Prognostic factors are clinical and pathological features that give information in estimating the likely clinical outcome of an individual suffering from cancer. The author gives a short review of the most important prognostic factors in breast cancer. 376 breast cancer cases of a ten year interval in a county hospital are summarized. Traditional clinico-pathological parameters i.e. TNM and steroid receptor status are discussed. The more common karyotipic, oncogene and tumor suppressor gene alterations are outlined in the study. Methods for their detection are presented and their value in prognostication is reviewed. Emphasis was laid on steroid receptors, c-erpB-2, p53 and bcl-2 alterations. Genes responsible for heritable forms of increased breast cancer risk are briefly reviewed.

Prognostic factors in breast cancer

// Nicole M. Davis 1 , Melissa Sokolosky 1 , Kristin Stadelman 1 , Stephen L. Abrams 1 , Massimo Libra 2 , Saverio Candido 2 , Ferdinando Nicoletti 2 , Jerry Polesel 3 , Roberta Maestro 4 , Antonino D’Assoro 5 , Lyudmyla Drobot 6 , Dariusz Rakus 7 , Agnieszka Gizak 7 , Piotr Laidler 8 , Joanna Dulinska-Litewka 8 , Joerg Basecke 9 , Sanja Mijatovic 10 , Danijela Maksimovic-Ivanic 10 , Giuseppe Montalto 11,12 , Melchiorre Cervello 12 , Timothy L. Fitzgerald 13 , Zoya N. Demidenko 14 , Alberto M. Martelli 15 , Lucio Cocco 15 , Linda S. Steelman 1 and James A. McCubrey 1 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University Greenville, NC 27858 USA 2 Department of Bio-Medical Sciences, University of Catania, Catania, Italy 3 Unit of Epidemiology and Biostatistics, Centro di Riferimento Oncologico, IRCCS, Aviano, Italy 4 Experimental Oncology 1, CRO IRCCS, National Cancer Institute, Aviano, Pordenone, Italy 5 Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA 6 Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv, Ukraine 7 Department of Animal Molecular Physiology, Institute of Experimental Biology, Wroclaw University, Wroclaw, Poland 8 Chair of Medical Biochemistry, Jagiellonian University Medical College, Krakow, Poland 9 Department of Medicine University of Gottingen, Gottingen, Germany 10 Department of Immunology, Institute for Biological Research “Sinisa Stankovic” University of Belgrade, Belgrade, Serbia 11 Biomedical Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy 12 Consiglio Nazionale delle Ricerche,Istituto di Biomedicina e Immunologia Molecolare “Alberto Monroy”, Palermo, Italy 13 Department of Surgery, Brody School of Medicine at East Carolina University, Greenville, NC 14 Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA 15 Dipartimento di Scienze Biomediche e Neuromotorie, Universita di Bologna, Bologna, Italy Correspondence: James A. McCubrey, email: // Keywords : Targeted Therapy, Therapy Resistance, Mutations, PI3K, mTOR, rapamycin Received : June 04, 2014 Accepted : July 11, 2014 Published : July 12, 2014 Abstract The EGFR/PI3K/PTEN/Akt/mTORC1/GSK-3 pathway plays prominent roles in malignant transformation, prevention of apoptosis, drug resistance and metastasis. The expression of this pathway is frequently altered in breast cancer due to mutations at or aberrant expression of: HER2 , ER alpha, BRCA1, BRCA2, EGFR1 , PIK3CA , PTEN , TP53 , RB as well as other oncogenes and tumor suppressor genes. In some breast cancer cases, mutations at certain components of this pathway ( e.g. , PIK3CA ) are associated with a better prognosis than breast cancers lacking these mutations. The expression of this pathway and upstream HER2 has been associated with breast cancer initiating cells (CICs) and in some cases resistance to treatment. The anti-diabetes drug metformin can suppress the growth of breast CICs and herceptin-resistant HER2+ cells. This review will discuss the importance of the EGFR/PI3K/PTEN/Akt/mTORC1/GSK-3 pathway primarily in breast cancer but will also include relevant examples from other cancer types. The targeting of this pathway will be discussed as well as clinical trials with novel small molecule inhibitors. The targeting of the hormone receptor, HER2 and EGFR1 in breast cancer will be reviewed in association with suppression of the EGFR/PI3K/PTEN/Akt/mTORC1/GSK-3 pathway.

/pdf/deregulation-of-the-egfr-pi3k-pten-akt-mtorc1-pathway-in-3t16n69jco.pdf

Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention

Breast cancer has seriously been threatening physical and mental health of women in the world, and its morbidity and mortality also show clearly upward trend in China over time. Through inquiry, we find that survival rate of patients with early-stage breast cancer is significantly higher than those with middle- and late-stage breast cancer, hence, it is essential to conduct research to quickly diagnose breast cancer. Until now, many methods for diagnosing breast cancer have been developed, mainly based on imaging and molecular biotechnology examination. These methods have great contributions in screening and confirmation of breast cancer. In this review article, we introduce and elaborate the advances of these methods, and then conclude some gold standard diagnostic methods for certain breast cancer patients. We lastly discuss how to choose the most suitable diagnostic methods for breast cancer patients. In general, this article not only summarizes application and development of these diagnostic methods, but also provides the guidance for researchers who work on diagnosis of breast cancer.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/cpr.12822

A review on methods for diagnosis of breast cancer cells and tissues.

