Displaying publications 1 - 20 of 21 in total

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  1. Wan Mohamad Darani WNS, Mat Ruzlin AN, Azhar ZI, Chen XW
    Sci Rep, 2024 Mar 22;14(1):6890.
    PMID: 38519534 DOI: 10.1038/s41598-024-57593-y
    The growing Human Immunodeficiency Virus (HIV) incidences and insufficient HIV knowledge among Malaysian late adolescents necessitate immediate attention to HIV prevention via education. This study aims to develop and validate an Information-Motivation-Behavioural skills (IMB) model-based education kit for adolescents, PREM-Kit, to educate on HIV prevention among Malaysian late adolescents. Utilizing the Analysis, Design, Development, Implementation, and Evaluation model, we conducted the study in three phases: needs assessment, development of PREM-Kit, and validation of PREM-Kit by applying the IMB model to map the PREM-Kit's contents. PREM-Kit, developed in Malay language, consisted of an infographic flip chart and videos. Five multi-disciplinary experts validated the PREM-Kit using the content validity index (CVI), and 13 end-users validated the PREM-Kit using the Malay version of the Patient Education Materials Assessment Tool for Printable and Audiovisual Materials. The infographic flip chart comprised three modules covering 15 topics, and an animated video accompanied each module. PREM-Kit achieved CVI scores of 1.0 and median scores of over 80% for understandability and actionability. Overall, the newly developed IMB model-based HIV education kit has good content validity, is simple to comprehend and apply, and is ready for testing its effectiveness in improving adolescents' knowledge, attitudes, and practices for HIV prevention.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  2. Cho BC, Kim DW, Batra U, Park K, Kim SW, Yang CT, et al.
    Cancer Res Treat, 2023 Jan;55(1):83-93.
    PMID: 35344649 DOI: 10.4143/crt.2021.1571
    PURPOSE: Previous report from the ASCEND-8 trial showed consistent efficacy with less gastrointestinal (GI) toxicity in patients with anaplastic lymphoma kinase-rearranged (ALK+) advanced/metastatic non-small cell lung cancer (NSCLC) treated with ceritinib 450-mg with food compared with 750-mg fasted. In this subgroup analysis, we report outcomes in Asian patients of the ASCEND-8 trial.

    MATERIALS AND METHODS: Key efficacy endpoints were blinded independent review committee (BIRC)-assessed overall response rate (ORR) and duration of response (DOR) evaluated per Response Evaluation Criteria in Solid Tumors v1.1. Other efficacy endpoints were investigator-assessed ORR and DOR; BIRC- and investigator-assessed progression-free survival (PFS) and disease control rate; overall survival (OS). Safety was evaluated by frequency and severity of adverse events.

    RESULTS: At final data cutoff (6 March 2020), 198 treatment-naïve patients were included in efficacy analysis, of which 74 (37%) comprised the Asian subset; 450-mg fed (n=29), 600-mg fed (n=19), and 750-mg fasted (n=26). Baseline characteristics were mostly comparable across study arms. At baseline, more patients in 450-mg fed arm (44.8%) had brain metastases than in 750-mg fasted arm (26.9%). Per BIRC, patients in the 450-mg fed arm had a numerically higher ORR, 24-month DOR rate and 24-month PFS rate than the 750-mg fasted arm. The 36-month OS rate was 93.1% in 450-mg fed arm and 70.9% in 750-mg fasted arm. Any-grade GI toxicity occurred in 82.8% and 96.2% of patients in the 450-mg fed and 750-mg fasted arms, respectively.

    CONCLUSION: Asian patients with ALK+ advanced/metastatic NSCLC treated with ceritinib 450-mg fed showed numerically higher efficacy and lower GI toxicity than 750-mg fasted patients.

