• Contact Us
  • Indexing
  • Submit Manuscript
  • Open Access
  • Journals
  • Home
  • ISSN: 2373-9436
    Breast Cancer Therapeutics
    Special Issue on Breast Cancer Therapeutics
    Gloria Joan Morris
    Assistant Professor
    Hematology and Medical Oncology
    The Mount Sinai Hospital
    USA
    Special Issue on Breast Cancer Therapeutics
    Editorial
    Masataka Sawaki*
    Recently, two pivotal papers with Intraoperative radiotherapy (IORT) are published [1,2]. The standard treatment for early breast cancer is breast-conserving therapy (BCT) with whole breast external irradiation therapy (WBI) [3]. Even in highly selected patients, omission of radiotherapy increases the risk of local recurrence [4].
    Manuel Ruiz-Borrego*
    The publication of the BOLERO 2 trial [1], made progress in identifying a way to approach different from the patients who make resistance to hormone therapy, everolimus is a drug that acts on the m- Tor [2] complex, which is in the center of the PI3K signaling pathway. Today is underway BOLERO 6 trial [3] , ("A phase II , randomized, open-label, three-arm , of everolimus in combination with exemestane versus everolimus monotherapy versus capecitabine , for the treatment of postmenopausal women with breast cancer with estrogen receptor positive , locally advanced , recurrent or metastatic after recurrence or progression to letrozole or anastrozole prior") that attempt to clarify its advantage over chemotherapy (capecitabine) in first line in patients with breast cancer metastatic hormone receptor-positive who have resorted to treatment with an aromatase inhibitor .
    Case Report
    Hussein A Assi, Katia E Khoury,Tarek H Mouhieddine, Lana E Khalil and Nagi S El Saghir*
    Abstract: Metastasis to the breast represents 0.4-1.3% of all breast malignancies. In those rare instances, the primary site is usually leukemia, lymphoma, or melanoma. Lung cancer, mostly adenocarcinoma, has been reported to be associated with metastasis to the breast. We report the first case of a female patient with a rapidly growing breast metastasis from a small cell lung cancer, as a first site of recurrence, misread as a triple negative breast cancer. We include clinical, radiological, pathological and immunohistochemical features of differential diagnosis.
    Perspective
    Sameer Berry1,2*
    Breast cancer represents the most common non-cutaneous cancer amongst women in the United States with over 300,000 cases diagnosed each year [1]. Breast Conserving Therapy (BCT) represents a breakthrough in the management of breast cancer allowing women to preserve their breast without compromising their cancer outcomes based on long term follow up from several randomized Phase III trials [2,3].
    Short Communication
    Yong Zhao1*, Chengfeng Yang2, Sandra Z Haslam2 and Richard C Schwartz3
    The heterogeneous disease Breast Cancer (BC) is an ancient disease which was noted 3500 years ago by ancient Egyptians [1] .The heterogeneity, including intratumor heterogeneity and intertumor heterogeneity, is influenced by genetic and non-genetic factors. Furthermore, BC is the most common malignant tumor and the second leading cause of cancer death in women.
    Mini Review
    Melissa R Gillette1 and Tracy Vargo-Gogola1,2*
    Abstract: Deregulation of Rho GTPase expression and activity levels is found in a number of cancers, including breast cancers. Aberrant Rho GTPase signaling promotes tumorigenic behaviors in a cell-autonomous manner. The development of conditional knockout and over expression mouse models of Rho GTPases and their regulators has allowed for investigation of the impact of aberrant Rho signaling in the context of the complex in vivo environment. These studies, including studies from our laboratory investigating the effects of Cdc42 and p190B RhoGAP over expression in the developing mammary gland, indicate that altered Rho signaling in the epithelium impacts the microenvironment. We propose that hyperactivated Rho signaling in neoplastic cells may contribute to tumor formation by promoting the development of a pro-tumorigenic and pro-invasive microenvironment. The availability of conditional Rho GTPase mouse models will facilitate these studies in the future.
    Review Article
    Nada Alwan*
    Abstract:
    Breast cancer is the commonest malignancy among women in countries within the Eastern Mediterranean Regions (EMR). In Iraq, it comprises approximately one third of the registered female cancers. Other features that justify increasing efforts for breast cancer control in the EMR include the obvious rise in the incidence rates, the higher frequencies of younger ages and advanced stages at the time of presentation and the likely prevalence of more aggressive tumors resulting in high mortality/incidence ratios.
    At the level of national registration, most of the cancer registries of those countries lack data regarding tumour staging and mortality rates. In fact, within the hospital records, there is no proper documentation on critically important risk factors and clinical characteristics of the disease including stage distribution at the time of initial diagnosis, hormonal receptor status, proportion of women presenting with distant metastases, treatment modalities and survival rates.
    In an attempt to address the aforementioned information needs on the clinical profile of breast cancer patients, and emphasizing the role of research as one of the basic pillars in the adoption of the cancer control strategy, a "National Breast Cancer Research Program-NBCRP" was established in Iraq in 2009. In collaboration with the International Agency for Research on Cancer (IARC) and WHO, the Iraqi researchers developed a comprehensive information system for Iraqi patients diagnosed with breast cancer. Thereafter, that data base model was utilized to compare the demographic characteristics, clinicopathological presentations and management outcomes of breast cancer patients inhabiting selected countries in the EMR (so far Iraq, Jordan, Lebanon and Egypt are included).
