Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 2nd World Congress on Breast Cancer Phoenix, Arizona,USA.

Day 1 :

Keynote Forum

Shahla Masood

University of Florida College of Medicine, USA

Keynote: Why the term of low-grade ductal carcinoma in situ should be abandoned: Minimizing over diagnosis and overtreatment

Time : 08:30-09:00

OMICS International Breast Cancer Congress-2016 International Conference Keynote Speaker Shahla Masood photo
Biography:

Shahla Masood, M.D. is an professor in the department of Pathology and Laboratory Medicine at the University of Florida College of Medicine–Jacksonville. She is Chair, Department of Pathology and Laboratory Medicine; Program Director, Breast Pathology Fellowship; Medical Director, Breast Health Center; Program Director, Cytopathology Fellowship; Director of Research. Clinical Special Interests: Breast pathology, cytopathology. Research Special Interests: Early breast cancer detection; use of minimally invasive procedures to provide optimal samples for analysis; prognostic/predictive index.

Abstract:

During the last several years, increased public awareness, advances in breast imaging and enhanced screening programs have led to early breast cancer detection and attention to cancer prevention. The numbers of image-detected biopsies have increased and pathologists are expected to provide more information with smaller tissue samples. These biopsies have resulted in detection of increasing numbers of high-risk proliferative breast disease and in situ cancers. The general hypothesis is that some forms of breast cancers may arise from established forms of ductal carcinoma in situ (DCIS) and atypical ductal hyperplasia (ADH) and possibly from more common forms of ductal hyperplasia. However, this is an oversimplification of a very complex process, given the fact that the majority of breast cancers appears to arise de-novo or from a yet unknown precursor lesion. Currently, ADH and DCIS are considered as morphologic risk factors and precursor lesions for breast cancer. However, morphologic distinction between these two entities has remained a real issue that continues to lead to over-diagnosis and overtreatment. Aside from morphologic similarities between ADH and low grade DCIS, biomarker studies and molecular genetic testing’s have shown that morphologic overlaps are reflected at the molecular levels and raise questions about the validity of separating these two entities. It is hoped that as we better understand the genetic basis of these entities in relation to ultimate patient outcome, the suggested use of the term of “Borderline Breast Disease” can minimize the number of patients who are subject to over treatment.

During the last several years, increased public awareness, advances in breast imaging and enhanced screening programs have led to early breast cancer detection and attention to cancer prevention. The numbers of image-detected biopsies have increased and pathologists are expected to provide more information with smaller tissue samples. These biopsies have resulted in detection of increasing numbers of high-risk proliferative breast disease and in situ cancers. The general hypothesis is that some forms of breast cancers may arise from established forms of ductal carcinoma in situ (DCIS) and atypical ductal hyperplasia (ADH) and possibly from more common forms of ductal hyperplasia. However, this is an oversimplification of a very complex process, given the fact that the majority of breast cancers appears to arise de-novo or from a yet unknown precursor lesion. Currently, ADH and DCIS are considered as morphologic risk factors and precursor lesions for breast cancer. However, morphologic distinction between these two entities has remained a real issue that continues to lead to over-diagnosis and overtreatment. Aside from morphologic similarities between ADH and low grade DCIS, biomarker studies and molecular genetic testing’s have shown that morphologic overlaps are reflected at the molecular levels and raise questions about the validity of separating these two entities. It is hoped that as we better understand the genetic basis of these entities in relation to ultimate patient outcome, the suggested use of the term of “Borderline Breast Disease” can minimize the number of patients who are subject to over treatment.

Keynote Forum

Colleen Huber

Naturopathic Oncology Research Institute, USA

Keynote: Breast cancer survivors’ choices in treatment and diet

Time : 09:00-09:30

OMICS International Breast Cancer Congress-2016 International Conference Keynote Speaker Colleen Huber photo
Biography:

Colleen Huber NMD is a Naturopathic Medical Doctor in Tempe, Arizona.  She is President of the Naturopathic Cancer Society.  She is a Naturopathic Oncologist and Fellow of the Naturopathic Oncology Research Institute.    Her writing includes her book, Choose Your Foods Like Your Life Depends On Them, and she has been featured in the Defeat Cancer book.  She authored the largest and longest study in medical history on sugar intake in cancer patients, which was reported in media around the world in 2014.  Her academic writing has appeared in The Lancet and Cancer Strategies Journal, and other medical journals.