    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  3. Abbaspour Babaei M, Kamalidehghan B, Saleem M, Huri HZ, Ahmadipour F
    Drug Des Devel Ther, 2016;10:2443-59.
    PMID: 27536065 DOI: 10.2147/DDDT.S89114
    c-Kit, a receptor tyrosine kinase, is involved in intracellular signaling, and the mutated form of c-Kit plays a crucial role in occurrence of some cancers. The function of c-Kit has led to the concept that inhibiting c-Kit kinase activity can be a target for cancer therapy. The promising results of inhibition of c-Kit for treatment of cancers have been observed in some cancers such as gastrointestinal stromal tumor, acute myeloid leukemia, melanoma, and other tumors, and these results have encouraged attempts toward improvement of using c-Kit as a capable target for cancer therapy. This paper presents the findings of previous studies regarding c-Kit as a receptor tyrosine kinase and an oncogene, as well as its gene targets and signaling pathways in normal and cancer cells. The c-Kit gene location, protein structure, and the role of c-Kit in normal cell have been discussed. Comprehending the molecular mechanism underlying c-Kit-mediated tumorogenesis is consequently essential and may lead to the identification of future novel drug targets. The potential mechanisms by which c-Kit induces cellular transformation have been described. This study aims to elucidate the function of c-Kit for future cancer therapy. In addition, it has c-Kit inhibitor drug properties and their functions have been listed in tables and demonstrated in schematic pictures. This review also has collected previous studies that targeted c-Kit as a novel strategy for cancer therapy. This paper further emphasizes the advantages of this approach, as well as the limitations that must be addressed in the future. Finally, although c-Kit is an attractive target for cancer therapy, based on the outcomes of treatment of patients with c-Kit inhibitors, it is unlikely that Kit inhibitors alone can lead to cure. It seems that c-Kit mutations alone are not sufficient for tumorogenesis, but do play a crucial role in cancer occurrence.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/antagonists & inhibitors*; Receptor Protein-Tyrosine Kinases/metabolism*; Receptor Protein-Tyrosine Kinases/chemistry
  4. Tablit S, Krache R, Amroune S, Jawaid M, Hachaichi A, Ismail AS, et al.
    J Mech Behav Biomed Mater, 2024 Apr;152:106438.
    PMID: 38359736 DOI: 10.1016/j.jmbbm.2024.106438
    Arundo donax L. is investigated in this study as a suitable reinforcing agent for PLA/PP waste blend 3D printing filament. To improve the compatibility of the fibre and polymer, the Arundo fibre was chemically modified using alkali and silane treatment. Untreated and treated fibres were extruded with Polymer blends before being 3D printed. Effect of chemical treatment on thermal, mechanical, and morphological properties of the composites was investigated. The tensile, Izod impact, and water absorption of the 3D printed specimens were also tested. The Alkali treated (ALK) and combination of alkali and silane treatment (SLN) composites displayed good results. Tensile strength and modulus of the materials increased, as well as their maintained stability in the Izod impact test, demonstrating that the incorporation of ArF did not result in a loss in performance. SEM examination supported these findings by confirming the creation of beneficial interfacial contacts between the matrix and fibre components, as demonstrated by the lack of void between the matrix and the fibre surface. Furthermore, the alkali treatment of the ArF resulted in a considerable reduction in water absorption inside the biocomposite, with a 64% reduction seen in ALK composite comparison to the untreated composite (Un). After the 43-day assessment period.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  5. Omar E, Othman NH
    Med J Malaysia, 2003 Aug;58(3):461-2.
    PMID: 14750392
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/genetics*
  6. Patmanathan SN, Wang W, Yap LF, Herr DR, Paterson IC
    Cell Signal, 2017 06;34:66-75.
    PMID: 28302566 DOI: 10.1016/j.cellsig.2017.03.002
