MyMedR

Fulltext Estimates of Glomerular filtration rate by the chronic kidney disease epidemiology collaboration equations best correlates with kinetic estimates of Glomerular filtration rates in the critically ill

Azrina Md Ralib, Farah Nadia Mohd Hanafiah, Fatimah Dzaharudin, Muhammad Rasydan Abd Ghani, Mohd Nizamudin Ismail, Mohd Basri Mat Nor

International Medical Journal Malaysia, 2017;16(11):51-51.

MyJurnal

Kinetic estimate of GFR (keGFR) is a more accurate estimate of GFR in the
acute settings with rapidly changing kidney functions. It takes into account the changes
of creatinine over time, creatinine production rate, and the volume of distribution,
however needs serial measurement of creatinine. We evaluated which methods of the
conventional eGFR measurement best correlates with keGFR. This could assist clinicians
in using a simpler method of calculation and is useful in the absence of serial plasma
creatinine. (Copied from article).

Matched MeSH terms: Receptor, Epidermal Growth Factor

Fulltext Are there useful molecular diagnostic tests for predicting responses to targeted therapies in cancer treatment?

HENG, FONG SEOW

Buletin Persatuan Genetik Malaysia, 2011;18(1):7-9.

MyJurnal

Targeted therapies for cancer are designed to inhibit speci c cellular changes or signals required for tumour cells to proliferate, survive, promote angiogenesis and metastasize. Examples include trastuzumab (a monoclonal antibody that targets the human epidermal growth factor receptor 2 [HER2]), imatinib ( a small molecule inhibitor of bcl-abr, an oncogenic kinase) and cetuximab ( a monoclonal antibody that binds to the extracellular domain of the epidermal growth factor receptor [EGFR]).

Matched MeSH terms: Receptor, Epidermal Growth Factor

Fulltext EGFR mutations in Asian patients with advanced lung adenocarcinoma

Liam CK, Pang YK, Poh ME

J Thorac Oncol, 2014 Sep;9(9):e70-1.

PMID: 25122441 DOI: 10.1097/JTO.0000000000000251

Matched MeSH terms: Receptor, Epidermal Growth Factor/genetics*

Fulltext EGFR mutation detection by polymerase chain reaction-direct sequencing and allele-specific real-time PCR

Liam CK, Wong CK, Tan JL

J Thorac Oncol, 2014 Sep;9(9):e71-2.

PMID: 25122442 DOI: 10.1097/JTO.0000000000000261

Matched MeSH terms: Receptor, Epidermal Growth Factor/genetics*

Differential effects of two-pore channel protein 1 and 2 silencing in MDA-MB-468 breast cancer cells

Jahidin AH, Stewart TA, Thompson EW, Roberts-Thomson SJ, Monteith GR

Biochem Biophys Res Commun, 2016 Sep 02;477(4):731-736.

PMID: 27353380 DOI: 10.1016/j.bbrc.2016.06.127

Two-pore channel proteins, TPC1 and TPC2, are calcium permeable ion channels found localized to the membranes of endolysosomal calcium stores. There is increasing interest in the role of TPC-mediated intracellular signaling in various pathologies; however their role in breast cancer has not been extensively evaluated. TPC1 and TPC2 mRNA was present in all non-tumorigenic and tumorigenic breast cell lines assessed. Silencing of TPC2 but not TPC1 attenuated epidermal growth factor-induced vimentin expression in MDA-MB-468 breast cancer cells. This effect was not due to a general inhibition of epithelial to mesenchymal transition (EMT) as TPC2 silencing had no effect on epidermal growth factor (EGF)-induced changes on E-cadherin expression. TPC1 and TPC2 were also shown to differentially regulate cyclopiazonic acid (CPA)-mediated changes in cytosolic free Ca(2+). These findings indicate potential differential regulation of signaling processes by TPC1 and TPC2 in breast cancer cells.

Matched MeSH terms: Receptor, Epidermal Growth Factor/metabolism*

Fulltext Recurrent cerebral infarcts secondary to marantic endocarditis in a patient with adenocarcinoma of the lung

Tai ML, Tan EC, Ang CC, Liam CK

Singapore Med J, 2016 Sep;57(9):524-5.