Abstract:

In this study we followed breast cancer survivors up to 7 years following initial encounter in a naturopathic clinic.  Most survivors had surgical resection of their entire tumor burden, followed by at least 36 intravenous nutrient treatments, administered under the medical direction of the author.  Some of those in remission chose to return for follow-up intravenous nutrients once per month after they were observed to achieve remission from their cancers.  We compare this group with those who had the intravenous nutrients without any surgery, as well as those who had the surgery plus IV nutrients, plus chemotherapy.  We compare the different cohorts for survival, treatment choices, disease status, current dietary habits and self-reported quality of life.  Comparison is also made among those whose initial diagnosis was Stage I, II, III or IV.  We examine in particular detail the diet and lifestyle of the cancer survivors.  97 total cancer survivors responded fully and promptly to detailed questionnaires, in which they indicated whether they had 3 times or more per week items from a long list of foods and beverages, and whether they exercised.  37 of those were breast cancer patients.  We compare the diets and lifestyles of those in remission versus those who continue to suffer from breast cancer.

  • Workshop on Bio-active natural products in breast cancer therapy
Location: Hall A
Speaker

Chair

Shahla Masood

University of Florida College of Medicine, USA

Speaker

Co-Chair

Colleen Huber

Naturopathic Oncology Research Institute, USA

Session Introduction

Alexander Herzog

University of Sevilla, Spain

Title: The role of hyperthermia as complementary treatment in metastatic breast cancer

Time : 10:15-10:45

Speaker
Biography:

Medical degree at the university of Heidelberg, Germany in 1984. Afterwards research at the German Cancer Research Center in Heidelberg about vaccine treatments against cancer in animal models. Specialization in internal medicine and oncology in the university hospital of Heidelberg. Consultant and head physician in different oncological hospitals. For more than 20 years he has been working in his own hospital specialized in hyperthermia complementary treatments in oncology. He is professor at the University of Sevilla, Spain, but also gives lectures at the University of Gießen.

 

Abstract:

Background:

Hyperthermia as complementary treatment is an important tool to improve the efficacy of chemotherapy and radiation in cancer. Hyperthermia treatment includes superficial hyperthermia, deep regional hyperthermia but also whole body hyperthermia. Beside a temperature dependent increase of the efficacy of cytostatic drugs or radiation there are also direct effects of hyperthermia on cancer cells at temperatures around 42 C° (107,6 F°).

Methods:

Hyperthermia is used together with radiation in locally recurrent disease or together with chemotherapy in patients with metastatic disease.

Superficial hyperthermia with water filtered infrared-A light (1200 nm, Hydrosun device)

  1. Local regional hyperthermia is used for superficial disease, e.g. inflammatory skin involvement with short wave irradiation with 13,56 MHz (Oncotherm EHY 2000 device is used for the localized breast tumor or metastatic tissues e.g. liver metastases.
  2. Whole body hyperthermia is performed by whole body radiation with water filtered infrared-A light (1200 nm) for patients with metastatic disease.

Chemotherapies are given to local hyperthermia session or to whole body hyperthermia.  

Results:

Early studies about simultaneously hyperthermia and radiation showed about doubled response rates compared to radiation alone. Even in pretreated patients with metastatic breast cancer using a combination of whole body hyperthermia and chemotherapy showed response rates between 70- 80%. Using cytostatic drugs in more moderate doses together with hyperthermia patients had only little side effects.

Conclusion:

Studies and own experiences show that hyperthermia in metastatic breast cancer shows promising results, in particular as breast cancer is a disease sensitive to different types of chemotherapy and radiation.

Biography:

Dr. Oertle is the lead physician at Envita Medical Centers where he instructs physicians, sits on the medical treatment review board, and specializes in chronic
disease, immunotherapy and oncology. He actively participates in research and development alongside Vertisis Custom Pharmacy. In addition to his roles at Envita,
Dr. Oertle is the director of nutrition for Bene Plates; co-founder and board member of Solidarity Health Share; and member of the Arizona Naturopathic Medical
Association, International Organization of Integrative Cancer Physicians, Catholic Medical Association, National Comprehensive Cancer Network, American
College for Advancement in Medicine, Association of American Physicians and Surgeons, American Naturopathic Clinical Research Institute and Naturopathic
Oncology Research Institute.

