Biologic characteristics of premalignant breast disease

Cole, Kimberly; Tabernero, María Dolores; Anderson, Karen S.

doi:10.3233/cbm-2011-0187

Cited by 17 publications

(14 citation statements)

References 191 publications

(202 reference statements)

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“…As opposed to the physiologic transient phosphorylation of extracellular signal-regulated kinase (ERK1/2) observed with the testosterone treatment, they demonstrate that the addition of ErbB2 inhibition leads to a persistent phosphorylation of ERK1/2, which negatively regulates the downstream signaling and cell growth (41). Most cases of DCIS show high levels of TFF3 and overexpression of ErbB-2 (42). Other studies have found that Fig.…”

Section: Discussionmentioning

confidence: 94%

Inhibition of ErbB-2 induces TFF3 downregulation in breast cancer cell lines

Xiang

Shen

et al. 2013

APMIS

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ErbB-2 gene plays an important role in carcinoma formation whose overexpression was observed in many types of tumors, including breast cancer. Dysregulation of Trefoil factor 3 (TFF3), which is thought to function in the development and progression of breast cancer, was found to be upregulated in ErbB2-overexpressing breast cancers and cells. However, a putative interaction between ErbB-2 and TFF3 in breast cancer remains unknown. To determine whether TFF3 has an important role in breast tumor, its levels were measured by immunohistochemistry in 130 cases of breast infiltrating duct carcinoma and 30 cases of normal breast tissue with a specific monoclonal antibody raised against human TFF3. Patients who were positive for ErbB-2 also had high expression levels of TFF3 (p < 0.05). Also, after infecting the SK-BR-3 cells with lentivirus-mediated ErbB2-specific shRNA (Lenti-ShERBB2), we detected the expressions of ErbB-2 and TFF3 by real-time polymerase chain reaction and Western blotting, respectively. Compared with the control groups, ErbB-2 mRNA expression was decreased in the Lenti-ShERBB2 infection group, and Western blotting indicated a concordant ErbB-2 protein reduction. On the other hand, TFF3 expression at both mRNA and protein levels was significantly downregulated by ErbB-2 silencing in SK-BR-3. These findings are a proof of the foundation for a certain relationships of ErbB-2 and TFF3, which may serve as novel therapeutic markers of ErbB2-overexpressing breast cancers in the future.

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Section: Discussionmentioning

confidence: 94%

Inhibition of ErbB-2 induces TFF3 downregulation in breast cancer cell lines

Xiang

Shen

et al. 2013

APMIS

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“…5,8 Despite recent advances in imaging, the rates of false positives (FPs) and false negatives (FNs) represent a significant problem in the early diagnosis of BC. [9][10][11][12] The sensitivities and specificities of various imaging modalities and/or their various combinations widely range from 50% upwards. [13][14][15][16][17] A comprehensive study by Berg et al evaluated the supplemental cancer detection yield of US or MRI, when used in addition to mammography, in a large cohort of women (n ¼ 2809; 21 sites) at elevated risk for BC.…”

Section: Introductionmentioning

confidence: 99%

“…15 In recent years, the role of protein biomarkers in the detection of BC has undergone a major shift from investigational use to evaluation of prognostic value for a given BC subtype. 11 With the discovery of key protein biomarkers and protein signatures for BC, proteomic technologies are currently poised to serve as an ideal diagnostic adjunct to imaging. 3,18 Previous research studies have shown that breast tumors are associated with systemic changes in both serum protein biomarkers (SPBs) and tumor-associated autoantibodies (TAAbs).…”

Section: Introductionmentioning

confidence: 99%

A Noninvasive Blood-based Combinatorial Proteomic Biomarker Assay to Detect Breast Cancer in Women Under the Age of 50 Years

Lourenço

Benson²,

Henderson³

et al. 2017

Clinical Breast Cancer

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“…The stem cells for neoplasias of the breast are perhaps the best characterized; the stem cells of the breast express aldehyde dehydrogenase activity (ALDH) and the ALDH1 protein. These stem cells also are CD44-v6 + and CD24 − and LIN − [23,73]. …”

Section: Stochastic Versus Stem Cell Models In the Development Of mentioning

confidence: 99%

The biology of incipient, pre-invasive or intraepithelial neoplasia

Grizzle

Srivastava

Manne

2011

CBM

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Invasive tumors (cancers or malignant lesions) typically develop in the setting in which there is the presence of putative non-invasive lesions and the development of these non-invasive lesions frequently precedes the development of cancers. For some organs, such as the oral cavity, cervix and skin, the respective putative pre-invasive lesions can be observed over time and documented to progress to invasive lesions. However, for less readily observable lesions, such as those of the prostate, the progression of the pre-invasive lesions, e.g., prostatic intraepithelial neoplasia (PIN) and prostatic proliferative inflammatory atrophy (PIA) to prostatic cancer are more difficult to document. Thus, for most organ systems, specific pre-invasive neoplastic lesions have been proposed based upon the apparent observations of one or more of the following: 1) microinvasive disease developing from a pre-invasive neoplastic lesion, 2) the general association of the pre-invasive lesion with invasive lesions, 3) the subsequent development of invasive lesions following diagnosis of the pre-invasive lesion, 4) correlations of the molecular features of the putative pre-invasive lesion with the matching invasive lesions, and 5) reductions in the rate of cancer following removal of the pre-invasive lesion. When there are mixtures of pre-invasive lesions with actual cancers in the same case, some of the above specific associations are more difficult to make. Several terms have been used to describe pre-invasive lesions, many of which are now less useful as our knowledge of these lesions increases. It is now commonly accepted that these lesions are a features of the spectrum of neoplastic development and most are accepted as “neoplastic lesions” with associated molecular features, even though they may be reversible even if they have mutations in suppressor genes (e.g., p53) or are associated with viral etiologies (e.g., cervical intraepithelial neoplasia). The overall term, “pre-invasive neoplasia”, seems to best describe these putative pre-invasive lesions. Thus, terms such as incipient neoplasia should be abandoned. The term “intra-epithelial neoplasia” with an associated grade, which has been developed for pre-invasive neoplastic lesions of the cervix, i.e. cervical intraepithelial neoplasia (CIN), seems to be a terminology that adds consistency across epithelial organs. Thus, adoption of these terms for the additional organ sites of pancreas (PanIN) and prostate (PIN) seems accepted. Less descriptive terms such as the degrees of dysplasia of the oral cavity and bronchopulmonary system and actinic keratosis and Bowen's disease of the skin might be better designated as oral intraepithelial neoplasia (OIN), pulmonary intraepithelial neoplasia (PulIN) and dermal intraepithelial neoplasia (DIN). The etiology of pre-invasive neoplasia is the etiology of the matching cancers. Some obvious initiating factors include exposure to the whole range of ionizing and non-ionizing radiation, tobacco abuse and a broad range of other carcinogens (e....

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Biologic characteristics of premalignant breast disease

Cited by 17 publications

References 191 publications

Inhibition of ErbB-2 induces TFF3 downregulation in breast cancer cell lines

Inhibition of ErbB-2 induces TFF3 downregulation in breast cancer cell lines

A Noninvasive Blood-based Combinatorial Proteomic Biomarker Assay to Detect Breast Cancer in Women Under the Age of 50 Years

The biology of incipient, pre-invasive or intraepithelial neoplasia

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