MH, Pastor-Barriuso R, Chang Y, Ryu S, Zhang Y, et al.
    Invest Ophthalmol Vis Sci, 2014 Oct;55(10):6244-50.
    PMID: 25183763 DOI: 10.1167/iovs.14-14151
    To examine the longitudinal association between age and intraocular pressure (IOP) in a large sample of Korean men and women.
    Matched MeSH terms: Disease Progression
  7. Zhang Y, Yan W, Collins MA, Bednar F, Rakshit S, Zetter BR, et al.
    Cancer Res, 2013 Oct 15;73(20):6359-74.
    PMID: 24097820 DOI: 10.1158/0008-5472.CAN-13-1558-T
    Pancreatic cancer, one of the deadliest human malignancies, is almost invariably associated with the presence of an oncogenic form of Kras. Mice expressing oncogenic Kras in the pancreas recapitulate the stepwise progression of the human disease. The inflammatory cytokine interleukin (IL)-6 is often expressed by multiple cell types within the tumor microenvironment. Here, we show that IL-6 is required for the maintenance and progression of pancreatic cancer precursor lesions. In fact, the lack of IL-6 completely ablates cancer progression even in presence of oncogenic Kras. Mechanistically, we show that IL-6 synergizes with oncogenic Kras to activate the reactive oxygen species detoxification program downstream of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling cascade. In addition, IL-6 regulates the inflammatory microenvironment of pancreatic cancer throughout its progression, providing several signals that are essential for carcinogenesis. Thus, IL-6 emerges as a key player at all stages of pancreatic carcinogenesis and a potential therapeutic target.
    Matched MeSH terms: Disease Progression
  8. Zaini ZM, McParland H, Møller H, Husband K, Odell EW
    Sci Rep, 2018 10 26;8(1):15874.
    PMID: 30367100 DOI: 10.1038/s41598-018-34165-5
    The value of image cytometry DNA ploidy analysis and dysplasia grading to predict malignant transformation has been determined in oral lesions considered to be at 'high' risk on the basis of clinical information and biopsy result. 10-year follow up data for 259 sequential patients with oral lesions clinically at 'high' risk of malignant transformation were matched to cancer registry and local pathology database records of malignant outcomes, ploidy result and histological dysplasia grade. In multivariate analysis (n = 228 patients), 24 developed carcinoma and of these, 14 prior biopsy samples were aneuploid. Aneuploidy was a significant predictor (hazard ratio 7.92; 95% CI 3.45, 18.17) compared with diploidy (p 
    Matched MeSH terms: Disease Progression
  9. Zaid OI, Abd Majid R, Sidek HM, Noor SM, Abd Rachman-Isnadi MF, Bello RO, et al.
    Trop Biomed, 2020 Mar 01;37(1):29-49.
    PMID: 33612716
    Treatment Failure with chloroquine is one of the challenges that faced the dedicated efforts to eradicate malaria This study aims at investigating the impact of treatment failure with chloroquine on the progression of the disease-induced histo-pathogenic and immunogenic outcomes. To achieve this, Rane's protocol with modifications was applied on a model of Plasmodium berghei ANKA infected ICR mice to determine the dose response curve of chloroquine and to screen the treatment impact on the disease progression. Chloroquine was given at 1, 5, 10, 15 and 20 mg/kg once the parasitemia reached to 20-30% (the experimental initiation point). During the subsequent days, the mice were monitored for changes in the clinical signs, hematology parameters and the progress of the parasitemia until the parasitemia reached to 60-70% (the experimental termination point) or up to 10 days after chloroquine administration in case of achieving a complete eradication of the parasite. At the end, the mice were exsanguinated and their blood and organs were collected for the biochemistry and the histology study. A complete eradication of the parasite was achieved at 20 mg/kg while recrudescence was observed at the lower doses. At 1 mg/kg, the parasite growth was comparable to that of the positive control. The histo-pathogenic and immunogenic changes were stronger in the groups that experienced recrudescence (at 5 and 10 mg/kg). All in all, the study highlights the possibility of having a worsened clinical condition when chloroquine is given at its sub-therapeutic doses during malaria treatment.