Abstract:

Resistance to chemotherapy after successive dosing regimens is a common theme for cancer progression that all oncologists
face. Similarly, the resistance to antimicrobial agents on infections can render similar complications especially with the
broad use of antibiotics. P-glycoprotein (Pgp), also known as multidrug resistance protein 1 (MDR-1), is found on the surface
membrane of both bacteria and mammalian cells, and acts to remove toxins or other harmful agents from the cell. Thus,
inhibition of Pgp and MDR-1 as a treatment adjuvant is of great interest within the fields of oncology and infectious disease
alike.
There are several naturally occurring agents that forego an inhibitory effect on MDR-1 and Pgp with varying amount of
literature to support its claims. As attractive as these previously noted natural agents have on inhibition of MDR-1, preliminary
data suggests a pattern may emerge from clinical data obtained from a natural supplement PGP-x1 utilizing a plant alkaloid.
Its active constituents have led to promising research revealing data which suggest it enhances chemotherapy and antibiotic
treatment via a mechanism involving the inhibition of MDR-1, Pgp and MRP-1 related transport. The data is consistent in
several experimental models that show the active alkaloid has the ability to inhibit expression of Pgp in cancer cells. The active
ingredient used in PGP-x1, which was utilized in the patient case studies to be discussed, utilizes a proprietary extraction
methodology. Each patient in this cohort of case studies was identified to have overexpression of MDR-1 resistance. They were
treated with genetically targeted chemotherapy in a metronomic dosing strategy with insulin as a biological response modifier
concomitantly with PGP-x1.

Ellie Wright

Southwest College of Naturopathic Medicine, USA

Title: Punica grantum role in breast cancer prevention and suppression

Time : 10:45-11:15

Speaker
Biography:

In 2008 obtained a Bachelor Degree at Arizona State University with Summa cum Laude. In 2010 graduated with a Master degree and a graduate certificate in Geriatric and Gerontology. In 2015, received a doctoral degree from Southwest College of Naturopathic Medicine.

 

Abstract:

The new studies shows exciting results in anti tumoral properties of Punica Grantum. The components of Punica Grantum are ellagic acid, ellagitannins (including punicalagins and punicalin) punicic acid, flavonoids, anthrocyanidins, anthorcyanis, estrogenic flavonols and flavons. Punicalgin can be found in seeds, peels juice of pomegranate. Both punicalgin and punicalin can be hydrolyzed to ellagic acid, a natural phenol. Pomegranate juice is rich in polyphenols, tannins, anthocyannins, includind vit C, vit E, co Q10 and lipoic acid. The synergisitic effect of all these components is superior than each individual constituents. The ellagic acid induces cell cycle arrest and apoptosis through TGF-B pathway in human breast cancer MCF- 7 cells. Pomegranate extract reduces the production of vascular endothelial growth factor (VEGF). Pomegranates extracts ellagitannins and punicalagin directly suppress inflammatory cell signaling, inhibits cytochrome P450 enzyme lowering the risk of cancer, inhibits production of VEGF while upregulating production of migratory inhibitory factor (MIF). Punic acid is omega 5 polyunsaturated fatty acid that inhibits both estrogen dependent and estrogen independent breast cancer cell proliferation in lab. Pomegranate ellagitannin-derived compounds exhibit antiaromatase activity and affect the growth of breast cancer cells. Βeta-sitosterol (β-SITO), a phytosterol present in pomegranate is a potent anticancer compound that interferes with microtubule.

William Nelson

Naturopathic Medical Doctors of Arizona, USA

Title: Biochemical effects of pomegranate on cancer
Biography:

William Nelson has a BS in Engineering and attended National College of Naturopathic Medical School in Portland, OR. He has 20 years of experience in private
practice and specializes in the metabolic treatment of cancer. Currently, he is on staff at Naturopathic Medical Doctors of Arizona which is the largest Naturopathic
Cancer Clinic.

