<scp>EGFR</scp>overexpression in canine primary lung cancer: pathogenetic implications and impact on survival

Sabattini, Silvia; Mancini, Fr; Marconato, Laura; Bacci, Barbara; Rossi, Federica; Vignoli, Massimo; Bettini, Giuliano

doi:10.1111/vco.12002

Cited by 35 publications

(31 citation statements)

References 40 publications

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“…With regard to EGFR expression, a significant association with tumour size (P ¼ 0.001), necrosis (P ¼ 0.001), mitotic index (P ¼ 0.022), histological grade of malignancy (P ¼ 0.041) and lymph node (Shiomitsu et al, 2009), gliomas (Higgins et al, 2010), lung tumours (Sabattini et al, 2012) and osteosarcomas (Selvarajah et al, 2012) and is associated with malignancy. However, further studies are necessary, with long-term followup, in order to clarify this subject.…”

Section: Discussionmentioning

confidence: 96%

Concurrent Expression of Cyclo-oxygenase-2 and Epidermal Growth Factor Receptor in Canine Malignant Mammary Tumours

Guimarães

Carvalho

Pires

et al. 2014

Journal of Comparative Pathology

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Section: Discussionmentioning

confidence: 96%

Concurrent Expression of Cyclo-oxygenase-2 and Epidermal Growth Factor Receptor in Canine Malignant Mammary Tumours

Guimarães

Carvalho

Pires

et al. 2014

Journal of Comparative Pathology

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“…19,33,36 The EGFR pathway is also reportedly overexpressed in approximately 75% of canine lung tumors, many of which also express TTF-1. 26,29 A combination of immunohistochemical markers, including TTF-1, napsin A, and SP-A, is used to diagnose human pulmonary tumors. 12,18,[20][21][22]30,34,42 Expressed in normal lung and thyroid, TTF-1 is a nuclear transcription factor detected in more than 70% of human lung tumors.…”

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confidence: 99%

Surfactant Protein A and Napsin A in the Immunohistochemical Characterization of Canine Pulmonary Carcinomas: Comparison With Thyroid Transcription Factor-1

et al. 2017

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Thyroid transcription factor-1 (TTF-1) is a specific and sensitive marker for canine pulmonary tumors but is also expressed in thyroid carcinomas, which commonly metastasize to lung. Napsin A and surfactant protein A (SP-A) are used in the histologic diagnosis of non-small-cell lung cancer in humans but have not been thoroughly evaluated in neoplasms of dogs. The objective of this study was to compare the efficacy of immunohistochemistry for SP-A, napsin A, and TTF-1 in the diagnosis of canine pulmonary carcinomas. TTF-1, napsin A, and SP-A antibodies were applied to 67 formalin-fixed, paraffin-embedded canine pulmonary tumors. Although each marker had good sensitivity, only 3% (2/67) of lung tumors were negative for SP-A compared with 7% (5/67) and 9% (6/67) for napsin A and TTF-1, respectively. Each antigen was detected in a greater percentage of cells of tumors with acinar or papillary patterns compared with those with squamous differentiation. SP-A immunoreactivity was absent in all 113 nonpulmonary tumors tested. Of 108 normal tissues, SP-A was detected only in lung and in 1 of 6 adrenal, 1 of 3 endometrial, and 1 of 4 hepatic sections. Based on these findings, SP-A and napsin A are useful markers of canine lung epithelial neoplasia. Of these, SP-A is the most sensitive and specific (a possible pitfall is the need to distinguish entrapped normal pulmonary epithelial cells or alveolar macrophages from neoplastic cells) and can be used in combination with TTF-1 or napsin A to improve detection and differentiation of pulmonary carcinomas from metastatic tumors in the canine lung.