    Matched MeSH terms: Disease Progression
  10. Yusof MI, Hassan E, Rahmat N, Yunus R
    Spine (Phila Pa 1976), 2009 Apr 1;34(7):713-7.
    PMID: 19333105 DOI: 10.1097/BRS.0b013e31819b2159
    Pedicle involvement in spinal tuberculosis (TB), the prevertebral abscess formation, severity of vertebral body, and disc collapse were evaluated from magnetic resonance imaging (MRI) of the patients.
    Matched MeSH terms: Disease Progression
  11. Yusof HM, Ab-Rahim S, Suddin LS, Saman MSA, Mazlan M
    Malays J Med Sci, 2018 Sep;25(5):16-34.
    PMID: 30914860 MyJurnal DOI: 10.21315/mjms2018.25.5.3
    Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. Early diagnosis and accurate staging of the disease is vital to improve the prognosis. Metabolomics has been used to identify changes in metabolite profiles in the different stages of cancer in order to introduce new non-invasive molecular tools for staging. In this systematic review, we aim to identify the common metabolite changes in human biological samples and the dominant metabolic pathways associated with CRC progression. A broad systematic search was carried out from selected databases. Four reviewers screened and reviewed the titles, abstracts, and full-text articles according to the inclusion and exclusion criteria. Quality assessment was conducted on the eight articles which met the criteria. Data showed that the metabolites involved with redox status, energy metabolism and intermediates of amino acids, choline and nucleotides metabolism were the most affected during CRC progression. However, there were differences in the levels of individual metabolites detected between the studies, and this might be due to the study population, sample preparation, analytical platforms used and statistical tools. In conclusion, this systematic review highlights the changes in metabolites from early to late stages of CRC. Moreover, biomarkers for prognosis are important to reduce CRC-related mortality.
    Matched MeSH terms: Disease Progression
  12. Yow, K.S., Sapar, S.H., Atan, K.A.
    MyJurnal
    This paper investigates and determines the solutions for the Diophantine equation x2 + 4.7b = y2r, where
    x, y, b are all positive intergers and r > 1. By substituting the values of r and b respectively, generators of
    x and yr can be determined and classified into different categories. Then, by using geometric progression
    method, a general formula for each category can be obtained. The necessary conditions to obtain the
    integral solutions of x and y are also investigated.
    Matched MeSH terms: Disease Progression
  13. Yousuf A, Mohd Arifin SR, Musa R, Md Isa ML
    PMID: 32174997 DOI: 10.2174/1745017901915010153
    Background: Depression is the most common mental disorder and a leading cause of disability, which commonly presents unexplained psychological and physical symptoms. Depression and HIV/AIDS are commonly comorbid. This review provides an insight into the effect of depression on disease progression among people living with HIV.

    Methods: A search for relevant articles was conducted using a database like MEDLINE, Scopus, PsycINFO and CINAHL. Peer-reviewed English journals published between 2015 and 2019 were included in the review.

    Results: A total of eight studies conducted in different settings were included in the review. This review has found that psychosocial, neurohormonal and virologic factors associated with depression affect HIV disease progression. Yet, the chronicity of depression, absence of the hormones that have a buffer effect on depression and lack of examination if depression is a predictor, or an outcome of disease progression, were some of the gaps that require further investigation.

    Conclusion: Considerably, more research is needed to better understand the effect of mental disorder, especially depression, on HIV disease progression to AIDS and future interventions should, therefore, concentrate on the integration of mental health screening in HIV clinical setup.

    Matched MeSH terms: Disease Progression
  14. Yeong KY, Berdigaliyev N, Chang Y
    ACS Chem Neurosci, 2020 12 16;11(24):4073-4091.
