Displaying publications 21 - 40 of 93 in total

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  1. Ang AH, Lambeth JT, Soo YS, Ong SC
    Med J Malaya, 1970 Sep;25(1):8-16.
    PMID: 4249503
    Matched MeSH terms: Kidney Neoplasms/radiography
  2. Singam P, Ho C, Hong GE, Mohd A, Tamil AM, Cheok LB, et al.
    Asian Pac J Cancer Prev, 2010;11(2):503-6.
    PMID: 20843141
    Renal cancer is rare and its incidence is 1.9 per 100,000 in the Malaysian population, which consists of three major ethnic groups (Malay, Chinese and Indians). A retrospective study was her conducted to identify clinical characteristics and ethnic background influences on presentation. The study included all renal cancer patients from a single medical institution over ten years, with a total of 75 cases. Seventy-three patients underwent surgery while 2 received only radiotherapy or chemotherapy. The male to female ratio was 2.75:1. Incidence was equal among the Malay (49.3%) and Chinese ethnic groups (45.3%). Mean age of patients were 57.1 (18-93) years old. There were 26 (37.4%) patients with Stage I disease, 14 (18.7%) at Stage II, 23 (30.7%) at Stage III and 12 (16%) at Stage IV. The Chinese race presented at mean older age (p= 0.02) and later stage of disease (p= 0.046). Patients above 40 years old had more advanced stage disease (p= 0.023). Tumour histology were clear cell (72%), urothelial cell (13.3%), sarcomatoid cell and nephroblastoma each contributed 2.7%. The mean tumour size was 8.1 (2-20) cm. There was substantial agreement between the pre and post operative staging (kappa 0.691). In conclusion we observed significant influences of age and race in the clinical presentation of renal cancer in our institution based population. There was larger male to female ratio and mean tumour size as compared to previous epidemiology studies.
    Matched MeSH terms: Kidney Neoplasms/pathology; Kidney Neoplasms/therapy*
  3. Yap NY, Ng KL, Ong TA, Pailoor J, Gobe GC, Ooi CC, et al.
    Asian Pac J Cancer Prev, 2013;14(12):7497-500.
    PMID: 24460324
    BACKGROUND: This study concerns clinical characteristics and survival of renal cell carcinoma (RCC) patients in University Malaya Medical Centre (UMMC), as well as the prognostic significance of presenting symptoms.

    MATERIALS AND METHODS: The clinical characteristics, presenting symptoms and survival of RCC patients (n=151) treated at UMMC from 2003-2012 were analysed. Symptoms evaluated were macrohaematuria, flank pain, palpable abdominal mass, fever, lethargy, loss of weight, anaemia, elevated ALP, hypoalbuminemia and thrombocytosis. Univariate and multivariate Cox regression analyses were performed to determine the prognostic significance of these presenting symptoms. Kaplan Meier and log rank tests were employed for survival analysis.

    RESULTS: The 2002 TNM staging was a prognostic factor (p<0.001) but Fuhrman grading was not significantly correlated with survival (p=0.088). At presentation, 76.8% of the patients were symptomatic. Generally, symptomatic tumours had a worse survival prognosis compared to asymptomatic cases (p=0.009; HR 4.74). All symptoms significantly affect disease specific survival except frank haematuria and loin pain on univariate Cox regression analysis. On multivariate analysis adjusted for stage, only clinically palpable abdominal mass remained statistically significant (p=0.027). The mean tumour size of palpable abdominal masses, 9.5±4.3cm, was larger than non palpable masses, 5.3±2.7cm (p<0.001).

    CONCLUSIONS: This is the first report which includes survival information of RCC patients from Malaysia. Here the TNM stage and a palpable abdominal mass were independent predictors for survival. Further investigations using a multicentre cohort to analyse mortality and survival rates may aid in improving management of these patients.

    Matched MeSH terms: Kidney Neoplasms/complications; Kidney Neoplasms/mortality*; Kidney Neoplasms/pathology; Kidney Neoplasms/therapy
  4. Mohtarrudin N, Ghazali R, Md Roduan MR
    Malays J Pathol, 2018 Dec;40(3):313-318.
    PMID: 30580362
    INTRODUCTION: Cyclooxygenase-2 (COX-2) promotes carcinogenesis by inducing proliferation and angiogenesis while decreasing apoptosis and immunosuppressive activity. It is overexpressed in many malignancies including renal cell carcinoma (RCC). The aim of this study was to investigate COX-2 expression in clear cell RCC and its association with tumour grades and demographic parameters.