    S1P is a small bioactive lipid which exerts its effects following binding to a family of five G protein-coupled receptors, known as S1P1-5. Following receptor activation, multiple signalling cascades are activated, allowing S1P to regulate a range of cellular processes, such as proliferation, apoptosis, migration and angiogenesis. There is strong evidence implicating the involvement of S1P receptors (S1PRs) in cancer progression and the oncogenic effects of S1P can result from alterations in the expression of one or more of the S1PRs and/or the enzymes that regulate the levels of S1P. However, cooperativity between the individual S1PRs, functional interactions with receptor tyrosine kinases and the sub-cellular localisation of the S1PRs within tumour cells also appear to play a role in mediating the effects of S1PR signalling during carcinogenesis. Here we review what is known regarding the role of individual S1PRs in cancer and discuss the recent evidence to suggest cross-talk between the S1PRs and other cellular signalling pathways in cancer. We will also discuss the therapeutic potential of targeting the S1PRs and their downstream signalling pathways for the treatment of cancer.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/metabolism
  7. Lai SK, Bakrin IH, Abd Rauf N, Abdul Raub SH
    Malays J Pathol, 2024 Apr;46(1):103-108.
    PMID: 38682850
    Spitz tumour with ALK rearrangement is a recently described entity and a rare tumour. The incidence of Spitz tumour was estimated at 3.63 per 100,000 persons in American paediatric population; while there is no data in Asian population. Here we reported a case of an eleven-year-old Asian boy who presented with a left shin nodule of two months' duration. The skin biopsy revealed a Spitz tumour with predominantly spindle cell morphology arranged in fascicles, vertically orientated nests and radial growth pattern. Junctional component, melanin pigment or Kamino bodies were not identified. Immunohistochemical study displayed homogenous cytoplasmic staining for ALK. Fluorescence in-situ hybridisation (FISH) analysis confirmed ALK rearrangement. Review of the literatures demonstrated that positive ALK immunohistochemistry may not correlate with ALK rearrangement. ALK-rearranged Spitz tumour confirmed with FISH analysis favour clinically benign behaviour despite atypical histomorphology or positive sentinel lymph node. Therefore, correlation of histomorphology, immunohistochemical stain and molecular study are important for the definitive diagnosis of this entity.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/genetics
  8. 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 Protein-Tyrosine Kinases
  9. Su KY, Balasubramaniam VRMT
    Front Microbiol, 2019;10:2715.
    PMID: 31824472 DOI: 10.3389/fmicb.2019.02715
    The ability of self-replicating oncolytic viruses (OVs) to preferentially infect and lyse cancer cells while stimulating anti-tumor immunity of the host strongly indicates its value as a new field of cancer therapeutics to be further explored. The emergence of Zika virus (ZIKV) as a global health threat due to its recent outbreak in Brazil has caught the attention of the scientific community and led to the discovery of its oncolytic potential for the treatment of glioblastoma multiforme (GBM), the most common and fatal brain tumor with poor prognosis. Herein, we evaluate the neurotropism of ZIKV relative to the receptor tyrosine kinase AXL and its ligand Gas6 in viral entry and the RNA-binding protein Musashi-1 (MSI1) in replication which are also overexpressed in GBM, suggesting its potential for specific targeting of the tumor. Additionally, this review discusses genetic modifications performed to enhance safety and efficacy of ZIKV as well as speculates future directions for the OV therapy.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  10. Mphahlele MJ, Paumo HK, Choong YS
    Pharmaceuticals (Basel), 2017 Nov 20;10(4).
    PMID: 29156606 DOI: 10.3390/ph10040087