    PMID: 33280374 DOI: 10.1021/acschemneuro.0c00696
    Sirtuins are class III histone deacetylase (HDAC) enzymes that target both histone and non-histone substrates. They are linked to different brain functions and the regulation of different isoforms of these enzymes is touted to be an emerging therapy for the treatment of neurodegenerative diseases (NDs), including Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS). The level of sirtuins affects brain health as many sirtuin-regulated pathways are responsible for the progression of NDs. Certain sirtuins are also implicated in aging, which is a risk factor for many NDs. In addition to SIRT1-3, it has been suggested that the less studied sirtuins (SIRT4-7) also play critical roles in brain health. This review delineates the role of each sirtuin isoform in NDs from a disease centric perspective and provides an up-to-date overview of sirtuin modulators and their potential use as therapeutics in these diseases. Furthermore, the future perspectives for sirtuin modulator development and their therapeutic application in neurodegeneration are outlined in detail, hence providing a research direction for future studies.
    Matched MeSH terms: Disease Progression
  15. Yap, Ivan K.S.
    MyJurnal
    Metabonomics can be used to quantitatively measure dynamic biochemical responses of living organisms to physiological or pathological stimuli. A range of analytical tools such as high-resolution nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry (MS) combined with multivariate statistical analysis can be employed to create comprehensive metabolic signatures of biological samples including urine, plasma, faecal water and tissue extracts. These metabolic signatures can reflect the physiological or pathological condition of the organism and indicate imbalances in the homeostatic regulation of tissues and extracellular fluids. This technology has been employed in a diverse range of application areas including investigation of disease mechanisms, diagnosis/prognosis of pathologies, nutritional interventions and drug toxicity. Metabolic profiling is becoming increasingly important in identifying biomarkers of disease progression and drug intervention, and can provide additional information to support or aid the interpretation of genomic and proteomic data. With the new generation of postgenomic technologies, the paradigm in many biological fields has shifted to either top down systems biology approaches, aiming to achieve a general understanding of the global and integrated response of an organism or to bottom up modelling of specific pathways and networks using a priori knowledge based on mining large bodies of literature. Whilst metabolic profiling lends itself to either approach, using it in an exploratory and hypothesis generating capacity clearly allows new mechanisms to be uncovered.
    Matched MeSH terms: Disease Progression
  16. Yap YF, Puthucheary SD
    Singapore Med J, 1998 Jun;39(6):260-2.
    PMID: 9803814
    Typhoid fever, which is endemic in Malaysia, affects all age groups and it has been stated that classical features described in textbooks were absent in children. The aim of this study was to find out whether this was true in the local setting and hence a retrospective study was undertaken.
    Matched MeSH terms: Disease Progression
  17. Yang SC, Mustafar R, Kamaruzaman L, Wei Yen K, Mohd R, Cader R
    Acta Med Indones, 2019 Oct;51(4):338-343.
    PMID: 32041918
    A 59-year-old lady with underlying hypothyroidism presented with acute contact dermatitis progressed to cellulitis with superimposed bacterial infection and acute kidney injury. She responded to initial management with antibiotics, but a week later, she had cutaneous and systemic vasculitis. Her skin biopsy consistent with immune-mediated leuko-cytoclastic vasculitis and her blood test was positive for cytoplasmic-anti-neutrophil cytoplasmic antibody (c-ANCA). A diagnosis of ANCA-associated vasculitis was made and she was treated with immunosuppressant with plasmapheresis and hemodialysis support for her kidney failure. Despite aggressive measures, the patient succumbed to her illness. This case report demonstrates that soft tissue infection could trigger the development of ANCA-associated vasculitis whilst a background of hypothyroidism serves as a predisposing factor as both condition were reported separately in a couple of case studies before.
    Matched MeSH terms: Disease Progression
  18. Yang QH, Zhang Y, Zhang XM, Li XR
    Int J Ophthalmol, 2019;12(2):302-311.
    PMID: 30809489 DOI: 10.18240/ijo.2019.02.19
    AIM: To investigate the pooled prevalence of diabetic retinopathy (DR), proliferative DR (PDR) and nonproliferative DR (NPDR) in Asian type 2 diabetes mellitus (T2DM) patients.
    METHODS: We performed a systematic search online search using PubMed, EMBASE, Web of Science, the Cochrane Library, and China WeiPu Library to identify eligible studies that reported the prevalence of DR, PDR and NPDR in Asian T2DM patients. Effect size (ES) with 95% confidence interval (CI) was used to evaluate the prevalence of DR, PDR and NPDR in Asian T2DM patients, respectively.