    MATERIALS AND METHODS: Thirty-six clear cell RCC cases were selected. There were 21 (58.3%) men and 15 (41.7%) women with median age of 56.6 years (range: 16-74 years). Chinese constituted 16 (44.4%) of the cases; Malays 14 (38.9%) cases and Indian 6 (16.7%) cases. There were 6 (16.7%) grade 1, 20 (55.6%) grade 2, 10 (27.8%) grade 3 and none was grade 4. The paraffin embedded tissues were cut at 4 μm thick and stained with COX-2 monoclonal antibody.

    RESULTS: Eighteen (50%) of the RCC cases were immunopositive, of which all showed strong positivity. The immunopositive cases showed cytoplasmic membrane positivity.

    CONCLUSION: There was no significant association between COX-2 expression with grade, age, sex and ethnicity (p=0.457, p=0.054, p=0.389 and p=0.568 respectively). Strong positivity of COX-2 suggest that COX-2 may play a role in cell proliferation and in carcinogenesis.

    Matched MeSH terms: Kidney Neoplasms/metabolism*; Kidney Neoplasms/pathology
  5. Rajandram R, Razack AH, Ng KL, Gobe GC
    J Kidney Cancer VHL, 2016;3(1):1-11.
    PMID: 28326275 DOI: 10.15586/jkcvhl.2016.47
    Although primary localised tumours of renal cell carcinoma (RCC) can be treated relatively successfully with surgery, metastatic RCC has poor prognosis because of late diagnosis and resistance to therapies. In the present study, we were interested in profiling the protein expression of "inhibitor of caspase-activated DNase" (ICAD), an apoptosis inhibitor, in kidney cancer and its paired normal kidney. Immunohistochemistry with automated batch staining and morphometry using digital pathology were used to compare ICAD in 121 RCC specimens with their paired normal kidney tissue. Tissue microarray of formalin-fixed, paraffin-embedded archival tissue was used. Intensity and localisation of ICAD were compared between normal and cancer samples, and against grading within the cancers. The results demonstrated that, in this cohort, ICAD was highly expressed in the proximal tubular epithelium of normal kidney, and significantly decreased in clear cell RCC tissue (p < 0.05) as well as other subtypes of RCC (p < 0.01) compared with normal kidney. There was a tendency towards nuclear localisation of ICAD in clear cell RCC, but not in other subtypes of RCC. No significant association was found between ICAD intensity and grade of RCC. In summary, down-regulation of ICAD occurs in RCC. ICAD normally inhibits DNA fragmentation and apoptosis; thus, its down-regulation was unexpected in a cancer known for its resistance to apoptosis. However, these RCC samples were from primary, not metastatic, RCC sites, and down-regulated ICAD may be part of a progressive pathway that promotes RCC metastasis.
    Matched MeSH terms: Kidney Neoplasms
  6. Gobe GC, Ng KL, Small DM, Vesey DA, Johnson DW, Samaratunga H, et al.
    Biochem Biophys Res Commun, 2016 Apr 22;473(1):47-53.
    PMID: 26995091 DOI: 10.1016/j.bbrc.2016.03.048
    Apoptosis repressor with caspase recruitment domain (ARC), an endogenous inhibitor of apoptosis, is upregulated in a number of human cancers, thereby conferring drug resistance and giving a rationale for the inhibition of ARC to overcome drug resistance. Our hypothesis was that ARC would be similarly upregulated and targetable for therapy in renal cell carcinoma (RCC). Expression of ARC was assessed in 85 human RCC samples and paired non-neoplastic kidney by qPCR and immunohistochemistry, as well as in four RCC cell lines by qPCR, Western immunoblot and confocal microscopy. Contrary to expectations, ARC was significantly decreased in the majority of clear cell RCC and in three (ACHN, Caki-1 and 786-0) of the four RCC cell lines compared with the HK-2 non-cancerous human proximal tubular epithelial cell line. Inhibition of ARC with shRNA in the RCC cell line (SN12K1) that had shown increased ARC expression conferred resistance to Sunitinib, and upregulated interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF). We therefore propose that decreased ARC, particularly in clear cell RCC, confers resistance to targeted therapy through restoration of tyrosine kinase-independent alternate angiogenesis pathways. Although the results are contrary to expectations from other cancer studies, they were confirmed here with multiple analytical methods. We believe the highly heterogeneous nature of cancers like RCC predicate that expression patterns of molecules must be interpreted in relation to respective matched non-neoplastic regions. In the current study, this procedure indicated that ARC is decreased in RCC.
    Matched MeSH terms: Kidney Neoplasms/metabolism*
  7. Caunter G, Faeez Md Noh MS, Safri LS, Kumar K, Md Idris MA, Harunarashid H, et al.
    EJVES Short Rep, 2019;44:19-22.
    PMID: 31453386 DOI: 10.1016/j.ejvssr.2019.06.003
    Introduction: The development of metastatic renal cell carcinoma (RCC) many years after a nephrectomy is not common but has been reported. A metastasis appearing as a hypervascular tumour, mimicking an arteriovenous malformation (AVM), is a highly unusual phenomenon, with a biopsy required for diagnostic confirmation. Surgery is an option for a solitary metastatic lesion amenable to complete excision, with proven survival benefits. However, widespread metastatic disease carries a very poor prognosis, and is best treated with systemic agents such as anti-angiogenic drugs or tyrosine kinase inhibitors.