    Series of the 2-unsubstituted and 2-(4-chlorophenyl)-substituted 4-anilino-6-bromoquinazolines and their 6-(4-fluorophenyl)-substituted derivatives were evaluated for in vitro cytotoxicity against MCF-7 and HeLa cells. The 2-unsubstituted 4-anilino-6-bromoquinazolines lacked activity, whereas most of their 2-(4-chlorophenyl) substituted derivatives were found to exhibit significant cytotoxicity and selectivity against HeLa cells. Replacement of bromine with 4-fluorophenyl group for the 2-unsubstituted 4-anilinoquinazolines resulted in superior activity against HeLa cells compared to Gefitinib. The presence of a 4-fluorophenyl group in the 2-(4-chlorophenyl) substituted derivatives led to increased cytotoxicity against HeLa cells, except for the 3-chloroanilino derivative. The most active compounds, namely, 3g, 3l, and 4l, were found to exhibit a moderate to significant inhibitory effect against epidermal growth factor receptor tyrosine kinase (EGFR-TK). The EGFR molecular docking model suggested that these compounds are nicely bound to the region of EGFR.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  11. Prasher P, Sharma M, Chan Y, Singh SK, Anand K, Dureja H, et al.
    Curr Med Chem, 2023;30(13):1529-1567.
    PMID: 34766883 DOI: 10.2174/0929867328666211111161811
    Protein kinases modulate the structure and function of proteins by adding phosphate groups to threonine, tyrosine, and serine residues. The phosphorylation process mediated by the kinases regulates several physiological processes, while their overexpression results in the development of chronic diseases, including cancer. Targeting of receptor tyrosine kinase pathways results in the inhibition of angiogenesis and cell proliferation that validates kinases as a key target in the management of aggressive cancers. As such, the identification of protein kinase inhibitors revolutionized the contemporary anticancer therapy by inducing a paradigm shift in the management of disease pathogenesis. Contemporary drug design programs focus on a broad range of kinase targets for the development of novel pharmacophores to manage the overexpression of kinases and their pathophysiology in cancer pathogenesis. In this review, we present the emerging trends in the development of rationally designed molecular inhibitors of kinases over the last five years (2016-2021) and their incipient role in the development of impending anticancer pharmaceuticals.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  12. Che Mat MF, Abdul Murad NA, Ibrahim K, Mohd Mokhtar N, Wan Ngah WZ, Harun R, et al.
    Int J Oncol, 2016 Dec;49(6):2359-2366.
    PMID: 27840905 DOI: 10.3892/ijo.2016.3755
    Glioblastoma multiforme (GBM) is an aggressive brain tumor and most patients have poor prognosis. Despite many advances in research, there has been no significant improvement in the patient survival rate. New molecular therapies are being studied and RNA interference (RNAi) therapy is one of the promising approaches to improve prognosis and increase survival in patients with GBM. We performed a meta‑analysis of five different microarray datasets and identified 460 significantly upregulated genes in GBM. Loss‑of‑function screening of these upregulated genes using LN18 cells was performed to identify the significant target genes for glioma. Further investigations were performed using siRNA in LN18 cells and various functional assays were carried out on the selected candidate gene to understand further its role in GBM. We identified PROS1 as a candidate gene for GBM from the meta‑analysis and RNAi screening. Knockdown of PROS1 in LN18 cells significantly induced apoptosis compared to siPROS1‑untreated cells (p<0.05). Migration in cells treated with siPROS1 was reduced significantly (p<0.05) and this was confirmed with wound-healing assay. PROS1 knockdown showed substantial reduction in cell invasion up to 82% (p<0.01). In addition, inhibition of PROS1 leads to decrease in cellular proliferation by 18%. Knockdown of PROS1 in LN18 cells caused activation of both of the extrinsic and intrinsic apoptotic pathways. It caused major upregulation of FasL which is important for death receptor signaling activation and also downregulation of GAS6 and other members of TAM family of receptors. PROS1 may play an important role in the development of GBM through cellular proliferation, migration and invasion as well as apoptosis. Targeting PROS1 in GBM could be a novel therapeutic strategy in GBM treatment.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/biosynthesis
