Displaying publications 1 - 20 of 37 in total

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  1. Inn FX, Ahmed N, Hing EY, Jasman MH
    Urol Ann, 2017 5 10;9(2):194-196.
    PMID: 28479777 DOI: 10.4103/0974-7796.204178
    Tyrosine kinase inhibitor (TKI) and its side effects are well known. However, these are mainly descriptive, with pictorial data lacking. Here, in we report a case of metastatic renal cell carcinoma, treated with TKI, with classic side effects; supplemented with images that demonstrate the adverse effects of the drug. In addition, we discuss and demonstrate the computed tomography changes.
    Matched MeSH terms: Protein-Tyrosine Kinases
  2. 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: Protein-Tyrosine Kinases/genetics*; Protein-Tyrosine Kinases/metabolism; 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. Chear CT, Ripen AM, Mohamed SA, Dhaliwal JS
    Gene, 2015 Apr 15;560(2):245-8.
    PMID: 25680287 DOI: 10.1016/j.gene.2015.02.019
    Bruton's tyrosine kinase (BTK), encoded by the BTK gene, is a cytoplasmic protein critical in B cell development. Mutations in the BTK gene cause X-linked agammaglobulinemia (XLA), a primary immunodeficiency with characteristically low or absent B cells and antibodies. This report describes a five year-old boy who presented with otitis externa, arthritis, reduced immunoglobulins and no B cells. Flow cytometry showed undetectable monocyte BTK expression. Sequencing revealed a novel mutation at exon 13 of the BTK gene which created a de novo splice site with a proximal 5 nucleotide loss resulting in a truncated BTK protein. The patient still suffered from ear infection despite intravenous immunoglobulin replacement therapy. In this study, mosaicism was seen only in the mother's genomic DNA. These results suggest that a combination of flow cytometry and BTK gene analysis is important for XLA diagnosis and carrier screening.
    Matched MeSH terms: Protein-Tyrosine Kinases/genetics*
  5. Beniddir MA, Le Borgne E, Iorga BI, Loaëc N, Lozach O, Meijer L, et al.
    J. Nat. Prod., 2014 May 23;77(5):1117-22.
    PMID: 24798019 DOI: 10.1021/np400856h
    Two new acridone alkaloids, chlorospermines A and B (1 and 2), were isolated from the stem bark of Glycosmis chlorosperma, together with the known atalaphyllidine (3) and acrifoline (4), by means of bioguided isolation using an in vitro enzyme assay against DYRK1A. Acrifoline (4) and to a lesser extent chlorospermine B (2) and atalaphyllidine (3) showed significant inhibiting activity on DYRK1A with IC50's of 0.075, 5.7, and 2.2 μM, respectively. Their selectivity profile was evaluated against a panel of various kinases, and molecular docking calculations provided structural details for the interaction between these compounds and DYRK1A.
    Matched MeSH terms: Protein-Tyrosine Kinases/antagonists & inhibitors
  6. Chear CT, Gill HK, Ramly NH, Dhaliwal JS, Bujang N, Ripen AM, et al.
    Asian Pac. J. Allergy Immunol., 2013 Dec;31(4):320-4.
    PMID: 24383975 DOI: 10.12932/AP0304.31.4.2013
    X-linked agammaglobulinemia (XLA) is a rare genetic disorder caused by mutations in the Bruton's tyrosine kinase (BTK) gene. These mutations cause defects in early B cell development. A patient with no circulating B cells and low serum immunoglobulin isotypes was studied as were his mother and sister. Monocyte BTK protein expression was evaluated by flow cytometry. The mutation was determined using PCR and followed by sequencing. Flow cytometry showed the patient lacked BTK protein expression in his monocytes while the mother and sister had 62% and 40% of the monocytes showing BTK protein expressions respectively. The patient had a novel base substitution in the first nucleotide of intron 9 in the BTK gene, and the mutation was IVS9+1G
    Matched MeSH terms: Protein-Tyrosine Kinases/genetics*
  7. 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
  8. Omar E, Othman NH
    Med. J. Malaysia, 2003 Aug;58(3):461-2.
    PMID: 14750392
    Matched MeSH terms: Receptor Protein-Tyrosine Kinases/genetics*
  9. Yaakup H, Sagap I, Fadilah SA
    Singapore Med J, 2008 Oct;49(10):e289-92.
    PMID: 18946602
    Primary oesophageal lymphoma is a very rare entity, with fewer than 30 reported cases worldwide. It represents an important cause of dysphagia. Most of the oesophageal lymphomas are diffuse large B-cell type, with only one reported case of anaplastic large cell lymphoma (ALCL) of T-cell phenotype. Primary oesophageal lymphomas that are not associated with an immunocompromised state tend to affect elderly patients. We describe the first case of primary oesophageal Ki (CD30)-positive ALK+ALCL of T-cell phenotype in a 34-year-old immunocompetent woman, who presented with a two-year history of dysphagia. She was treated with chemotherapy and endoscopic oesophageal dilations and stenting, resulting in complete remission of the lymphoma and resolution of the dysphagia. She then underwent autologous peripheral blood haematopoietic stem cell transplantation and remained disease-free two years after the diagnosis.
    Matched MeSH terms: Protein-Tyrosine Kinases/biosynthesis*; Receptor Protein-Tyrosine Kinases
  10. 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
  11. Bennett NC, Rajandram R, Ng KL, Gobe GC
    J Kidney Cancer VHL, 2014;1(2):17-25.
    PMID: 28326246 DOI: 10.15586/jkcvhl.2014.9