PMID: 27663211 DOI: 10.11622/smedj.2016157

Matched MeSH terms: Receptor, Epidermal Growth Factor/metabolism

Outcomes of Malaysian patients with advanced lung adenocarcinoma and unknown epidermal growth factor receptor mutation status treated with gefitinib

Liam CK, Ruthranesan M, Lee CH, Pang YK, Chua KT, Lim BK

Asia Pac J Clin Oncol, 2012 Sep;8(3):267-74.

PMID: 22897510 DOI: 10.1111/j.1743-7563.2011.01509.x

To evaluate the response and progression-free survival (PFS) of Malaysian patients with advanced lung adenocarcinoma and unknown epidermal growth factor receptor (EGFR) mutation status treated with gefitinib.

Matched MeSH terms: Receptor, Epidermal Growth Factor/antagonists & inhibitors; Receptor, Epidermal Growth Factor/genetics

Epidermal growth factor receptor targeted therapy with gefitinib in locally advanced and metastatic primary lung adenocarcinoma

Liam CK, Pang YK, Leow CH

Respirology, 2006 May;11(3):287-91.

PMID: 16635086

To describe the efficacy of monotherapy with the epidermal growth factor receptor-tyrosine kinase inhibitor, gefitinib in patients with locally advanced and metastatic primary lung adenocarcinoma.

Matched MeSH terms: Receptor, Epidermal Growth Factor/drug effects*; Receptor, Epidermal Growth Factor/metabolism

Fulltext Advanced right lung adenocarcinoma with ipsilateral breast metastasis

Liam CK, Pang YK, Poh ME, Kow KS, Wong CK, Varughese R

Respirol Case Rep, 2013 Sep;1(1):20-2.

PMID: 25473531 DOI: 10.1002/rcr2.14

Breast metastases from non-small cell lung carcinoma are rarely reported. We report a case of a female patient with primary adenocarcinoma of the lower lobe of her right lung presenting with a massive right-sided malignant pleural effusion. The tumor harbored an epidermal growth factor receptor insertion mutation in exon 20 but was anaplastic lymphoma kinase translocation negative. She did not respond to treatment with erlotinib. First- and second-line cytotoxic chemotherapy resulted in stable disease as the best responses. She developed right breast metastasis 20 months after her initial presentation. The rarity of the condition and the likely mechanism of the breast metastasis are discussed.

Matched MeSH terms: Receptor, Epidermal Growth Factor

Fulltext EGFR mutation testing for squamous cell lung carcinoma

Liam CK, Leow HR, Pang YK

J Thorac Oncol, 2013 Dec;8(12):e114.

PMID: 24389448 DOI: 10.1097/JTO.0b013e3182a4e111

Matched MeSH terms: Receptor, Epidermal Growth Factor/genetics*

Fulltext Synthesis, Biological Evaluation and Molecular Docking of Novel Indole-Aminoquinazoline Hybrids for Anticancer Properties

Mphahlele MJ, Mmonwa MM, Aro A, McGaw LJ, Choong YS

Int J Mol Sci, 2018 Jul 31;19(8).

PMID: 30065164 DOI: 10.3390/ijms19082232

A series of indole-aminoquinazolines was prepared via amination of the 2-aryl-4-chloroquinazolines with the 7-amino-2-aryl-5-bromoindoles. It was then evaluated for cytotoxicity in vitro against human lung cancer (A549), epithelial colorectal adenocarcinoma (Caco-2), hepatocellular carcinoma (C3A), breast adenocarcinoma (MCF-7), and cervical cancer (HeLa) cells. A combination on the quinazoline and indole moieties of a 2-phenyl and 2-(4-fluorophenyl) rings in compound 4b; 2-(4-fluorophenyl) and 3-chlorophenyl rings in compound 4f; or the two 2-(4-fluorophenyl) rings in compound 4g, resulted in significant and moderate activity against the Caco-2 and C3A cell lines. The indole-aminoquinazoline hybrids compounds 4f and 4g induced apoptosis in Caco-2 and C3A cells, and were also found to exhibit moderate (IC50 = 52.5 nM) and significant (IC50 = 40.7 nM) inhibitory activity towards epidermal growth factor receptor (EGFR) against gefitinib (IC50 = 38.9 nM). Molecular docking suggests that 4a⁻h could bind to the ATP region of EGFR like erlotinib.