  13. Hooi Yeen Yap, Jack Bee Chook, Sin Yeang Teow
    MyJurnal
    ntroduction: Nasopharyngeal carcinoma (NPC) is a prevalent cancer among human population in Southern China, Hong Kong and Southeast Asia. In Malaysia, NPC is the fourth most common cancer in both sexes, predominantly in the Chinese. Epstein-Barr virus (EBV) infection is known to be highly associated with NPC. Fibroblast growth factor receptor-4 (FGFR4) is part of the family of tyrosine kinase receptors that regulate cell survival, differentiation and pro-liferation. The binding of FGFR4 ligands such as fibroblasts growth factors (FGFs) has been shown to activate various oncogenic signalling pathway including MAPK, Ras and PI3K-Akt pathways. In the past, FGFR4 has been shown to promote tumorigenesis and tumour progression in various cancers such as liver, colon, breast and pancreatic and gastric cancers. However, its role in NPC establishment and pathogenesis is under-explored. This study aimed to evaluate the FGFR4 expression in NPC using various cell lines and its potential as a therapeutic target for NPC treat-ment by gene silencing. Methods: The basal FGFR4 level of NPC (EBV-positive: C666-1 and EBV-negative: HONE1 and HK1) and nasopharyngeal epithelial (NPE) normal (NP69 and NP460) cell lines was determined by western blot analysis and RT-qPCR. FGFR4 level at different time points (0, 24, 48, and 72 hours) in HONE1 and C666-1 cell lines were determined by western blot analysis. Luminescence-based assay was performed to determine the cell prolifer-ation of NPC cells in correlation with the FGFR4 expression. NPC cells were then treated with the optimised FGFR4 siRNA or FGFR inhibitor, BLU-9931 and the silencing/ inhibition of FGFR4 expression was confirmed by western blot analysis. The effect of FGFR4 inhibition on the cell proliferation and aggressiveness of NPC cells was then investigat-ed through wound healing assay and invasion marker analysis. Results: Out of the five tested cell lines, HONE1 and C666-1 highly expressed FGFR4, NP69 showed very low expression while HK1 and NP460 did not express FGFR4. In the time-point study, the FGFR4 level of HONE1 and C666-1 peaked at 24-48 hours which is the exponential phase of cells. Following that, the FGFR4 level decreased corresponding to the decreased cell growth rate due to the nutrient deprivation. siRNA experiments showed that 6.25nM of four siRNAs (5, 6, 9 and 10) could effectively target and silence the FGFR4 expression of HONE1, but not in C666-1 even up to 250nM was tested. When BLU-9931 was used, only modest inhibition was observed in both cells at 3uM. Compared to the untreated control, FGFR4-inhibited HONE1 exhibited decreased cell proliferation rate. Cell migration and invasion capabilities of HONE1 were also significantly reduced following the FGFR4 silencing, suggesting the potential of utilising FGFR4 as the therapeutic target. Conclusion: FGFR4 is highly expressed in C666-1 (EBV-positive) and HONE1 (initially EBV-positive, but lost EBV genome in subsequent in vitro passage) NPC cells, but not in EBV-negative HK1 NPC cell and normal NPE cells. FGFR4 gene silencing effectively inhibited the cell proliferation, migration and invasive potentials of NPC cell line. These findings highlight the therapeutic value of targeting FGFR4 for NPC treatment. Further investigations are war-ranted to reveal the molecular mechanism and the possible role of EBV in regulating FGFR4 pathway.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  14. Lee JS, Choi SJ, Kim L, Park IS, Han JY, Kim JM, et al.
    Malays J Pathol, 2019 Aug;41(2):213-222.
    PMID: 31427559
    INTRODUCTION: Anaplastic lymphoma kinase-positive (ALK+) anaplastic large cell lymphoma (ALCL) with a non-common pattern can be diagnostic challenging. Pathologists can be unavoidably and unintentionally blind to non-descript tumor cells in a lymphohistiocytic- (LH) or small-cell (SC)-pattern. We report a case of primary systemic ALK+ ALCL with a SC pattern that presented as secondary gastric lesions with a mixed LH and SC pattern that was masqueraded as inflammatory lesions.