Abstract:

Pomegranates have been shown to contain over 100 different phytochemicals, including ellagitannins, punicic acid,
flavonoids, anthocyanidins, estrogenic flavonols, and flavones. The highest concentration of ellagitannins is in the freshly
prepared juice. Recent research shows remarkable results in reducing atherosclerosis, obesity, insulin resistance, intestinal
inflammation and cancer. Pomegranate has been shown to have breast cancer preventive effects through modulation of
endogenous sex hormone levels. Ellagitannins prevents estrogen-responsive breast cancer by inhibiting the growth of cultured
breast cancer cells. Ellagic acid also inhibits the enzyme known as aromatase that converts androgen to estrogen hormones.
The anti-cancer effect is also expressed through inhibition of vascular endothelial growth factor (VEGF) that promotes new
vasculature and tumor growth and metastasis. Pomegranate juice lowers the risk of cancer through inhibiting several of the
cytochrome P450 enzymes that can activate carcinogen metabolites. Pomegranates are rich in fatty acids (80%) specifically
conjugated linolenic acids (cLNA) which constitute anti-inflammatory and anti-cancer effects. Research shows pomegranate
is anti-proliferative, anti-invasive, and anti-metastatic by inducing apoptosis and blocking the activation of inflammatory
pathways. These mechanisms of anti-inflammatory, anti-cancer and anti-angiogenesis are expressed through inhibition of
cyclooxygenase (COX), lipooxygenase (LOX), cytochrome P450 (CYP450) and last but not least the master inflammatory
switch in the body NF-kB.

Linda Isaacs

Nutritional Research and Educational Foundation, USA

Title: Pancreatic enzymes and cancer

Time : 11:15-11:45

Speaker
Biography:

Linda L. Isaacs, M.D., received her medical degree from Vanderbilt University School of Medicine and is certified by the American Board of Internal Medicine. She has written papers published in the peer-reviewed journals Nutrition and Cancer and Alternative Therapies in Health and Medicine, and has served as a reviewer for Alternative Therapies in Health and Medicine. She is the co-author, with Dr. Nicholas Gonzalez, of the book The Trophoblast and the Origins of Cancer. Her website is www.DrLindaI.com.

Abstract:

Pancreatic proteolytic enzymes have been used in the management of cancer for more than 100 years. The theoretical rationale was described by the embryologist Dr. John Beard, who noted the similarity of cancer cells to the trophoblast and who may have been the first researcher to speculate that cancer originates from stem cells. Various other practitioners have used pancreatic enzymes against cancer since Dr. Beard’s time. In her lecture, Dr. Isaacs will review this history, and describe case reports of breast cancer patients successfully treated with enzymes.

  • Breast Cancer Therapy
    Biology of Breast Cancer
Location: Hall A
Speaker

Chair

Colleen Huber

Naturopathic Oncology Research Institute, USA

Speaker

Co-Chair

Alexander Herzog

University of Sevilla,Spain

Session Introduction

Bolin Liu

University of Colorado Anschutz Medical Campus, USA

Title: RTK signaling in therapeutic resistance of erbB2-targeted therapy

Time : 12:45-13:10

Speaker
Biography:

Dr. Bolin Liu is an Associate Professor at the Department of Pathology, School of Medicine, University of Colorado Anschutz Medical Campus. He received extensive postdoctoral training in the Department of Experimental Therapeutics at MD Anderson Cancer Center from 1998-2002. Since becoming an independent investigator in 2007, Dr. Liu has focused on studying the role of erbB3 in breast cancer development. The main research program in Dr. Liu’s laboratory is to understand the biology of receptor tyrosine kinase (RTK) signaling in drug resistance and tumor metastasis, and to identify novel approach overcoming the resistance and enhancing therapeutic efficacy in cancer treatment.

Abstract:

