ArticleBreast cancer research : BCR2009
Increased levels of active c-Src distinguish invasive from in situ lobular lesions.
Article in Breast cancer research : BCR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 30 citations in OpenAlex.
- Riluzole Suppresses Growth and Enhances Response to Endocrine Therapy in ER+ Breast Cancer.Journal of the Endocrine Society · 2023Article
- Article
- The Differential Impact of SRC Expression on the Prognosis of Patients with Head and Neck Squamous Cell Carcinoma.Cancers · 2019Article
- Constitutive activation of STAT3 in breast cancer cells: A review.International journal of cancer · 2016Review
- Molecular drivers of lobular carcinoma in situ.Breast cancer research : BCR · 2015Review
- Src, a potential target for overcoming trastuzumab resistance in HER2-positive breast carcinoma.British journal of cancer · 2014Article
- First report of the safety, tolerability, and pharmacokinetics of the Src kinase inhibitor saracatinib (AZD0530) in Japanese patients with advanced solid tumours.Investigational new drugs · 2013Article
- Phase I study of saracatinib (AZD0530) in combination with paclitaxel and/or carboplatin in patients with solid tumours.British journal of cancer · 2012Article
- Subcellular localization of total and activated Src kinase in African American and Caucasian breast cancer.PloS one · 2012Article
- Abl kinases are required for invadopodia formation and chemokine-induced invasion.The Journal of biological chemistry · 2010Article
- Oleic acid promotes MMP-9 secretion and invasion in breast cancer cells.Clinical & experimental metastasis · 2010Article
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7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionMounting molecular evidence suggests that invasive lobular carcinoma (ILC) is developing from in situ lesions, atypical lobular hyperplasia (ALH), and lobular carcinoma in situ (LCIS). However, little is known about the mechanisms promoting the progression of lobular breast cancer (LBC) to invasive disease. Here, we investigated whether c-Src kinase, an established inducer of invasive states, contributes to the progression from ALH/LCIS to ILC.
methodsImmunochemistry for c-Src and other cancer-related molecules was performed on archived tissue specimens from 57 LBC patients. Relative c-Src activity was estimated by comparing fluorescence intensity of ILC with that of adjacent ALH/LCIS and nonneoplastic epithelia after staining with an antibody against active c-Src. Expression of active c-Src was correlated with markers of invasion and malignancy and with relapse among LBC patients.
resultsLevels of activated c-Src were increased in ILC relative to ALH/LCIS (1.63-fold +/- 0.24 SD) and nonneoplastic epithelia (1.47 +/- 0.18 SD). Increased c-Src levels correlated with the activation of c-Src downstream targets (Fak, Stat-3) and the expression of mesenchymal markers. ILC cells with activated c-Src co-expressed metastatic markers (Opn, Cxcr4) and included cells positive for the cancer stem cell marker Aldh1. A tendency for high c-Src levels (P = 0.072) was observed among the seven LBC patients with relapsed disease.
conclusionsOur data indicate elevated c-Src activity in ILC relative to noninvasive neoplastic tissue. The associated molecular changes suggest that c-Src promotes LBC invasiveness by inducing an epithelial-mesenchymal transition. Therefore, c-Src antagonists might counteract the acquisition of invasiveness during LBC progression. Inhibition of c-Src may also affect ILC cells thought to have a high metastatic potential and to be capable of initiating/maintaining tumor growth. Together with the possible association between high c-Src levels and disease recurrence, our findings encourage the evaluation of c-Src antagonists for the treatment of LBC.
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