    CASE REPORT: A 34-year-old woman with intractable epigastric pain was referred to have repeated endoscopy with biopsy. She was found to multiple gastric erosions and nodules that were diagnosed as inflammatory lesions both endoscopically and histologically. Meanwhile, she developed an acute onset of severe back pain associated with a pathologic compression fracture in the T3 thoracic vertebral body. Imaging studies disclosed a disseminated systemic disease involving abdominopelvic lymph nodes and cervical and thoracic vertebral bodies. The needle biopsy of the pelvic lymph node disclosed diffuse proliferation of monomorphic small round cells that were diffusely positive for CD30 and ALK. A diagnosis of ALK+ ALCL with a monomorphic SC pattern was rendered.

    DISCUSSION: A retrospective review of the gastric biopsies with the aid of immunohistochemistry enabled us to recognise the presence of lymphomatous infiltrates with a mixed LH and SC pattern in every piece of gastric biopsies that were repeatedly misdiagnosed as inflammatory lesions. This case illustrates a significant diagnostic pitfall of the LH- and SC-patterns in ALK+ ALCL, in which the tumour cells featuring lymphoid, plasmacytoid or histiocytoid appearance can be masqueraded as inflammatory cells.

    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  15. 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 Protein-Tyrosine Kinases
  16. Siti-Aishah, M.A., Salwati, S., Idrus, M., Rahimah, R., Salmi, A., Leong, C.F., et al.
    Medicine & Health, 2008;3(1):69-74.
    MyJurnal
    Anaplastic large cell lymphoma (ALCL) is a rare tumour, accounting for approximately 3% of adult non-Hodgkin lymphomas.1 Primary systemic ALCL frequently involves both lymph nodes and extranodal sites. A 44-year-old woman presented with a firm, mobile mass in the left iliac fossa region. Ultrasound findings showed a well defined inhomogenous soft tissue mass, measuring 4x4x2.6cm in the deep subcutaneous region. Histopathological examination revealed that the mass was infiltrated by large lymphoid cells with marked nuclear atypia including kidney-shaped nuclei. These neoplastic cells expressed anaplastic lymphoma kinase (ALK) (both nuclear & cytoplasmic staining), CD30 and EMA but not for T-cell (CD45RO and CD3), and B-cell (CD20 & CD79α) markers. Fluorescence in situ hybridization (FISH) analysis showed a t(2;5)(p23;q35) chromosomal translocation. Subsequently the patient developed shortness of the breath and a thoracic computed tomography (CT) scan showed a mass encasing the right upper lobe bronchus. She also had bilateral axillary lymph nodes, measuring 1 cm in diameter (biopsy was not done). The mediastinum and endobronchial region did not show any abnormalities. She received 6 cycles of CHOP chemotherapy and remained disease free 2 years after diagnosis. ALCL, rarely present as a soft tissue tumour and this disease should be included as a differential diagnosis of any soft tissue mass.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
  17. Ameli F, Rose IM, Masir N
    Asian Pac J Cancer Prev, 2015;16(6):2385-90.
    PMID: 25824769
    BACKGROUND: Invasive ductal (IDC) and lobular (ILC) carcinomas are the common histological types of breast carcinoma which are difficult to distinguish when poorly differentiated. Discoidin domain receptor (DDR1) and Drosophila dishevelled protein (DVL1) were recently suggested to differentiate IDC from ILC.