Gene amplification/overexpression of erbB2 (HER2/neu) is observed in approximately 25-30% of invasive breast cancers and significantly associated with a worse prognosis. ErbB2-targeted therapies, including trastuzumab (or Herceptin) and lapatinib (or Tykerb) have been successfully used in breast cancer patients with erbB2-positive tumors. However, both de novo and acquired resistance to these agents frequently occurs, representing a significant clinical problem. Our recent studies revealed a co-expression of three receptor tyrosine kinases (RTKs), erbB2, erbB3, and the insulin-like growth factor-I receptor (IGF-IR), in both trastuzumab-resistant and -sensitive breast cancer cells, and an enhanced activation of the downstream signaling in the resistant cells. The three RTKs actually interacted with each other to form a heterotrimeric complex only in the trastuzumab-resistant breast cancer cells. Specific knockdown of either erbB3 or IGF-IR expression was able to re-sensitize the resistant cells to trastuzumab-mediated inactivation of downstream signaling and growth inhibition. Interestingly, the trastuzumab-resistant sublines also exhibited refractoriness to lapatinib. While knockdown of erbB3 dramatically re-sensitized the cells to lapatinib-induced apoptosis, specific knockdown of IGF-1R did not alter the cells’ responsiveness to lapatinib. Moreover, a specific inhibitor of Akt, but not Src, significantly enhanced lapatinib-mediated anti-proliferative/anti-survival effects on the trastuzumab-resistant cells. These data indicate that erbB3 signaling is critical for both trastuzumab and lapatinib resistances mainly through activation of the PI-3K/Akt pathway, whereas IGF-1R-initiated Src activation results in trastuzumab resistance without affecting lapatinib sensitivity. Our findings may facilitate the development of precision therapeutic regimens for erbB2-positive breast cancer patients who become resistant to erbB2-targeted therapy.

Speaker
Biography:

Dr. Thangaraju has completed his PhD from the University of Madras, India and postdoctoral studies from the McGill University, Montreal, Canada, Mayo Clinic, Rochester, MN, and National Cancer Institute (NCI), Fredrick, MD. He is an Associate Professor in the department of Biochemistry and Molecular Biology at the Georgia Regents University, Augusta, GA. He has published more than 65 manuscripts in well reputed journals and a recipient of various NIH and DOD research grants and has been serving as a member in various NIH  and DoD study sections.

Abstract:

In recent years, impressive technical advancements have been made in the isolation and validation of the mammary stem cells (MaSCs) and cancer stem cells (CSCs). However, the signaling pathways that regulate stem cell self-renewal are largely unknown. Further, CSCs are believed to contribute to resistance to chemotherapy and radiation therapy. However, an effective therapeutic strategy to overcome this resistance is yet to be identified. Using MMTV-Neu-Tg mouse mammary tumor model, we found that both luminal progenitor and basal stem cells are susceptible to genetic and epigenetic modifications, which in turn reprogram normal MaSCs into cancer propagating CSCs.  Combination of 5-Azacytidine, a DNMT inhibitor, and butyrate, a HDAC inhibitor, markedly reduces CSCs and consequently increases the overall survival of the animal. RNA-seq analysis of the CSCs treated with 5-AzaC+butyrate provides evidence that combined inhibition of DNMTs and HDACs reduces CSCs pool in the mammary gland by blocking growth-promoting signaling molecules like RAD51AP1 and SPC25. RAD51AP1 and SPC25, which are known to play a key role in DNA damage repair and kinetochore assembly, are significantly overexpressed in breast tumor tissues and associated with decreased overall patients’ survival. In conclusion, our studies provide strong evidence that breast CSCs (both basal stem cells and luminal progenitor cells) are susceptible for genetic and epigenetic modifications and associated with resistance to chemo- and radiotherapy. Thus, combination of DNMT and HDAC inhibitors can serve as an effective therapeutic strategy to block mammary tumor growth and to overcome drug resistance by inhibiting CSCs.

Speaker
Biography:

Prof. Sribatsa Kumar Mahapatra, M.S. F.R.C.S. (EDIN.) D.N.B. F.I.C.S. PROF. & H.O.D. Dept. of General Surgery Veer Surendra Sai Institute Of Medical Science & Research, Burla, Sambalpur, Odisha, India, Completed his MBBS with Honors from MKCG Medical College, Berhampur University, Odisha in 1977. He completed his M.S. (General Surgery) in 1982 from Post Graduate Institute of Medical Education & Research, Chandigarh (India) & obtained Diplomate of National Board (General Surgery) form National Board of Examination in 1988 & obtained F.R.C.S. (Edin.) in 1995 from Royal College of Surgeons of Edinburg (U.K.)

He joined as a Medical Teacher in 1984 and working in different capacities became Professor of Surgery in 2008. He became Head of the Dept. of Surgery in 2013. He has presented his experience in Autologous Stemcell Therapy in refractory leg ulcers in 5th World Congress of Cell & Stemcell therapy at Chicago with appreciation of the delegates & organizers. He is actively involved in teaching, under graduate & post graduate students in General Surgery and treating the Surgical Patients in a busy 1000 beded institute hospital.