    Report: A 58 year old man developed an AVM mimicking a vascular tumour within his left brachioradialis muscle 10 years after a nephrectomy for RCC. Ultrasound and magnetic resonance imaging did not reveal any suspicious features of the vascular lesion.The lesion was successfully removed surgically, and was later proven histopathologically to be metastatic RCC. Further imaging showed widespread metastatic disease, and the patient survived only 15 months after receiving tyrosine kinase inhibitor therapy.

    Discussion: This case report aims to highlight a few important points: RCC metastases may be hypervascular, mimicking an AVM. A long disease free interval does not necessarily exclude recurrence or metastasis, as in this case, therefore long term surveillance is recommended. A high index of suspicion must be maintained to avoid delay in treatment, and biopsy of any suspicious lesion for histological examination is mandatory, albeit after many years of cancer remission. Whole body imaging with computed tomography or positron emission tomography computed tomography may detect clinically occult recurrence or metastases, and is important to guide further treatment.

    Matched MeSH terms: Kidney Neoplasms
  8. Chan VW, Tan WS, Leow JJ, Tan WP, Ong WLK, Chiu PK, et al.
    World J Urol, 2021 Dec;39(12):4295-4303.
    PMID: 34031748 DOI: 10.1007/s00345-021-03734-1
    PURPOSE: The COVID-19 pandemic has led to the cancellation or deferment of many elective cancer surgeries. We performed a systematic review on the oncological effects of delayed surgery for patients with localised or metastatic renal cell carcinoma (RCC) in the targeted therapy (TT) era.

    METHOD: The protocol of this review is registered on PROSPERO(CRD42020190882). A comprehensive literature search was performed on Medline, Embase and Cochrane CENTRAL using MeSH terms and keywords for randomised controlled trials and observational studies on the topic. Risks of biases were assessed using the Cochrane RoB tool and the Newcastle-Ottawa Scale. For localised RCC, immediate surgery [including partial nephrectomy (PN) and radical nephrectomy (RN)] and delayed surgery [including active surveillance (AS) and delayed intervention (DI)] were compared. For metastatic RCC, upfront versus deferred cytoreductive nephrectomy (CN) were compared.

    RESULTS: Eleven studies were included for quantitative analysis. Delayed surgery was significantly associated with worse cancer-specific survival (HR 1.67, 95% CI 1.23-2.27, p 

    Matched MeSH terms: Kidney Neoplasms/mortality*; Kidney Neoplasms/pathology; Kidney Neoplasms/surgery*
  9. Cheng JY, Samudram H, Lee Lai Ling C, Nadarajan VS
    Transfus Med, 2022 Dec;32(6):484-491.
    PMID: 36239101 DOI: 10.1111/tme.12924
    OBJECTIVES: To evaluate the performance and utility of a time-temperature indicator (TTI) to determine the cumulative exposure time (CET) of red cell components (RCC) to temperatures above 10°C occurring within and outside the transfusion laboratory.

    BACKGROUND AND OBJECTIVES: Blood centres often use the '30 or 60-min rule' for accepting RCC exposed to room temperature (RT) back into inventory. Effective monitoring of these temperature deviations is however lacking.

    MATERIALS AND METHODS: A Timestrip PLUS® TP153 10°C (TS + 10) TTI was attached to RCC units after preparation of the unit in the blood bank or on issue to the ward, to track the CET > 10°C during laboratory processing and outside the transfusion laboratory.

