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

Cancer is the leading cause of human deaths in the world and produces serious economic burdens. On September 12, 2018, the academic journal A Cancer Journal for Clinicians published an article about the latest statistics of cancers worldwide, which provided a status report on the global burden of 36 cancers in 185 countries worldwide. Cancer has also become a serious public health problem in China and caused more and more attention of the government and people in recent years. This review analyzes the incidence, mortality and prevalent trend of cancers in China, discusses the reasons behind this status, and reviews the potential countermeasures for cancer prevention and control in China.

Analysis of status and countermeasures of cancer incidence and mortality in China.

Is early-onset cancer an emerging global epidemic? Current evidence and future implications

// 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

Immunotherapy has recently entered a renaissance phase with the approval of multiple agents for the treatment of cancer. Immunotherapy stands ready to join traditional modalities, including surgery, chemotherapy, radiation, and hormone therapy, as a pillar of cancer treatment. Although immunotherapy has begun to have success in advanced cancer treatment, its scheduling and efficacy with surgery to treat earlier stages of cancer and prevent distant metastases has not been systematically examined. Here, we have used two models of spontaneously metastatic breast cancers in mice, to illustrate the significantly greater therapeutic power of neoadjuvant, compared with adjuvant immunotherapies in the context of primary tumor resection. Elevated and sustained peripheral tumor-specific immune responses underpinned the outcome, and blood sampling of tumor-specific CD8+ T cells immediately prior and post surgery may provide a predictor of outcome. These data now provide strong rationale to extensively test and compare neoadjuvant immunotherapy in humans. Citation Format: Jing Liu, Stephen Blake, Michelle Yong, Heidi Harjunpaa, Shin Foong Ngiow, Kazuyoshi Takeda, Arabella Young, Stacey Allen, Mark J. Smyth, Michele WL Teng. Improved efficacy of neoadjuvant compared to adjuvant immunotherapy to eradicate metastatic disease [abstract]. In: Proceedings of the Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; 2016 Sept 25-28; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2016;4(11 Suppl):Abstract nr B115.

Abstract B115: Improved efficacy of neoadjuvant compared to adjuvant immunotherapy to eradicate metastatic disease

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

// Shicong Tang 1 , Hong Pan 2 , Wei Wei 1 , Huawei Yang 1 , Jianlun Liu 1 and Rirong Yang 3 1 Department of Breast Surgery, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi, People’s Republic of China 2 Department of Thoracic Surgery, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi, People’s Republic of China 3 Department of Immunology, School of Preclinical Medicine, Guangxi Medical University, Guangxi, People’s Republic of China Correspondence to: Rirong Yang, email: 520yrr@163.com Jianlun Liu, email: liu_jianlun@126.com Keywords: GOLPH3; breast cancer; chemotherapy; survival Received: May 19, 2017     Accepted: August 04, 2017     Published: October 19, 2017 ABSTRACT The association between Golgi phosphoprotein 3 (GOLPH3) and clinical pathological characteristics, as well as the clinical outcomes of both neoadjuvant and adjuvant chemotherapies in breast cancer, remain largely unknown. In this study, we investigated the biological role and clinical significance of GOLPH3 in breast cancer. We found that GOLPH3 expression in tumor tissue was higher than that in adjacent noncancerous tissue (ANT) and fibroadenoma. GOLPH3 silencing reduced the migration, invasion, and proliferation of breast cancer cells and promoted apoptosis of the cells. Importantly, patients with high GOLPH3 expression had worse disease-free survival (DFS) and overall survival (OS), and GOLPH3 expression was correlated with clinical pathological characteristics such as molecular subtype, tumor-node-metastasis classification, and age but was not associated with surgery type. Patients with high GOLPH3 expression had poor DFS and OS in every molecular subtype, and an increase in tumor invasion and lymph node metastasis. The risk of recurrence increased with age in patients with high GOLPH3 expression, and surgery type had no influence on patient survival. This is the first study to investigate the correlation between GOLPH3 and response to chemotherapy in breast cancer. Patients with high GOLPH3 expression showed resistance to neoadjuvant and adjuvant chemotherapies, and GOLPH3 overexpression indicated a high risk of recurrence in patients who received adjuvant chemotherapy. These data suggest that GOLPH3 may be a novel biomarker that correlates with poor survival and resistance to chemotherapy in breast cancer.

/pdf/golph3-a-novel-biomarker-that-correlates-with-poor-survival-2ac4e4o57u.pdf

GOLPH3: a novel biomarker that correlates with poor survival and resistance to chemotherapy in 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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