Abstract:

Modified Radical Mastectomy is the standard surgical procedure for locally advanced Breast Cancer and other early Breast Cancer in developing countries. Breast Flap Complications like Seroma, Flap Necrosis, Marginal Flap Necrosis, Wound infection, Shoulder stiffness, hypertrophic scarp, kelloid formation & local recurrence are some of the complications seen commonly following Modified Radical Mastectomy.

Bone Marrow is harvested just before MRM from the patients sternum under anesthesia  & kept aside in heparinised solution. Flaps are raised  above & below as per standard procedure and Mastectomy completed with the tumour in toto alongwith auxiliary dissection. Haemostasis is achieved in Breast bed under the flap and axilla.

Autologous bone marrow  is infiltrated under the flap and infiltrated to axiliary walls and pectoral bed. Would closed with a dynamic drain to axila and upper flap. Post Operative observation of local pain, amount of drain collection, duration of the drain stay and shoulder stiffness symptoms are compared with a group of standard MRM without bone marrow application.

It is observed that autologus bone marrow therapy is helpful in preventing local flap problems. Postoperative pain is found to be significantly less, local seroma formation is less making early drain removal, post operative would infection is less, & shoulder stiffness is less. Regarding local hypertrophic scarp, kelloid & local recurrence we need further followup in the study.

Speaker
Biography:

Dr. Li finished his breast pathology fellowship at the MD Anderson Cancer Center.  Dr. Li is an assistant professor in the Department of Pathology and the Associate Director of the Glenn Family Breast Center, Winship Cancer Institute at Emory University, Atlanta.  He has published more than 25 peer reviewed articles in breast diseases.

Abstract:

Background: Male breast carcinoma (MBC) is treated similarly to female breast carcinoma (FBC), and similar survival rates for both have been assumed. We analyzed prognostic and clinico-pathologic features of MBC to determine whether MBC subtypes differ from FBC subtypes.

Methods: We reviewed data for 172,847 FBC and 1,442 MBC patients from 2010 to 2012 from the National Cancer Institute Surveillance, Epidemiology, and End Results database.  Carcinomas were subtyped by hormone receptor (HR) and human epidermal growth factor 2 (HER2) status as HR+/HER2–, HR+/HER2+, HR–/HER2+, and HR–/HER2–.

Results: The overall incidence of MBC in all breast carcinoma cases was 0.8%. MBC was more frequently HR+/HER2 than FBC was (78.3% vs 67.4%) and less frequently HR/HER2 (2.1% vs 10.9%). More MBC was staged as III or IV (24.9% vs 17.2%). MBC had significantly worse overall survival (OS) than FBC (P<0.0001). After adjustment for age, ethnicity, and tumor grade, stage I and II MBC had significantly worse OS time than stage-matched FBC had (P=0.0011 for stage I, P=0.0229 for stage II). When stage- and subtype-matched patients were compared, MBC had significantly worse OS than FBC for stage I overall, for sub-stages IA and IIB HR+/HER2– carcinoma, and for stage III HR+/HER2+ carcinoma.  Furthermore, MBC patients with HR+/HER2– T1aN0 carcinomas had worse OS than FBC patients had.

Conclusions: Patients with MBC have worse survival than patients with FBC, especially for early-stage HR+ breast cancers. More studies are needed optimize treatment for MBC.

Hong (Amy) Zhang

The University of Texas-M. D. Anderson Cancer Center, USA

Title: FOXK2: A novel oncogene that is amplified and over-expressed in breast cancer

Time : 14:55-15:15

Speaker
Biography:

Dr. Zhang has completed her M.D. training in China and completed her Ph.D. from the University of Texas (UT)-Graduate School of Biomedical Science in 2000. She receiveid residency training at UT-Medical School at Houston. She is a practicing surgical pathologist at UT-M D Anderson Cancer Center, majoring in breast pathology. She has published more than 38 papers in reputed journals and has been serving as an editorial board member of several journals. Her research interes focuses on identifying new molecular markers and novel therapeutic targets for breast cancers using modern biotechnologies of cytogenetics, molecular biology, biochemistry and animal models.