    Steroid hormones and their receptors have important roles in normal kidney biology, and alterations in their expression and function help explain the differences in development of kidney diseases, such as nephrotic syndrome and chronic kidney disease. The distinct gender difference in incidence of renal cell carcinoma (RCC), with males having almost twice the incidence as females globally, also suggests a role for sex hormones or their receptors in RCC development and progression. There was a peak in interest in evaluating the roles of androgen and estrogen receptors in RCC pathogenesis in the late 20th century, with some positive outcomes for RCC therapy that targeted estrogen receptors, especially for metastatic disease. Since that time, however, there have been few studies that look at use of steroid hormone modulators for RCC, especially in the light of new therapies such as the tyrosine kinase inhibitors and new immune therapies, which are having some success for treatment of metastatic RCC. This review summarises past and current literature and attempts to stimulate renewed interest in research into the steroid hormones and their receptors, which might be used to effect, for example, in combination with the other newer targeted therapies for RCC.
    Matched MeSH terms: Protein-Tyrosine Kinases
  12. Abushouk AI, Negida A, Elshenawy RA, Zein H, Hammad AM, Menshawy A, et al.
    CNS Neurol Disord Drug Targets, 2018 Apr 26;17(1):14-21.
    PMID: 28571531 DOI: 10.2174/1871527316666170602101538
    Parkinson's disease (PD) is the most prevalent movement disorder in the world. The major pathological hallmarks of PD are death of dopaminergic neurons and the formation of Lewy bodies. At the moment, there is no cure for PD; current treatments are symptomatic. Investigators are searching for neuroprotective agents and disease modifying strategies to slow the progress of neurodegeneration. However, due to lack of data about the main pathological sequence of PD, many drug targets failed to provide neuroprotective effects in human trials. Recent evidence suggests the involvement of C-Abelson (c-Abl) tyrosine kinase enzyme in the pathogenesis of PD. Through parkin inactivation, alpha synuclein aggregation, and impaired autophagy of toxic elements. Experimental studies showed that (1) c-Abl activation is involved in neurodegeneration and (2) c-Abl inhibition shows neuroprotective effects and prevents dopaminergic neuronal' death. Current evidence from experimental studies and the first in-human trial shows that c-Abl inhibition holds the promise for neuroprotection against PD and therefore, justifies the movement towards larger clinical trials. In this review article, we discussed the role of c-Abl in PD pathogenesis and the findings of preclinical experiments and the first in-human trial. In addition, based on lessons from the last decade and current preclinical evidence, we provide recommendations for future research in this area.
    Matched MeSH terms: Protein-Tyrosine Kinases
  13. Lim YM, Eng WL, Chan HK
    Asian Pac. J. Cancer Prev., 2017 07 27;18(7):1925-1930.
    PMID: 28749622
    Background: In Malaysia, the treatment for chronic myeloid leukemia (CML) has long been delivered under the
    Malaysian Patient Assistance Program (MYPAP), but research on identifying factors contributing to non-adherence to
    tyrosine kinase inhibitors (TKIs) is still limited. The current study explored understanding and challenges of Malaysian
    CML patients in taking imatinib and nilotinib. Methods: Semi-structured, face-to-face interviews were conducted
    with 13 CML patients receiving treatment at a public tertiary care center, and were analyzed using the content analysis
    approach. Results: The patients generally demonstrated inadequate knowledge, particularly of the natural history and
    staging of CML, the function of TKIs, and the methods used for monitoring the effectiveness of treatment. A number of
    them also had experiences of withholding, skipping or altering the treatment, mainly due to the life-disturbing adverse
    drug effects (ADRs), forgetfulness, and religious and social issues. Besides, most of them were found having limited
    skills in managing the ADRs, and not using prompts as reminders to take the medications. Furthermore, even though
    nilotinib was generally perceived as better tolerated as compared with imatinib, the inconvenience caused by the need
    to take it twice daily and on an empty stomach was constantly highlighted by the patients. Conclusion: While TKIs
    are widely used for CML treatment in Malaysia, the findings have revealed a lack of patient education and awareness,
    which warrants an integrated plan to reinforce medication adherence.
    Matched MeSH terms: Protein-Tyrosine Kinases
  14. Awang-Kechik NH, Ahmad R, Doustjalali SR, Sabet NS, Abd-Rahman AN
    J Clin Exp Dent, 2019 Mar;11(3):e269-e274.
    PMID: 31001398 DOI: 10.4317/jced.55546
    Background: The biological responses involved during retention phase have been studied for many years but little is known about the effect of saliva proteome during retention phase of post-orthodontic treatment. This study aims to identify the protein profiles during retention phase in relation to biological processes involved by Liquid Chromatography Mass Spectrometry (LC-MS) approach.

