Amplifications of EGFR gene and protein expression of EGFR, Her-2/neu, c-kit, and androgen receptor in phyllodes tumor of the prostate

Wang, Xiaoyan; Jones, Timothy D.; Zhang, Shaobo; Eble, John N.; Bostwick, David G.; Qian, Junqi; López-Beltrán, Antonio; Montironi, Rodolfo; Harris, Jennifer; Liu, Cheng

doi:10.1038/modpathol.3800724

Cited by 33 publications

(21 citation statements)

References 30 publications

(34 reference statements)

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“…[12][13][14][15][16] EGFR alterations have been implicated in the pathogenesis and progression of many malignancies. 13,[17][18][19][20][21] The incidence of EGFR mutations in unselected tumors with non-small cell histology ranges from 10 to 50%, depending upon the ethnic makeup of the patient population and the detection methods used for mutation analysis; 95% of such mutations have been found in adenocarcinomas. 12,13,16,[22][23][24][25][26][27][28][29][30][31][32][33][34] Although the exact molecular mechanisms resulting from these somatic mutations are not completely understood, it seems clear that mutant EGFR has enhanced tyrosine kinase activity.…”

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confidence: 99%

Molecular pathology of lung cancer: key to personalized medicine

et al. 2012

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The majority of lung adenocarcinoma patients with epidermal growth factor receptor-(EGFR) mutated or EML4-ALK rearrangement-positive tumors are sensitive to tyrosine kinase inhibitors. Both primary and acquired resistance in a significant number of those patients to these therapies remains a major clinical problem. The specific molecular mechanisms associated with tyrosine kinase inhibitor resistance are not fully understood. Clinicopathological observations suggest that molecular alterations involving so-called 'driver mutations' could be used as markers that aid in the selection of patients most likely to benefit from targeted therapies. In this review, we summarize recent developments involving the specific molecular mechanisms and markers that have been associated with primary and acquired resistance to EGFR-targeted therapy in lung adenocarcinomas. Understanding these mechanisms may provide new treatment avenues and improve current treatment algorithms.

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confidence: 99%

Molecular pathology of lung cancer: key to personalized medicine

et al. 2012

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“…In accordance with the criteria of Alvarez et al, 12 EGFR amplification was considered to be present if 410% of the nuclei contained multiple EGFR signals and the EGFR/ CEP7 ratio was 42. 10,11 Polysomy for an individual tumor was defined as follows: 410% of the nuclei contained 42 signals of CEP7 or EGFR and the EGFR/CEP7 ratio was o2. Individual tumors were considered to show disomy if the percentage of disomic cells (with two copies of EGFR and CEP7) fell into the range of summarized average±three standard deviations of the normal control cells and did not meet the criteria for amplification or polysomy.…”

Section: Fish Analysismentioning

confidence: 99%

“…Preparations were considered valid if 490% of the cells showed bright signals. 10,11 Statistical Analysis Data were analyzed using SAS version 9.1 (SAS Institute, Cary, NC, USA). Correlations between EGFR protein expression and gene amplification were evaluated by using Cochran-Mantel-Hanszel.…”

Section: Fish Analysismentioning

confidence: 99%

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Epidermal growth factor receptor protein expression and gene amplification in the chemorefractory metastatic embryonal carcinoma

et al. 2009

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Testicular cancer is the most common cancer in young male patients. The combination of cisplatin-based chemotherapy and surgery has resulted in high cure rates. However, a small percentage of patients have cancers that are refractory to chemotherapy; treatment options for these patients are limited, and their prognosis is generally poor. Further studies are needed to explore the molecular pathogenesis pathways and potential targets of therapy for this group of highly aggressive tumors. We analyzed 21 patients who presented with metastatic embryonal carcinoma, were treated with chemotherapy, and subsequently underwent retroperitoneal lymph node dissection. Immunostaining for epidermal growth factor receptor (EGFR) was performed on paraffin-embedded tissue sections containing tumor from these specimens, using the avidinbiotin-peroxidase method. EGFR gene amplification was performed by interphase fluorescence in situ hybridization (FISH). Immunohistochemically, 9 of 21 cases (43%) demonstrated positive EGFR staining; 12 of 21 cases (57%) had absent or very limited EGFR expression. FISH revealed EGFR amplification in 1 case (5%), polysomy in 15 of 21 cases (71%), and normal disomy pattern in 5 of 21 cases (24%). A significant correlation between EGFR protein expression level and its chromosome polysomy/amplification was established (P ¼ 0.02). Our study showed that EGFR protein is frequently expressed in a subset of patients with chemorefractory metastatic embryonal carcinoma. EGFR chromosomal polysomy/amplification may be one of the mechanisms that cause increased EGFR protein expression, and could potentially be used as indication for anti-EGFR therapy.

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“…1,10 Targeted therapies, including anti-eGFR and anti-androgen agents, may be used in patients with phyllodes tumour of the prostate. 1 …”

Section: Discussionmentioning

confidence: 99%

Benign phyllodes tumour of the prostate: An extremely rare entity

Aydoğdu

Atesci

Karakose

et al. 2014

CUAJ

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Benign phyllodes tumour (BPT) of the prostate is a very rare neoplasm. It is composed of hyperplastic and neoplastic glandular stromal proliferation. Patients with BPT of the prostate generally present with lower urinary tract symptoms and hematuria. BPT of the prostate can potentially cause recurrent obstructive symptoms. Complete transurethral resection (TUR) and close postoperative follow-up is recommended. A 59-year-old man presented with dysuria and obstructive urinary symptoms. Flexible cystoscopy revealed prostatic hyperplasia and a polypoidal lesion originating from the right lateral lobe of the prostate. Magnetic resonance imaging revealed a 3 × 2.5-cm mass lesion in the right lateral lobe of the prostate. TUR of the prostate was performed and the pathological examination revealed benign prostatic hyperplasia and benign phyllodes tumour of the prostate.

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Amplifications of EGFR gene and protein expression of EGFR, Her-2/neu, c-kit, and androgen receptor in phyllodes tumor of the prostate

Cited by 33 publications

References 30 publications

Molecular pathology of lung cancer: key to personalized medicine

Molecular pathology of lung cancer: key to personalized medicine

Epidermal growth factor receptor protein expression and gene amplification in the chemorefractory metastatic embryonal carcinoma

Benign phyllodes tumour of the prostate: An extremely rare entity

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