    RESULTS: There were 41 references and 48 995 T2DM patients involved in this study. The prevalence of DR, PDR, and NPDR was 28%, 6%, and 27% in T2DM patients, respectively; while the prevalence of PDR and NPDR in DR patients was 17% and 83%, respectively. Subgroup analysis showed that prevalence of DR in T2DM patients from Singaporean, Indian, South Korean, Malaysian, Asian, and Chinese was 33%, 42%, 16%, 35%, 21% and 25%, respectively. In T2DM patients with NPDR from Indian, South Korean, Malaysian, Asian, Chinese, higher prevalence was found than that in PDR patients (45% vs 17%, 13% vs 3%, 30% vs 5%, 23% vs 2% and 22% vs 3%), as well as in DR patients (74% vs 26%, 81% vs 19%, 86% vs 14%, 92% vs 8% and 85% vs 15%). The prevalence of PDR in T2DM from India was higher than patients from other locations of Asia, and the same results were also observed in NPDR patients.
    CONCLUSION: In either T2DM Asian patients or DR patients, NPDR is more common than PDR. Based on our results, we should pay more attention to NPDR screening and management in T2DM patients, and we also recommend suitable interventions to prevent its progression.
    Matched MeSH terms: Disease Progression
  19. Yam YY, Hoh BP, Othman NH, Hassan S, Yahya MM, Zakaria Z, et al.
    Genet. Mol. Res., 2013;12(1):319-27.
    PMID: 23420356 DOI: 10.4238/2013.February.7.1
    Colorectal cancer is one of the most common cancers in many countries, including Malaysia. The accumulation of genomic alterations is an important feature of colorectal carcinogenesis. A better understanding of the molecular events underlying the stages of colorectal carcinogenesis might be helpful in the detection and management of the disease. We used a commercially available single-nucleotide polymorphism genotyping array to detect both copy number abnormalities (CNAs) and copy-neutral loss of heterozygosity (LOH) in sporadic colorectal carcinomas. Matched tumor and normal tissues of 13 colorectal carcinomas (Dukes' stages A-D) were analyzed using a 250K single nucleotide polymorphism array. An additional assay was performed to determine the microsatellite instability status by using the National Cancer Institute-recommended BAT-26 panel. In general, copy number gain (92.3%) was most common, followed by copy number loss (53.8%) and copy-neutral LOH (46.2%). Frequent CNAs of gains and losses were observed on chromosomes 7p, 8, 13q, 17p, 18q, and 20q, and copy-neutral LOH was observed on chromosomes 2, 6, 12, 13q, 14q, 17, 20p, 19q, and 22q. Even though genomic alterations are associated with colorectal cancer progression, our results showed that DNA CNAs and copy-neutral LOH do not reflect disease progression in at least 50% tumors. Copy-neutral LOH was observed in both early and advanced tumors, which favors the involvement of these genomic alterations in the early stages of tumor development.
    Matched MeSH terms: Disease Progression
  20. Yahaya MAF, Lila MAM, Ismail S, Zainol M, Afizan NARNM
    J Immunol Res, 2019;2019:2368249.
    PMID: 30931335 DOI: 10.1155/2019/2368249
    Tumour-associated macrophage (TAM) serves as the site in which most inflammatory cells coreside. It plays an important role in determining the progression and metastasis of a tumour. The characteristic of TAM is largely dependent on the stimuli present in its tumour microenvironment (TME). Under this environment, however, M2 macrophages are found to be in abundance compared to M1 macrophages which later promote tumour progression. Numerous studies have elucidated the relationship between TAM and the progression of tumour; hence, TAM has now been the subject of interest among researchers for anticancer therapy. This review discusses the role of TAM in colorectal cancer (CRC) and some of the potential candidates that could reeducate TAM to fight against CRC. It is with hope that this review will serve as the foundation in understanding TAM in CRC and helping other researchers to select the most suitable candidate to reeducate TAM that could assist in enhancing the tumouricidal activity of M1 macrophage and eventually repress the development of CRC.
    Matched MeSH terms: Disease Progression
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