    RESULTS: The mean CET of 153 RCC tracked within the laboratory was 56 min. Sixty-four (41.8%) and 34 (22.2%) of RCC had core temperature (CT) >10°C for more than 30 and 60 min, respectively. Among the 69 RCC that were returned unused, 27 (39.1%), 17 (24.6%) and 5 (7.2%) RCC units had CT >10°C for more than 30, 60 and 120 min respectively.

    CONCLUSION: A large proportion of RCC have CT >10°C exceeding 30 min during handling within the transfusion laboratory, as well as when RCC are returned unused from transfusion locations. Corrective measures should be implemented to better manage the cold chain to avoid undesirable consequences to blood transfusion. A temperature sensitive device that can also indicate CET can be employed to objectively monitor the period that RCC remained at a CT that exceeds 10°C.

    Matched MeSH terms: Kidney Neoplasms*
  10. Rohana J, Boo NY, Hayati AR, Baizura J
    Med J Malaysia, 2002 Sep;57(3):364-7.
    PMID: 12440278
    A term newborn infant developed hypovolaemic shock shortly after birth. She was pale with gross hepatomegaly. She required multiple boluses of intravenous fluids, blood products as well as inotropic support. Blood investigations showed persistent thrombocytopenia, anaemia and disseminated intravascular coagulopathy (DIC). She also developed heart failure. She finally succumbed on the eleventh day of life. Autopsy revealed haemangiomatosis involving the liver, lungs, gastrointestinal tract, kidneys and adrenals.
    Matched MeSH terms: Kidney Neoplasms/complications*; Kidney Neoplasms/congenital*
  11. Poh ME, Liam CK, Pang YK, Chua KT
    Respirol Case Rep, 2013 Dec;1(2):26-7.
    PMID: 25473534 DOI: 10.1002/rcr2.16
    We report a man presenting with dyspnea, cough, and hemoptysis due to left lung collapse from an endobronchial tumor obstructing the left main bronchus. Endobronchial biopsy of the tumor showed renal cell carcinoma, identical to a previous specimen of renal cell carcinoma removed by a radical left nephrectomy five years ago. The endobronchial tumor was removed by snare diathermy through a flexible bronchoscope, following which his symptoms resolved and the left lung re-expanded. Endobronchial metastasis from renal cell carcinoma is rare and can mimic obstruction from other endobronchial etiologies, such as bronchogenic carcinoma. Total lung collapse as a result is even more uncommon, although atelectasis is well described. Endobronchial techniques, such as snare diathermy, can relieve obstruction, providing symptom palliation even in advanced disease.
    Matched MeSH terms: Kidney Neoplasms
  12. Zaini MN, Patel SA, Syafruddin SE, Rodrigues P, Vanharanta S
    Sci Rep, 2018 08 13;8(1):12063.
    PMID: 30104738 DOI: 10.1038/s41598-018-30499-2
    Tissue-specific transcriptional programs control most biological phenotypes, including disease states such as cancer. However, the molecular details underlying transcriptional specificity is largely unknown, hindering the development of therapeutic approaches. Here, we describe novel experimental reporter systems that allow interrogation of the endogenous expression of HIF2A, a critical driver of renal oncogenesis. Using a focused CRISPR-Cas9 library targeting chromatin regulators, we provide evidence that these reporter systems are compatible with high-throughput screening. Our data also suggests redundancy in the control of cancer type-specific transcriptional traits. Reporter systems such as those described here could facilitate large-scale mechanistic dissection of transcriptional programmes underlying cancer phenotypes, thus paving the way for novel therapeutic approaches.
    Matched MeSH terms: Kidney Neoplasms/genetics
  13. Yap NY, Ong TA, Morais C, Pailoor J, Gobe GC, Rajandram R
    Cell Biol Int, 2019 Jun;43(6):715-725.
    PMID: 31062478 DOI: 10.1002/cbin.11150
    Renal cell carcinoma (RCC) is one of the most lethal urogenital cancers and effective treatment of metastatic RCC remains an elusive target. Cell lines enable the in vitro investigation of molecular and genetic changes leading to renal carcinogenesis and are important for evaluating cellular drug response or toxicity. This study details a fast and easy protocol of establishing epithelial and fibroblast cell cultures or cell lines concurrently from renal cancer nephrectomy tissue. The protocol involves mechanical disaggregation, collagenase digestion and cell sieving for establishing epithelial cells while fibroblast cells were grown from explants. This protocol has been modified from previous published reports with additional antibiotics and washing steps added to eliminate microbial contamination from the surgical source. Cell characterisation was carried out using immunofluorescence and quantitative polymerase chain reaction. Eleven stable epithelial renal tumour cell lines of various subtypes, including rare subtypes, were established with a spontaneous immortalisation rate of 21.6% using this protocol. Eight fibroblast cell cultures grew successfully but did not achieve spontaneous immortalisation. Cells of epithelial origin expressed higher expressions of epithelial markers such as pan-cytokeratin, cytokeratin 8 and E-cadherin whereas fibroblast cells expressed high α-smooth muscle actin. Further mutational analysis is needed to evaluate the genetic or molecular characteristics of the cell lines.