Matched MeSH terms: Receptor, Epidermal Growth Factor/metabolism

Fulltext Small Cell Transformation and T790M Mutation as Coresistance Mechanisms for First-line Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitor (TKI) Therapy Failure

Shee-Chai C, Liam CK, Mun KS

J Thorac Oncol, 2017 10;12(10):e171-e173.

PMID: 28939153 DOI: 10.1016/j.jtho.2017.06.068

Matched MeSH terms: Receptor, Epidermal Growth Factor/genetics*

Successful pregnancy with epidermal growth factor receptor tyrosine kinase inhibitor treatment of metastatic lung adenocarcinoma presenting with respiratory failure

Lee CH, Liam CK, Pang YK, Chua KT, Lim BK, Lai NL

Lung Cancer, 2011 Nov;74(2):349-51.

PMID: 21920622 DOI: 10.1016/j.lungcan.2011.08.008

We report a woman presenting with respiratory failure due to a right-sided pleural effusion, lung metastases and lymphangitis carcinomatosis from advanced lung adenocarcinoma in the third trimester of pregnancy, who showed good response to EGFR tyrosine kinase inhibitor.

Matched MeSH terms: Receptor, Epidermal Growth Factor/antagonists & inhibitors; Receptor, Epidermal Growth Factor/genetics

Overexpression of phospho-Akt correlates with phosphorylation of EGF receptor, FKHR and BAD in nasopharyngeal carcinoma

Yip WK, Leong VC, Abdullah MA, Yusoff S, Seow HF

Oncol Rep, 2008 Feb;19(2):319-28.

PMID: 18202777

The Akt pathway is one of the most common molecular alterations in various human malignancies. However, its involvement in nasopharyngeal carcinoma (NPC) tumorigenesis has not been well established. In this study, the status of Akt activation and expression of its upstream and downstream molecules was investigated in 64 NPC and 38 non-malignant nasopharyngeal tissues by immunohistochemistry. The hotspot mutations of PIK3CA, encoding the p110alpha catalytic subunit of phosphatidylinositol 3-kinase (PI3K), were also determined in 25 of these NPC tissues. No hotspot mutations were found in any of the samples tested. Akt was activated in 27 (42.2%) and 23 (35.9%) NPCs, as indicated by p-Akt (Thr308) and p-Akt (Ser473) immunoreactivity, respectively. PTEN loss did not correlate statistically with activated Akt. However, a positive correlation was observed between activated Akt and phospho-epidermal growth factor receptor (p-EGFR), suggesting that the EGFR signaling might be one of the upstream regulators of the Akt pathway. The phosphorylation of forkhead (FKHR) and Bcl-2 associated death domain (BAD), but not mammalian target of rapamycin and glycogen synthase kinase-3beta, was significantly correlated with Akt activation. This implies that Akt promotes cell proliferation (as estimated by Ki-67) and survival, at least, through the inactivation of FKHR and BAD in NPC. Our data revealed that the EGFR/PI3K/Akt signaling pathway is important in NPC pathogenesis and that PIK3CA hotspot mutations are rare in NPC.

Matched MeSH terms: Receptor, Epidermal Growth Factor/analysis; Receptor, Epidermal Growth Factor/metabolism*

Mesua ferrea stem bark extract induces apoptosis and inhibits metastasis in human colorectal carcinoma HCT 116 cells, through modulation of multiple cell signalling pathways

Asif M, Shafaei A, Abdul Majid AS, Ezzat MO, Dahham SS, Ahamed MBK, et al.

Chin J Nat Med, 2017 Jul;15(7):505-514.