    Material and Methods: A total of 5 ml of unstimulated saliva was collected from each subject (10 non-orthodontic patients and 15 post-orthodontic patients with 6-months retention phase). Samples were then subjected to LC-MS analysis. The expressed proteins were identified and compared between groups. Incisor irregularity for both maxilla and mandible were determined with Little's Irregularity Index at 6-months retention phase.

    Results: 146 proteins and 135 proteins were expressed in control and 6-months retention phase group respectively. 15 proteins were identified to be co-expressed between groups. Immune system process was only detected in 6-months retention phase group. Detected protein in immune system process was identified as Tyrosine-protein kinase Tec. Statistical significant of incisor irregularity was only found in mandible at 6-months retention phase.

    Conclusions: Our study suggests that immune system process protein which is Tyrosine-protein kinase Tec could be used as biomarker for prediction of stability during retention phase of post-orthodontic treatment. Key words:Orthodontics, proteomics, retention, LC-MS, saliva.

    Matched MeSH terms: Protein-Tyrosine Kinases
  15. Sosroseno W, Bird PS, Seymour GJ
    J Microbiol Immunol Infect, 2003 Dec;36(4):229-35.
    PMID: 14723250
    The aim of this study was to determine the role of intracellular proteins in phagocytosis of opsonized Porphyromonas gingivalis by RAW264.7 cells, a murine macrophage-like cell line. This periodontopathogen was grown anaerobically and opsonized with an IgG2a murine monoclonal anti-P. gingivalis lipopolysaccharide antibody. RAW264.7 cells were preincubated with protein tyrosine kinase inhibitors (staurosporine and genistein), protein kinase C inhibitors (phorbol myristic acetate and bisindolylmaleimide), a serine/threonine phosphatase inhibitor (okadaic acid), a phosphatidylinositol 3-kinase inhibitor (worthmannin), phospholipase A2 inhibitors (bromophenacyl bromide and nordihydroguaiaretic acid), phospholipase C inhibitors (p-chloromercuriphenyl sulfonate and neomycin sulfate), an actin-filament depolymerizer (cytochalasin D), and a microtubule disrupting agent (colchicine). Inhibitor-treated macrophages were then incubated with the opsonized P. gingivalis and the phagocytosed cells determined microscopically. The results showed the percentage of the phagocytosed organisms decreased when the cells were preincubated with protein tyrosine kinase, protein kinase C, protein phosphatase and phosphatidylinositol 3-kinase inhibitors. Of interest, preincubation with phorbol myristic acetate for 30 min increased the ability of RAW264.7 cells to phagocytose the opsonized organisms. Phospholipase A2 and phospholipase C inhibitors only slightly reduced the number of phagocytosed organisms. The results indicated that opsonophagocytosis of P. gingivalis by RAW264.7 cells might be determined by the activation of protein tyrosine kinase, protein kinase C, protein phosphatases, and phosphatidylinositol 3-kinase inhibitor. Both phospholipase A2 and phospholipase C would appear to be involved to a lesser extent. The opsonophagocytosis of this periodontopathogen would also appear to be dependent upon actin and microtubule polymerization.
    Matched MeSH terms: Protein-Tyrosine Kinases/antagonists & inhibitors; Protein-Tyrosine Kinases/physiology*
  16. Kabir MZ, Feroz SR, Mukarram AK, Alias Z, Mohamad SB, Tayyab S
    J. Biomol. Struct. Dyn., 2016 Aug;34(8):1693-704.
    PMID: 26331959 DOI: 10.1080/07391102.2015.1089187
    Interaction of a tyrosine kinase inhibitor, vandetanib (VDB), with the major transport protein in the human blood circulation, human serum albumin (HSA), was investigated using fluorescence spectroscopy, circular dichroism (CD) spectroscopy, and molecular docking analysis. The binding constant of the VDB-HSA system, as determined by fluorescence quenching titration method was found in the range, 8.92-6.89 × 10(3 )M(-1) at three different temperatures, suggesting moderate binding affinity. Furthermore, decrease in the binding constant with increasing temperature revealed involvement of static quenching mechanism, thus affirming the formation of the VDB-HSA complex. Thermodynamic analysis of the binding reaction between VDB and HSA yielded positive ΔS (52.76 J mol(-1) K(-1)) and negative ΔH (-6.57 kJ mol(-1)) values, which suggested involvement of hydrophobic