Abstract:

The chromosome 17 is a frequent site of cancer-associated genetic anomalies and is strongly associated with poor prognosis. Previous studies of breast cancer have revealed the amplification of several genomic regions on 17q. These amplifications are typically discontinuous and complex in structure, suggesting that multiple oncogenes in this chromosomal segment may be co-selected during breast carcinogenesis.By integrative analysis of public genomic datasets of breast cancers from The Cancer Genome Atlas (TCGA) including 910 tumor cases and 981 normal controls, we have found that FOXK2 in 17q25 displayed frequent genomic amplifications and correlated gene expression changes in in all subtypes of breast cancers classified by PAM50 compared to normal controls. Its overexpression was associated with poor overall survival of breast cancer patients. FOXK2 knockdown using lentivirus mediated shRNAs inhibited breast cancer cell proliferation and anchorage-independent growth in four breast cancer cell lines with high FOXK2 expression status (MDA-MB-231, MCF-7, HCC1954 and MDA-MB-361). More importantly, overexpression of FOXK2 and oncogene RAS induced MCF10A cell colony formation, indicating that FOXK2 is an oncogene in breast cancer. The potential interacting molecules/pathways were explored using RNASeq technique on the FOXK2 knockdown breast cancer cells. Several pathways, including regulation of cell proliferation, regulation of cell division, cell adhesion and regulation of cell metabolism, were regulated by FOXK2 in breast cancer cells.Our data provide compelling evidence that FOXK2 is an oncogene in breast tumorigenesis, and it might be a novel therapeutic target and a biomarker predicting poor outcome.

Ebenezer Chitra

Institute of Medical Research, Malaysia

Title: Lactoferricin B peptide kills breast cancer cells in vitro: Potential for therapy

Time : 15:15-15:35

Speaker
Biography:

Dr. Ebenezer Chitra completed her Ph.D. from National Institute of Immunology, Jawaharlal Nehru University, New Delhi, India. She did her post-doctoral fellowship in National Health Research Institutes, Taiwan working on cell signaling in cancer. Currently, she is a faculty in the School of Medicine in International Medical University. Her research interest is in cancer biology. 

Abstract:

Breast cancer is one of the most common cancers in women and is currently treated by surgery and a combination of chemotherapy and radiotherapy. Lactoferricin B (Lfcin B) is a 25-mer natural peptide obtained from milk protein lactoferrin and is capable of inducing apoptosis in cancer cell lines. The effect of Lfcin B in breast cancer cell lines has not been tested so far. In this study, the effects of  Lfcin B peptide was tested on a panel of breast cancer cell lines comprising of MCF 7 (Luminal A type expressing estrogen receptor and progesterone receptor; triple negative), MDA-MB-231 (claudin low type; triple negative), SKBR3 (overexpressing HER2) and MDA-MB-468 (basal type). The mammary epithelial cell line, MCF-10a was used as a normal control. Lfcin B was dissolved in plain medium and the cells were treated with various concentrations of the peptide (100 µg/ml to 300 µg/ml) to study its effect on proliferation, cell migration and apoptosis. Apoptosis was studied by flow cytometry of annexin-PI stained cells and western blot while changes in the gene expression induced by Lfcin B was analyzed by quantitative RT-PCR. Lfcin B peptide induced significantly more apoptosis in all the breast cancer cell lines studied compared to normal breast epithelial cells. The peptide suppressed cell migration in the invasive cell lines MDA-MB-231 and MDA-MB-468. Our studies suggest a potential for Lfcin B to be developed for breast cancer therapy.

Ana T. Limon-Miro

The University of Sonora, Mexico

Title: Health care nurses: A systematic literature review

Time : 15:55-16:15

Speaker
Biography:

Ana T. Limon-Miro is a nutritionist with a master degree in Health Sciences at Universidad de Sonora. She is the coordinator of the nutrition area in the Navigator Program for Sonoran Breast Cancer patients at Universidad de Sonora. Limon-Miro is currently a PhD student in the Science Program of Centro de Investigación en Alimentación y Desarrollo A.C. interested in nutrition intervention programs in breast cancer patients.