PMID: 28807224 DOI: 10.1016/S1875-5364(17)30076-6

Considering the great potential of natural products as anticancer agents, the present study was designed to explore the molecular mechanisms responsible for anticancer activities of Mesua ferrea stem bark extract against human colorectal carcinoma. Based on MTT assay results, bioactive sub-fraction (SF-3) was selected for further studies using HCT 116 cells. Repeated column chromatography resulted in isolation of less active α-amyrin from SF-3, which was identified and characterized by GC-MS and HPLC methods. α-amyrin and betulinic acid contents of SF-3 were measured by HPLC methods. Fluorescent assays revealed characteristic apoptotic features, including cell shrinkage, nuclear condensation, and marked decrease in mitochondrial membrane potential in SF-3 treated cells. In addition, increased levels of caspases-9 and -3/7 levels were also observed in SF-3 treated cells. SF-3 showed promising antimetastatic properties in multiple in vitro assays. Multi-pathway analysis revealed significant down-regulation of WNT, HIF-1α, and EGFR with simultaneous up-regulation of p53, Myc/Max, and TGF-β signalling pathways in SF-3 treated cells. In addition, promising growth inhibitory effects were observed in SF-3 treated HCT 116 tumour spheroids, which give a hint about in vivo antitumor efficacy of SF-3 phytoconstituents. In conclusion, these results demonstrated that anticancer effects of SF-3 towards colon cancer are through modulation of multiple molecular pathways.

Matched MeSH terms: Receptor, Epidermal Growth Factor/genetics; Receptor, Epidermal Growth Factor/metabolism

Fulltext Epidermal growth factor receptor mutations in lung adenocarcinoma in Malaysian patients

Liam CK, Wahid MI, Rajadurai P, Cheah YK, Ng TS

J Thorac Oncol, 2013 Jun;8(6):766-72.

PMID: 23575413 DOI: 10.1097/JTO.0b013e31828b5228

Despite available data from other Asian countries, the prevalence of epidermal growth factor receptor (EGFR) mutations among lung adenocarcinoma patients has not been reported in Malaysia. This study sought to determine the frequency of EGFR mutations among multiethnic Malaysian patients diagnosed with lung adenocarcinoma.

Matched MeSH terms: Receptor, Epidermal Growth Factor/genetics*

Paronychia induced by the epidermal growth factor receptor inhibitor cetuximab

Lee SL, Tan BS, Chan LC

J Oncol Pharm Pract, 2013 Sep;19(3):273-8.

PMID: 23161875 DOI: 10.1177/1078155212461289

While the development of epidermal growth factor receptor inhibitors has been hailed as a remarkable triumph in the field of oncology, it has inherited with it a host of cutaneous side-effects that have been increasingly observed in a substantial number of patients in the recent years. One cutaneous manifestation that may inflict significant pain and affect activities of daily living among some of the patients receiving epidermal growth factor receptor inhibitors is paronychia. A case of paronychia associated with the use of cetuximab in the management of KRAS wild-type midrectal adenocarcinoma along with its management has been described.

Matched MeSH terms: Receptor, Epidermal Growth Factor/antagonists & inhibitors*

Carbonate apatite nanoparticles carry siRNA(s) targeting growth factor receptor genes egfr1 and erbb2 to regress mouse breast tumor

Tiash S, Kamaruzman NIB, Chowdhury EH

Drug Deliv, 2017 Nov;24(1):1721-1730.

PMID: 29119846 DOI: 10.1080/10717544.2017.1396385

Cancer cells lose their control on cell cycle by numerous genetic and epigenetic alterations. In a tumor, these cells highly express growth factor receptors (GFRs), eliciting growth, and cell division. Among the GFRs, epidermal growth factor receptor-1 (EGFR1) (Her1/ERBB1) and epidermal growth factor receptor-2 (EGFR2) (Her2/ERBB2) from epidermal growth factor (EGF) family and insulin-like growth factor-1 receptor (IGF1R) are highly expressed on breast cancer cells, thus contributing to the aggressive growth and invasiveness, have been focused in this study. Moreover, overexpression of these receptors is related to suppression of cell death and conferring resistance against the classical drugs used to treat cancer nowadays. Therefore, silencing of these GFRs-encoding genes by using selective small interfering RNAs (siRNAs) could be a powerful approach to treat breast cancer. The inorganic pH sensitive carbonate apatite nanoparticles (NPs) were used as a nano-carrier to deliver siRNA(s) against single or multiple GFR genes in breast cancer cells as well as in a mouse model of breast carcinoma. Silencing of egfr1 and erbb2 simultaneously led to a reduction in cell viability with an increase in cell death signal in the cancer cells and regression of tumor growth in vivo.

