Epidermal growth factor receptor (EGFR) expression in patients with laryngeal squamous cell carcinoma

Kontić, Mirko; Milovanović, Jovica; Čolović, Zaviša; Poljak, Nikola Kolja; Šundov, Željko; Sučić, Ante; Pešutić-Pisac, Valdi

doi:10.1007/s00405-014-3323-9

Cited by 14 publications

(11 citation statements)

References 15 publications

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“…Therefore, the previous researches of VEGFR2 focused on its function of angiogenesis. However, our research revealed that VEGFR2 expressed strongly not only in the endothelial cells but also in tumor cells in HNSCC, which consisted with reports in other cancer (Guo et al, 2010;Silva et al, 2011;Mokhtari, 2012;Kontic et al, 2014). This result indicated thatVEGFR2 might play an important role inprogression of HNSCC.…”

Section: Discussionsupporting

confidence: 85%

VEGFR2 Expression in Head and Neck Squamous Cell Carcinoma Cancer Cells Mediates Proliferation and Invasion

Xu¹,

Zhu²,

Gu³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Vascular endothelial growth factor 2 (VEGFR2) was initially identified as a receptor of VEGF on endothelial cells with a role in regulating angiogenesis during organism development and tumorigenesis. Previously, in cancer tissue, VEGFR2 has been reported to be expressed in endothelial cells. In our research, we found that VEGFR2 was expressed not only in endothelial cells but also cancer cells in head and neck squamous cell carcinomas (HNSCCs). Knockdown of VEGFR2 in Hep2 cells could arrest the cell cycle in G0/G1, leading to a decrease in proliferation. We also present evidence that MAPK/ERK signal pathways and expression of CDK1 downstream of VEGFR2 might regulate proliferation and cell cycle arrest. Furthermore, we discovered that down-regulate VEGRF2 in Hep2 cells could significantly affect the invasion ability. Taken together, our data suggest that VEGFR2 might regulate proliferation and invasion in HNSCC cancer cells in vivo.

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Section: Discussionsupporting

confidence: 85%

VEGFR2 Expression in Head and Neck Squamous Cell Carcinoma Cancer Cells Mediates Proliferation and Invasion

Xu¹,

Zhu²,

Gu³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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“…The use of EGFR as a biomarker for response to EGFR inhibitor is limited by the semiquantitative nature of and subjectivity of immunohistochemical scoring 100–102. It might be due to inaccurate assays as well as the nature of increased gene copy number being a less predictive biomarker compared to activating mutations 55.…”

Section: Introductionmentioning

confidence: 99%

<p>Novel genetic alterations and their impact on target therapy response in head and neck squamous cell carcinoma</p>

Jiang

Dong

et al. 2019

CMAR

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Head and neck squamous cell carcinoma (HNSCC) is highly variable by tumor site, histologic type, molecular characteristics, and clinical outcome. During recent years, emerging targeted therapies have been focused on driver genes. HNSCC involves several genetic alterations, such as co-occurrence, multiple feedback loops, and cross-talk communications. These different kinds of genetic alterations interact with each other and mediate targeted therapy response. In the current review, it is emphasized that future treatment strategy in HNSCC will not solely be based on “synthetic lethality” approaches directed against overactivated genes. More importantly, biologic, genetic, and epigenetic alterations of HNSCC will be taken into consideration to guide the therapy. The emerging genetic alterations in HNSCC and its effect on targeted therapy response are discussed in detail. Hopefully, novel combination regimens for the treatment of HNSCC can be developed.

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“…In our protein analysis, overexpression of the marker was correlated with the grade of the examined cases. Another study has shown similar association combined, also, with overall advanced disease characteristics, including stage and metastasizing potential leading to poor prognosis (14). in vivo 33: 815-819 (2019) Interestingly, another study has concluded that the synergetic over activation of EGFR and hepatocyte growth factor tyrosine kinase receptor MET proto-oncogene, (c MET-gene locus: 7q31) is associated with poor survival especially in patients with glottis LSCC (15).…”

Section: Discussionmentioning

confidence: 91%

Combined EGFR/ALK Expression Analysis in Laryngeal Squamous Cell Carcinoma

Politi¹,

Tsiambas²,

Mastronikolis³

et al. 2019

In Vivo

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Background/Aim: Epidermal growth factor receptor (EGFR) acts as an oncogene in malignancies. Our aim was to examine the role of combined EGFR/ anaplastic lymphoma kinase (ALK) expression as molecular markers in laryngeal squamous cell carcinoma (LSCC) patients. Materials and Methods: Fifty (n=50) tissue sections derived from twenty-five (n=25) primary LSCCs were analyzed by immunohistochemistry (IHC). Results: EGFR overexpression was observed in 17/25 (68%) cases. Concerning ALK, 23/25 (92%) demonstrated low expression. EGFR expression was associated with grade (p=0.049), whereas ALK expression was correlated with stage (p=0.048). ALK overexpression was detected at advanced-stage EGFR-positive cases. A biphasic EGFR protein expression pattern was observed in five (n=5) LSCC cases, whereas ALK expression was stable in all cases. Conclusion: EGFR overexpression is frequently observed in LSCC combined with low ALK expression. LSCC patients with EGFR/ALK protein overexpression should be eligible for targeted therapeutic strategies. Molecular analyses in solid malignancies-including laryngeal squamous cell carcinomas (LSCC)-have shown that upregulation of specific growth factor receptors critically destabilize the cell micro-environment inducing signal transduction from the membrane to the nucleus (1). Among these molecules, epidermal growth factor receptor (EGFR) plays a crucial role in this process. The EGFR (other names include: ERBB, ERBB1, or HER1) gene is located on the short (p) arm of chromosome 7 at position 12 (cytogenetic chr band 7p12.1) (2). The protein encoded by the corresponding gene acts as a transmembrane glycoprotein. It is a member of the verb -b2 erythroblastic leukemia viral oncogene (ErbB)/human epidermal receptor (HER) family of receptor tyrosine kinases, that includes also other three cell membrane receptor tyrosine kinases: HER2/c-neu (ERBB2), HER3 (ERBB3) and HER4 (ERBB4). Three main EGFR depended pathways have been already identified including the PI3K-AKT-PTEN-mTOR, the RAS-(B) RAF-MEK-ERK/MAPK and also the IL6-JAK1/2-STAT3 (3). Concerning LSCC, a subset of patients exhibits EGFR activating mutations (approximately 10-30%) and also gene amplification (approximately 10-35%) leading to protein overexpression (4, 5). Similarly, deregulation of anaplastic lymphoma kinase (ALK) seems to be a novel marker in handling LSCC patients with EGFR aberrant expression. ALK gene is located at chromosome 2 (2p23 band) encoding a protein which acts as a transmembrane receptor tyrosine kinase 815 This article is freely accessible online.

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Epidermal growth factor receptor (EGFR) expression in patients with laryngeal squamous cell carcinoma

Cited by 14 publications

References 15 publications

VEGFR2 Expression in Head and Neck Squamous Cell Carcinoma Cancer Cells Mediates Proliferation and Invasion

VEGFR2 Expression in Head and Neck Squamous Cell Carcinoma Cancer Cells Mediates Proliferation and Invasion

<p>Novel genetic alterations and their impact on target therapy response in head and neck squamous cell carcinoma</p>

Combined EGFR/ALK Expression Analysis in Laryngeal Squamous Cell Carcinoma

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