    Matched MeSH terms: Kidney Neoplasms/pathology
  14. Rohilla S, Singh M, Priya S, Almalki WH, Haniffa SM, Subramaniyan V, et al.
    PMID: 36734949 DOI: 10.1615/JEnvironPatholToxicolOncol.2022042088
    Melatonin is a serotonin-derived pineal gland hormone with many biological functions like regulating the sleep-wake cycle, circadian rhythm, menstrual cycle, aging, immunity, and antioxidants. Melatonin synthesis and release are more pronounced during the night, whereas exposure to light decreases it. Evidence is mounting in favor of the therapeutic effects of melatonin in cancer prevention, treatment and delayed onset in various cancer subtypes. Melatonin exerts its anticancer effect through modification of its receptors such as melatonin 1 (MT1), melatonin 2 (MT2), and inhibition of cancer cell proliferation, epigenetic alterations (DNA methylation/demethylation, histone acetylation/deacetylation), metastasis, angiogenesis, altered cellular energetics, and immune evasion. Melatonin performs a significant function in immune modulation and enhances innate and cellular immunity. In addition, melatonin has a remarkable impact on epigenetic modulation of gene expression and alters the transcription of genes. As an adjuvant to cancer therapies, it acts by decreasing the side effects and boosting the therapeutic effects of chemotherapy. Since current treatments produce drug-induced unwanted toxicities and side effects, they require alternate therapies. A recent review article attempts to summarize the mechanistic perspective of melatonin in different cancer subtypes like skin cancer, breast cancer, hepatic cancer, renal cell cancer, non-small cell lung cancer (NSCLC), colon oral, neck, and head cancer. The various studies described in this review will give a firm basis for the future evolution of anticancer drugs.
    Matched MeSH terms: Kidney Neoplasms*
  15. Morais C, Rajandram R, Blakeney JS, Iyer A, Suen JY, Johnson DW, et al.
    PLoS One, 2021;16(3):e0248983.
    PMID: 33765016 DOI: 10.1371/journal.pone.0248983
    Expression of the protease sensing receptor, protease activated receptor-2 (PAR2), is elevated in a variety of cancers and has been promoted as a potential therapeutic target. With the development of potent antagonists for this receptor, we hypothesised that they could be used to treat renal cell carcinoma (RCC). The expression of PAR2 was, therefore, examined in human RCC tissues and selected RCC cell lines. Histologically confirmed cases of RCC, together with paired non-involved kidney tissue, were used to produce a tissue microarray (TMA) and to extract total tissue RNA. Immunohistochemistry and qPCR were then used to assess PAR2 expression. In culture, RCC cell lines versus primary human kidney tubular epithelial cells (HTEC) were used to assess PAR2 expression by qPCR, immunocytochemistry and an intracellular calcium mobilization assay. The TMA revealed an 85% decrease in PAR2 expression in tumour tissue compared with normal kidney tissue. Likewise, qPCR showed a striking reduction in PAR2 mRNA in RCC compared with normal kidney. All RCC cell lines showed lower levels of PAR2 expression than HTEC. In conclusion, we found that PAR2 was reduced in RCC compared with normal kidney and is unlikely to be a target of interest in the treatment of this type of cancer.
    Matched MeSH terms: Kidney Neoplasms/genetics; Kidney Neoplasms/metabolism*; Kidney Neoplasms/pathology*
  16. Tan GC, Prasad V
    Int. J. Surg. Pathol., 2018 Feb;26(1):34.
    PMID: 28508688 DOI: 10.1177/1066896917709946
    Matched MeSH terms: Kidney Neoplasms/pathology*
  17. Wong KT, Khir AS, Noori S, Peh SC
    Aust N Z J Surg, 1994 Feb;64(2):128-9.
    PMID: 8291977
    Matched MeSH terms: Kidney Neoplasms/pathology
  18. Machiela MJ, Hofmann JN, Carreras-Torres R, Brown KM, Johansson M, Wang Z, et al.
    Eur Urol, 2017 Nov;72(5):747-754.
    PMID: 28797570 DOI: 10.1016/j.eururo.2017.07.015
    BACKGROUND: Relative telomere length in peripheral blood leukocytes has been evaluated as a potential biomarker for renal cell carcinoma (RCC) risk in several studies, with conflicting findings.