Defining the role of the RSK isoforms in cancer

Neoadjuvant treatment of breast cancer refers to the use of different treatment modalities prior to surgical excision of the tumor. It has been accepted as a treatment option for patients with nonmetastatic disease, because it renders inoperable tumors operable and increases the rates of breast-conserving surgery, while achieving similar long-term clinical outcomes as adjuvant treatment. The neoadjuvant setting is being increasingly perceived as a research platform, where the biologic effects of traditional anticancer agents can be delineated, prognostic and predictive biomarkers can be identified, and the development of targeted agents can be expedited. Surrogate endpoints that can predict long-term clinical outcome and are evaluable early on, such as the pathologic complete response, offer valuable opportunities for rapid assessment of anticancer agents. Additionally, efforts for molecular profiling of the post-neoadjuvant residual disease hold the potential to lead to personalized therapy for breast cancer patients with early-stage high-risk disease.

Neoadjuvant therapy for breast cancer

Arachidonate lipoxygenases (ALOX) have been implicated in playing a critical role in tumorigenesis, development, and metastasis. We previously reported that ALOX12 is involved in breast cancer chemoresistance. In this study, we demonstrate that the ALOX5 activation correlates with the HER2 expression and mediates breast cancer growth and migration. We found that the ALOX5 expression and activity were upregulated in breast cancer patients, particularly in those tissues with HER2-positive. ALOX5 upregulation was also observed in HER2-positive breast cancer cells. In contrast, HER2 inhibition led to decreased expression and activity of ALOX5 but not ALOX5AP, suggesting that HER2 specifically regulates the ALOX5 expression and activity in breast cancer cells. We further demonstrated that ALOX5 is important for breast cancer biological activities with the predominant roles in growth and migration, likely through RhoA, focal adhesion, and PI3K/Akt/mTOR signaling but not epithelial mesenchymal transition (EMT). Our work is the first to report a correlation between the ALOX5 activity and HER2 overexpression in breast cancer. Our findings also highlight the therapeutic value of inhibiting ALOX5 in breast cancer, particularly those patients with the HER2 overexpression.

/pdf/aberrant-alox5-activation-correlates-with-her2-status-and-2evphnlelp.pdf

Aberrant ALOX5 Activation Correlates with HER2 Status and Mediates Breast Cancer Biological Activities through Multiple Mechanisms.

β-Glucosidase inhibition sensitizes breast cancer to chemotherapy.

BRCA1 is a susceptibility gene that has a genetic predisposition for breast cancer. BRCA1 gene mutation is closely associated with familial hereditary breast cancer, but the BRCA1 gene mutation is rarely found in sporadic breast cancer. According to previous studies, decreased expression of BRCA1 was detected in certain types of sporadic breast cancer. Aberrant methylation of DNA promoter CpG islands is one of the mechanisms by which tumor suppressor gene expression and function is lost. The aim of the present study was to investigate BRCA1 gene expression, methylation status and clinical significance in sporadic types of breast cancer. Quantitative polymerase chain reaction (PCR) and bisulfite sequencing PCR were respectively used to detect expression differences of BRCA1 mRNA and BRCA1 methylation in the 49 cancerous and paired non-cancerous samples from patients with breast cancer. The associations of BRCA1 expression and methylation status with the clinicopathologic characteristics were analysed. BRCA1 mRNA expression levels in the 49 breast cancer tissues were lower than those in the paired non-cancerous tissues. There was a significant statistical difference (P=0.001). BRCA1 mRNA expression was not associated with the main clinicopathologic characteristics. Frequency of the BRCA1 promoter methylation in the breast cancerous tissues was significantly higher than that in the non-cancerous tissues (P=0.007); BRCA1 gene methylation status was negatively correlated with mRNA expression (P=0.029); and BRCA1 methylation exhibited no association with all clinicopathological features. DNA promoter hypermethylation may be the potential mechanism accounting for BRCA1 expression silence in part of sporadic types of breast cancer. Some patients with hypermethylated BRCA1 may display favorable clinicopathological status.

/pdf/promoter-methylation-and-expression-changes-of-brca1-in-1wta87tk4j.pdf

Promoter methylation and expression changes of BRCA1 in cancerous tissues of patients with sporadic breast cancer.

Breast cancer is one of the most common cancers and is the second leading cause of cancer-related death in women worldwide. Ribosomal s6 kinase4 (RSK4) is a potential tumor suppressor in multiple cancers, while its role in breast cancer is largely unknown. Our study here aimed to explore the relationship between RSK4 expression with the clinicopathologic characteristics and the promoter methylation status of RSK4. Real-time PCR and bisulfite sequencing PCR were, respectively, used to detect the expression difference of RSK4 mRNA and RSK4 methylation in the 49 breast cancer and paired non-cancerous samples. The associations of RSK4 expression and methylation status with the clinicopathologic characteristics were analyzed. In the 49 breast cancer patients' specimens, RSK4 mRNA expression was found to be significantly decreased in most of breast cancer tissues compared with paired non-cancerous tissues (p = 0.002), which was largely due to the promoter hypermethylation (p = 0.005). Frequency of RSK4 promoter methylation in breast cancers was significantly higher than paired non-cancerous tissues (p = 0.009); RSK4 methylation was not associated with all clinicopathological features. The silencing of RSK4 due to promoter hypermethylation is a frequent event in breast cancer. The majority of cancers have a higher level of methylation status when compared with non-cancerous tissues. RSK4 may be a valuable biomarker for the study of breast cancer carcinogenesis and progression.

Frequent epigenetic inactivation of RSK4 by promoter methylation in cancerous and non-cancerous tissues of breast cancer

Clinical utility of the additional use of blue dye for indocyanine green for sentinel node biopsy in breast cancer.

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