    OBJECTIVES: To assess the expression of DDR1 and DVL1 and their association with histological type, grading and hormonal status of IDC and ILC.

    MATERIALS AND METHODS: This cross sectional study was conducted on IDC and ILC breast tumours. Tumours were immunohistochemically stained for (DDR1) and (DVL1) as well as estrogen receptor (ER), progesterone receptor (PR) and C-erbB2 receptor. Demographic data including age and ethnicity were obtained from patient records.

    RESULTS: A total of 51 cases (30 IDCs and 21 ILCs) were assessed. DDR1 and DVL1 expression was not significantly associated with histological type (p=0.57 and p=0.66 respectively). There was no association between DDR1 and DVL1 expression and tumour grade (p=0.32 and p=1.00 respectively), ER (p=0.62 and 0.50 respectively), PR (p=0.38 and p=0.63 respectively) and C-erbB2 expression (p=0.19 and p=0.33 respectively) in IDC. There was no association between DDR1 and DVL1 expression and tumour grade (p=0.52 and p=0.33 respectively), ER (p=0.06 and p=0.76 respectively), PR (p=0.61 and p=0.43 respectively) and C-erbB2 expression (p=0.58 and p=0.76 respectively) in ILC.

    CONCLUSIONS: This study revealed that DDR1 and DVL1 are present in both IDC and ILC regardless of the tumour differentiation. More studies are needed to assess the potential of these two proteins in distinguishing IDC from ILC in breast tumours.

    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/metabolism*
  18. Tiash S, Chua MJ, Chowdhury EH
    Int J Oncol, 2016 Jun;48(6):2359-66.
    PMID: 27035628 DOI: 10.3892/ijo.2016.3452
    Treatment of breast cancer, the second leading cause of female deaths worldwide, with classical drugs is often accompanied by treatment failure and relapse of disease condition. Development of chemoresistance and drug toxicity compels compromising the drug concentration below the threshold level with the consequence of therapeutic inefficacy. Moreover, amplification and over-activation of proto-oncogenes in tumor cells make the treatment more challenging. The oncogene, ROS1 which is highly expressed in diverse types of cancers including breast carcinoma, functions as a survival protein aiding cancer progression. Thus we speculated that selective silencing of ROS1 gene by carrier-mediated delivery of siRNA might sensitize the cancer cells to the classical drugs at a relatively low concentration. In this investigation we showed that intracellular delivery of c-ROS1-targeting siRNA using pH-sensitive inorganic nanoparticles of carbonate apatite sensitizes mouse breast cancer cells (4T1) to doxorubicin, but not to cisplatin or paclitaxel, with the highest enhancement in chemosensitivity obtained at 40 nM of the drug concentration. Although intravenous administrations of ROS1-loaded nanoparticles reduced growth of the tumor, a further substantial effect on growth retardation was noted when the mice were treated with the siRNA- and Dox-bound particles, thus suggesting that silencing of ROS1 gene could sensitize the mouse breast cancer cells both in vitro and in vivo to doxorubicin as a result of synergistic effect of the gene knockdown and the drug action, eventually preventing activation of the survival pathway protein, AKT1. Our findings therefore provide valuable insight into the potential cross-talk between the pathways of ROS1 and doxorubicin for future development of effective therapeutics for breast cancer.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/genetics*
  19. Omar E, Madhavan M, Othman NH
    Pathology, 2004 Apr;36(2):152-9.
    PMID: 15203751
    To investigate RET and p53 expression in local thyroid lesions, in order to shed light on the pathogenesis of papillary carcinoma and explain the high prevalence of this condition among the nodular hyperplasia (multi-nodular goitre) cases.
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/metabolism*
  20. Tai YC, Kim LH, Peh SC
    Pathology, 2003 Oct;35(5):436-43.
    PMID: 14555389
    AIMS: The most common recurrent genetic aberration in anaplastic large cell lymphoma (ALCL) is translocation involving the ALK gene that results in ectopic expression of ALK protein in lymphoid tissue. This study aims to investigate the frequency of ALK gene rearrangement in a series of Asian ALCL.

    METHODS: ALK gene rearrangement was detected by immunostaining of ALK protein and fluorescence in situ hybridisation (FISH) targeting at the 2p23 region.

    RESULTS: The expression of ALK protein was detected in 24/34 (71%) of the cases, and it was significantly higher in childhood cases (100%) when compared to adult cases (47%). The analyses by FISH were consistent with the results from immunostaining of ALK protein, but the analyses were only successful in 15/34 (44%) cases. FISH analyses detected extra copies of ALK gene in three cases, including one case that expressed ALK protein and showed 2p23 rearrangement.

    CONCLUSIONS: The current series revealed a high frequency of ALK gene rearrangement, especially in the children. Immunostaining of ALK protein is a reliable indication of ALK gene rearrangement, and is superior to FISH. However, FISH analysis is useful in detecting other genetic aberrations that are not related to ALK gene rearrangement.

    Matched MeSH terms: Receptor Protein-Tyrosine Kinases
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