interactions and hydrogen bonding in stabilizing the VDB-HSA complex. Far-UV and near-UV CD spectral results suggested alterations in both secondary and tertiary structures of HSA upon VDB-binding. Three-dimensional fluorescence spectral results also showed significant microenvironmental changes around the Trp residue of HSA consequent to the complex formation. Use of site-specific marker ligands, such as phenylbutazone (site I marker) and diazepam (site II marker) in competitive ligand displacement experiments indicated location of the VDB binding site on HSA as Sudlow's site I (subdomain IIA), which was further established by molecular docking results. Presence of some common metal ions, such as Ca(2+), Zn(2+), Cu(2+), Ba(2+), Mg(2+), and Mn(2+) in the reaction mixture produced smaller but significant alterations in the binding affinity of VDB to HSA.
    Matched MeSH terms: Protein-Tyrosine Kinases/antagonists & inhibitors
  17. Wong PF, Abubakar S
    Cell. Mol. Biol. Lett., 2008;13(3):375-90.
    PMID: 18311544 DOI: 10.2478/s11658-008-0009-6
    Malignant prostate tissues have markedly reduced zinc (Zn(2+)) contents in comparison to non-malignant tissues. In this study, we restored a high intracellular Zn(2+) level to LNCaP prostate cancer cells by culturing the cells in a growth medium supplemented with a supraphysiological concentration of Zn(2+) (10 microg/ml) over 5 weeks. The intracellular Zn(2+) level increased in the Zn(2+)-treated cells, and there was a marked increase in the presence of zincosomes, a Zn(2+)-specific intracellular organelle. The proliferation rate of the Zn(2+)-treated cells was markedly reduced. There was also a significant increase (36.6% +/- 6.4%) in the total tyrosine phosphorylated proteins. Vaccinia H1-related (VHR) phosphatase, zeta chain-associated protein-70 (ZAP-70) kinase and phosphorylated extracellular signal-regulated protein kinase 1 and 2 (p-ERK 1 and 2) were also present in higher abundance. Treatment with TPEN, which chelates Zn(2+), reduced the abundance of VHR phosphatase and ZAP-70 kinase, but increased the abundance of p-ERK 1. However, the TPEN treatment restored the Zn(2+)-treated LNCaP cell proliferation to a rate comparable to that of the non Zn(2+)-treated cells. These results highlight the importance of a high intracellular Zn(2+) content and the VHR/ZAP-70-associated pathways in the modulation of LNCaP prostate cancer cell growth.
    Matched MeSH terms: Protein-Tyrosine Kinases/metabolism
  18. Zhou Q, Cheung YB, Jada SR, Lim WT, Kuo WL, Gray JW, et al.
    Cancer Biol. Ther., 2006 Nov;5(11):1445-9.
    PMID: 17102595
    AIM: The purpose of this study was to test the hypothesis if longer CA dinucleotide repeats are more common in the Asian population and also to gain insights into the interplay between the CA dinucleotide repeats and the frequencies of EGFR gene expression and amplifications as this might have therapeutic implications with regards to treatment with tyrosine kinase inhibitors.

    MATERIALS AND METHODS: The EGFR intron 1 polymorphism was analysed in three distinct healthy Asian subjects, namely, Chinese (N = 96), Malays (N = 98) and Indians (N = 100). Comparative genomic hybridisation was performed to investigate for changes in DNA copy number in relation to the polymorphic CA dinucleotide repeats in breast tumor tissues (N = 22).

    RESULTS: The frequency of short alleles with 14 and 15 CA repeats were most common in the Asian populations and significantly higher than those reported for Caucasians. The frequency of 20 CA repeats was 5%, almost 13-fold lower than previous reports. EGFR amplifications were detected in 23% and 11% of breast tumor tissues harboring short and long CA repeats, respectively.

    CONCLUSION: Our results show that the frequency of alleles encoding for short CA dinucleotide repeats is common in Asian populations. EGFR expression and amplification levels were also higher in Asian breast tumor tissues with short CA dinucleotide repeats. These findings suggest that the EGFR intron 1 polymorphism may influence response to treatment with tyrosine kinase inhibitors in breast cancer patients and further studies are warranted.

    Matched MeSH terms: Protein-Tyrosine Kinases/antagonists & inhibitors
  19. 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
  20. 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
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