Abstract:

Studies have shown that nutrition interventions in breast cancer patients improve their nutritional status and quality of life. Data about costs of specialized nutrition intervention programs regarding their cultural and socioeconomic status is limited. The aim of this study was to design an individualized diet for each breast cancer patient in a Navigator Program (NP) and determine the economic cost of the nutritional plan according to their socioeconomic status. Total energy expenditure was calculated and a caloric restriction was done according to the patient's nutritional status. The nutritional plan followed NIH guidelines and was adapted to the Mexican Food Equivalent System. A weekly menu was provided by a nutritionist based on four different configurations (w leguminous + w/wo milk or wo leguminous + w/wo milk) generated from the patient's usual diet. Weekly costs were calculated for each configuration based on local market prices in Hermosillo, Sonora, Mexico. From 27 subjects, 85%(23/27) had overweight or obesity, 61%(11/18) had a weekly income above 5 minimum wages, and 41%(11/27) received a 1500 kcal/d nutrition plan. The average weekly cost of a 1500 kcal nutritional menu was $504 MNX ±46 [$27 USD ±2], equivalent to 7 minimum wages/week ($73 MNX [$4 USD], minimum wage in Mexico). Animal protein was the most expensive food group, followed by vegetables and fruits. Health professionals in navigator programs should be aware of diet costs and socioeconomic data of breast cancer patients in order to improve their adherence to treatment, nutritional status and quality of life.

Maria E. Sales

University of Buenos Aires, Argentina

Title: Muscarinic modulation of paclitaxel actions on human breast cancer

Time : 16:15-16:35

Speaker
Biography:

Maria E. Sales is working in 1Centro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET), Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.

Abstract:

Cholinergic modulation of tumor progression has been described in differentexperimental models. In our laboratory, we demonstrated that long term treatment of murine mammary tumors with the non-selective agonist, carbachol (CARB) promotes cell death through the activation of muscarinic (M) receptors. We studied the effect of acombination of sub threshold doses of CARB (10-12M) with paclitaxel (PX) (10-8M) acytotoxic agent used in the treatment of breast cancer, on MDA-MB231 cells derived from a human triple negative breast tumor. The combination of CARB+PX reduced cell viability by 27±3% (p <0.01 vs. control). In addition, the combination of the M2 selective agonist, arecaidine (ARE) (12.5 ıM) that promotes cell death in glioblastomas, with PX (10-9M) produced a similar reduction in cell viability (24±7%; p<0.05) effect that was not observed with drugs added separately. By Western blot we detected the expression of M receptors (M5> M1=M2). The silencing of M2 receptor with a specific siRNA increased cell viability to control values. ARE+PX also reduced by 98ı7% mRNA levels of the drug transporter ABCG2 and by 97ı8% the expression of the epidermal growth factor receptor (p<0.001 vs. control). The combination did not modify the viability of MCF-10A cells derived from human normal mammary gland that do not express M receptors. These results suggest that M receptors could be considered as therapeutic targets in breast cancer and that the combination of cholinergic agonists plus cytotoxic agents, as PX may represent a novel therapeutic tool for the treatment of this illness

Biography:

He was Born in 1956, in Barakaldo-Bizkaia (Basque Country), SPAIN.Doctor in Medicine, Basque Country University. Radiologist. Accredited university Professor
in Health Sciencies, Basque Country University.Founding member and past President of the “Spanish Society of Breast Imaging” (SEDIM).Founding member of the
“European Society of Breast Imaging” (EUSOBI). Founding member and Past-Vicepresident of the “Iberoamerican Society of Breast Imaging” (SIBIM). Founding
member and President of the “Basque Society of Breast Diseases”. Author of numerous articles and book chapters about breast diseases.

Abstract:

Background: According to some authors, there is the possibility of obtaining a valid analysis of the tumor genetic fingerprint
using paraffin blocks containing samples obtained via radio-guided large needle biopsy.
Methods: We present 15 cases, with samples obtained via echo-guided biopsy with a 12 G needle (3 to 4 samples) through
malignant solid masses during the diagnostic procedure. The samples used for examination by Mamma print® came from the
paraffin blocks used for the conventional histological diagnosis, following assessment by a pathologist. A review of the available
literature on this subject was conducted.
Results: The number of samples varied from 3 to 4. In 12 cases (80%), we were able to obtain valid samples for Mamma print®
assessment. The results were “High Risk” in five cases and “Low Risk” in seven cases.
Conclusion: Upon our experience, the same samples obtained via per-cutaneous biopsy for assessment of suspicious lesions,
with a result of malignancy, can be used for the 70-gene prognosis signature assessment (Mamma print®).