    Zachary C. VanGundy1#, Joseph Markowitz2#, Julie D. Baker1, Heather R. Strange1 and Tracey L. Papenfuss1*
    Abstract:
    In cancer, immune dysfunction and immunosuppression contributes to the failure of cancer therapies and cancer-related mortality. Myeloid derived suppressor cells (MDSCs) are a potently immunosuppressive population of cells which contribute to dysfunction and immunosuppression. In breast cancer, MDSC levels are clinically relevant and correlate with disease outcome and response to treatment. In this study, the E0771 breast cancer adenocarcinoma cell line was used to induce MDSCs in vitro to recapitulate the in vivo induction of MDSC in immunocompetent C57BL/6 mice. In vivo, approximately 25% of splenocytes derived from the E0771 breast cancer model are phenotypically (CD11b+ GR-1+) and functionally MDSCs with the level of induction dependent on tumor location and burden. Approximately 70% of the cells differentiated in vitro from bone marrow precursors were phenotypically MDSCs and found to suppress the proliferation of responder immune cells. In this study, we describe a parallel in vivo and in vitro model system of MDSC induction utilizing the E0771 breast cancer cell line. The development of this model system in immunocompetent mice is a useful new method to investigate mechanistic questions of MDSC development and MDSC-immune interactions in breast cancer.
    Kara Britt1*, Wendy Ingman2, Cecilia Huo3, Grace Chew3 and Erik Thompson3,4
    Abstract:
    High mammographic density confers a significantly increased risk of breast cancer. As it is relatively common in the normal population the risk of cancer attributable to increased mammographic density could potentially account for an important percentage of total BCa cases. The underlying cause for high mammographic density and its association with increased BCa risk and progression is unknown. In this review we describe the work that has been done to define the histopathological characteristics of mammographic density. Mammograms define breast tissues with areas of high density due to an increased amount of radio-opaque tissue (stromal and epithelial cells) and also less areas of radiolucent fat. Histological work however can define the roles played by each cell type. We review the work that has been performed assessing changes in epithelial cells, stromal cells, the extracellular matrix, and immune infiltrate. To determine how these changes may be increasing breast cancer risk we also discuss the roles of each of the cell types in breast cancer initiation and progression.
    Amy L Strong1, Matthew E Burow2, Jeffrey M Gimble1,3 and Bruce A Bunnell1,4*
    Abstract: Obesity increases the incidence of many types of cancers, and as the incidence of obesity continues to rise, the frequency of obesity-associated cancers will likely increase. While obesity increases postmenopausal breast, endometrial, pancreatic, colorectal, and renal carcinomas, understanding the effects of obesity on postmenopausal breast cancer remains a priority, as it is the most common diagnosed cancer in women. Obesity is defined by the rapid expansion of adipose tissue, resulting in inflammation of the adipose tissue. This inflammatory environment may, in t urn, alter the Adipose-derived Stromal Cells (ASCs) within adipose tissue, influencing their effects on breast cancer cells. Recent studies demonstrate that ASCs in obese patients traffic through the circulation and into the tumor more frequently compared to lean patients. Furthermore, once at the tumor site, ASCs have been shown to alter the gene expression profile of cancer cells, leading to the expansion and enhanced invasiveness of these cancer cells. Together, these results suggest that obesity alters the ASCs within the tumor stroma, which in turn alters the cancer cells and leads to the development of aggressive breast cancer. Future studies investigating the precise mechanisms by which ASCs isolated from obese patients enhances breast cancer cell growth and developing new therapies to target these ASCs will decrease the morbidity and mortality from obesity-associated breast cancers.
  • Current Issue Highlights
  • BRAT1 was originally identified as a BRCA1 interacting protein [1], however, subsequent studies showed that it also binds to ATM, DNA-PK, and SMC1,
    Readmore...

    Mechanisms of detecting and repairing damaged DNA are conserved and controlled through the DNA damage response (DDR).
    Readmore...

    JSciMed Central Peer-reviewed Open Access Journals
    10120 S Eastern Ave, Henderson,
    Nevada 89052, USA
    Tel: (702)-751-7806
    Toll free number: 1-800-762-9856
    Fax: (844)-572-4633 (844-JSCIMED)
    E-mail: cancerbiology@jscimedcentral.com
    1455 Frazee Road, Suite 570
    San Diego, California 92108, USA
    Tel: (619)-373-8720
    Toll free number: 1-800-762-9856
    Fax: (844)-572-4633 (844-JSCIMED)
    E-mail: cancerbiology@jscimedcentral.com
    About      |      Journals      |      Open Access      |      Special Issue Proposals      |      Guidelines      |      Submit Manuscript      |      Contacts
    Copyright © 2016 JSciMed Central All Rights Reserved
    Creative Commons Licence Open Access Publication by JSciMed Central is licensed under a Creative Commons Attribution 4.0 International License.
    Based on a work at https://jscimedcentral.com/. Permissions beyond the scope of this license may be available at https://creativecommons.org/.