    OBJECTIVE: We performed an analysis of genetic variants associated with leukocyte telomere length to assess the relationship between telomere length and RCC risk using Mendelian randomization, an approach unaffected by biases from temporal variability and reverse causation that might have affected earlier investigations.

    DESIGN, SETTING, AND PARTICIPANTS: Genotypes from nine telomere length-associated variants for 10 784 cases and 20 406 cancer-free controls from six genome-wide association studies (GWAS) of RCC were aggregated into a weighted genetic risk score (GRS) predictive of leukocyte telomere length.

    OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Odds ratios (ORs) relating the GRS and RCC risk were computed in individual GWAS datasets and combined by meta-analysis.

    RESULTS AND LIMITATIONS: Longer genetically inferred telomere length was associated with an increased risk of RCC (OR=2.07 per predicted kilobase increase, 95% confidence interval [CI]:=1.70-2.53, p<0.0001). As a sensitivity analysis, we excluded two telomere length variants in linkage disequilibrium (R2>0.5) with GWAS-identified RCC risk variants (rs10936599 and rs9420907) from the telomere length GRS; despite this exclusion, a statistically significant association between the GRS and RCC risk persisted (OR=1.73, 95% CI=1.36-2.21, p<0.0001). Exploratory analyses for individual histologic subtypes suggested comparable associations with the telomere length GRS for clear cell (N=5573, OR=1.93, 95% CI=1.50-2.49, p<0.0001), papillary (N=573, OR=1.96, 95% CI=1.01-3.81, p=0.046), and chromophobe RCC (N=203, OR=2.37, 95% CI=0.78-7.17, p=0.13).

    CONCLUSIONS: Our investigation adds to the growing body of evidence indicating some aspect of longer telomere length is important for RCC risk.

    PATIENT SUMMARY: Telomeres are segments of DNA at chromosome ends that maintain chromosomal stability. Our study investigated the relationship between genetic variants associated with telomere length and renal cell carcinoma risk. We found evidence suggesting individuals with inherited predisposition to longer telomere length are at increased risk of developing renal cell carcinoma.

    Matched MeSH terms: Kidney Neoplasms/blood; Kidney Neoplasms/genetics*; Kidney Neoplasms/pathology
  19. Dutt AK
    Med J Malaya, 1969 Dec;24(2):161-3.
    PMID: 4244145
    Matched MeSH terms: Kidney Neoplasms*
  20. Ch'ng WC, Abd-Aziz N, Ong MH, Stanbridge EJ, Shafee N
    Cell Oncol (Dordr), 2015 Aug;38(4):279-88.
    PMID: 25930675 DOI: 10.1007/s13402-015-0229-5
    Newcastle disease virus (NDV) is an oncolytic virus that is known to have a higher preference to cancer cells than to normal cells. It has been proposed that this higher preference may be due to defects in the interferon (IFN) responses of cancer cells. The exact mechanism underlying this process, however, remains to be resolved. In the present study, we examined the antiviral response towards NDV infection of clear cell renal cell carcinoma (ccRCC) cells. ccRCC is associated with mutations of the von Hippel-Lindau tumor suppressor gene VHL, whose protein product is important for eliciting cellular responses to changes in oxygen levels. The most common first line treatment strategy of ccRCC includes IFN. Unfortunately, most ccRCC cases are diagnosed at a late stage and often are resistant to IFN-based therapies. Alternative treatment approaches, including virotherapy using oncolytic viruses, are currently being investigated. The present study was designed to investigate the mechanistic pathways underlying the response of ccRCC cells to oncolytic NDV infection.
    Matched MeSH terms: Kidney Neoplasms/genetics; Kidney Neoplasms/metabolism; Kidney Neoplasms/virology
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