Matched MeSH terms: Receptor, Epidermal Growth Factor/metabolism*

Fulltext Epidermal growth factor receptor (EGFR) gene alteration and protein overexpression in Malaysian triple-negative breast cancer (TNBC) cohort

Zakaria Z, Zulkifle MF, Wan Hasan WAN, Azhari AK, Abdul Raub SH, Eswaran J, et al.

Onco Targets Ther, 2019;12:7749-7756.

PMID: 31571924 DOI: 10.2147/OTT.S214611

Background: Epidermal growth factor receptor (EGFR) is a member of the ErbB family of tyrosine kinase receptor proteins that plays important roles in tumour cell survival and proliferation. EGFR has been reported to be overexpressed in up to 78% of triple-negative breast cancer (TNBC) cases suggesting it as a potential therapeutic target. The clinical trials of anti-EGFR agents in breast cancer showed low response rates. However, a subgroup of patients demonstrated response to EGFR inhibitors highlighting the necessity to stratify patients, who might benefit from effective combination therapy that could include anti EGFR-agents. Population variability in EGFR expression warrants systematic evaluation in specific populations.

Purpose: To study EGFR alterations and expressions in a multi ethnic Malaysian TNBC patient cohort to determine the possibility of using anti-EGFR combinatorial therapy for this population.

Patients and methods: In this study, we evaluated 58 cases of Malaysian TNBC patient samples for EGFR gene copy number alteration and EGFR protein overexpression using fluorescence in-situ hybridization (FISH) and immunohistochemistry (IHC) methods, respectively.

Results: EGFR protein overexpression was observed in about 30% while 15.5% displayed high EGFR copy number including 5.17% gene amplification and over 10% high polysomy. There is a positive correlation between EGFR protein overexpression and gene copy number and over expression of EGFR is observed in ten out of the 48 low copy number cases (20.9%) without gene amplification.

Conclusion: This study provides the first glimpse of EGFR alterations and expressions in a multi ethnic Malaysian TNBC patient cohort emphasising the need for the nationwide large scale EGFR expression evaluation in Malaysia.

Matched MeSH terms: Receptor, Epidermal Growth Factor

Fulltext Mapping 18F-Fluorodeoxyglucose metabolism using PET/CT for the assessment of treatment response in non-small cell lung cancer patients undergoing epidermal growth factor receptor inhibitor treatment: a single-centre experience

Subapriya Suppiah, Fathinul Fikri Ahmad Saad, Nur Hafizah Mohad Azmi, Abdul Jalil Nordin

Malaysian Journal of Medicine and Health Sciences, 2017;13(1):9-15.

MyJurnal

Introduction: Specific mutations in the epidermal growth factor receptor (EGFR) characterize a subgroup of nonsmall
cell lung cancer (NSCLC) patients that may be highly responsive to receptor inhibitor therapy. 18F-FDG PET/CT
scans can map the glucose metabolism and treatment response of NSCLC. Therefore, we aimed to assess the pattern
of metabolic response and outcome of inoperable NSCLC treated with epidermal growth factor receptor (EGFR)
inhibitors, using 18F-FDG PET/CT scan. Methods: A retrospective study of inoperable NSCLC patients on EGFR
inhibitor treatment that were referred for wholebody18F-FDG PET/CT scans was conducted based on cases scanned
from January 2011 to June 2014. Comparison was made among serial attenuation-corrected fused PET/CT images for
all study patients throughout the course of their treatment. Comparison based on PERCIST criteria was categorized
into 4 levels ie. complete response (CMR), partial response (PMR), stable disease (SMD), progressive metabolic
disease (PMD). Results: Overall, there were 5 patients identified, mean age: 57.4 years old +/- 2.9 years; The median
survival time from initiation of EGFR inhibitor treatment to death was 17 months. Two patients showed initial partial
metabolic response (PMR), two had progressive metabolic disease (PMD) and one had complete metabolic response
(CMR) after the initiation of treatment. The patient with initial CMR had relapse and PMD 5 months later. Majority of
patients eventually succumbed to their illness. Conclusions: Wholebody18F-FDG PET/CT is able to assess metabolic
treatment response of NSCLC towards EGFR inhibitor treatment.

Matched MeSH terms: Receptor, Epidermal Growth Factor

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