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“…Its ligands, EGF and transforming growth factor-α, bind to the ectodomain of EGFR to elicit biological effects through the RAS/RAF/mitogen-activated protein kinase kinase 1/extracellular signal-related kinase pathway, the phosphoinositide 3-kinase/AKT pathway, the phospholipase-Cγ/protein kinase C pathway, the SRC/signal transducer and activator of transcription pathway and the corresponding crosstalk, leading to the regulation of cellular proliferation, survival, apoptosis, invasion and metastasis (11,12). The overexpression of EGFR usually indicates rapid progress, resistance to chemoradiotherapy and a poor prognosis for patients with lung cancer (13,14). Various small-molecule tyrosine kinase inhibitors (TKIs) and anti-EGFR antibodies targeting EGFR have been developed over the previous 30 years.…”

Section: Introductionmentioning

confidence: 99%

Antitumor activity of nimotuzumab in combination with cisplatin in lung cancer cell line A549 inï¿½vitro

Yang

Zhou

et al. 2018

Oncol Lett

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Abstract. Nimotuzumab, a humanized IgG1 monoclonal antibody against epidermal growth factor receptor (EGFR), increases radiosensitivity in lung cancer. Cisplatin is an effective antitumor agent in lung cancer. In the present study, the antitumor activity of nimotuzumab combined with cisplatin was investigated in A549 lung cancer cells. Viability, cell cycle distribution and cyclin D1 expression were assessed following treatment with nimotuzumab alone, cisplatin alone, nimotuzumab in combination with cisplatin, and nimotuzumab followed sequentially by cisplatin. The inhibitory effect on cell viability of nimotuzumab sequentially followed by cisplatin was higher compared with cisplatin alone (82.17±1.62 vs. 56.97±1.42%). Compared with treatment by cisplatin alone, cell cycle analysis by flow cytometry demonstrated that the percentage of cells in the G 0 /G 1 phase was increased when A549 cells were treated with nimotuzumab followed sequentially by cisplatin (P<0.01). However, the proportion of cells in G 0 /G 1 phase was decreased when A549 cells were treated with nimotuzumab and cisplatin simultaneously compared with cisplatin alone (P<0.05). Cyclin D1 expression was decreased in all chemotherapy treatment groups; the most significant decrease was in A549 cells treated with nimotuzumab followed sequentially by cisplatin. Nimotuzumab may enhance the antitumor activity of cisplatin on A549 cells. The cell cycle arrest at G 0 /G 1 observed may have been due to decreased cyclin D1 levels. Potential antagonism was identified when A549 cells were treated with nimotuzumab and cisplatin simultaneously, indicating that targeted therapy may be more effective when administered prior to conventional chemotherapy. IntroductionLung cancer has been the most common cancer worldwide, and the leading cause of cancer-associated mortality, since 1985 (1). The 5-year survival rate for lung carcinoma overall is poor, at 16-17% (2). Surgery is not suitable for the majority of patients with lung cancer, as diagnoses are often obtained at advanced disease stages. The standard of care for advanced non-small cell lung cancer (NSCLC) is cisplatin in combination with 1 to 3 of the following drugs: Paclitaxel, gemcitabine and docetaxel (3). The efficacy of chemotherapy is limited due to its side effects and the lack of response in certain sub-populations of patients. Research efforts have focused on identifying molecular targets and developing molecular-targeted therapies based on the understanding of the molecular abnormalities associated with lung cancer (4-6).Insight into the pathobiology of NSCLC has facilitated the development of targeted molecular therapies that target specific mutations that serve critical roles in the progression to aggressive disease. Mutations in the epidermal growth factor receptor (EGFR), KRAS and anaplastic lymphoma kinase (ALK) genes are mutually exclusive in patients with NSCLC, and targeted therapy may be affected due to the existence of one mutation in lieu of another. Therefore, the detection of these mutati...

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EGFRoverexpression in canine primary lung cancer: pathogenetic implications and impact on survival

Cited by 35 publications

References 40 publications

Concurrent Expression of Cyclo-oxygenase-2 and Epidermal Growth Factor Receptor in Canine Malignant Mammary Tumours

Concurrent Expression of Cyclo-oxygenase-2 and Epidermal Growth Factor Receptor in Canine Malignant Mammary Tumours

Surfactant Protein A and Napsin A in the Immunohistochemical Characterization of Canine Pulmonary Carcinomas: Comparison With Thyroid Transcription Factor-1

Antitumor activity of nimotuzumab in combination with cisplatin in lung cancer cell line A549 inï¿½vitro

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