Dra. Isaura Meza obtained her PhD in Cell Biology from the University of California, Berkeley, CA, USA, and did a Postdoctoral work from the University of Geneva, Geneva, Switzerland.  She is currently working as a full professor in the Molecular Biomedicine Department at CINVESTAV. Her current investigation is on breast cancer signaling processes leading to Ephytelial-Mesenchymal-Transition.

Inflammation is considered a critical component of cancer progression. In breast cancer it has been proposed that increased levels of the inflammatory IL-1β, cytokine, derived from the microenvironment of malignant cells, promotes invasiveness. Previously, our group has shown that epithelial non-invasive MCF-7 breast cancer cells acquired a mesenchymal phenotype with increased migration and invasiveness, after binding to the IL-1RI receptor of the cytokine followed by activation of a novel signaling pathway called IL-1β /IL-1R/ β-catenin. This transition toward malignancy was initiated by remarkable modifications of the intercellular junctions and the actin cytoskeleton of the MCF-7 epithelial cells. Once detached from each other, the cells acquired mesenchymal morphology and functions characteristic of cancerous invasive cells, named 6D cells. Cannabidiol (CBD) has been used to treat a variety of cancers and inflammatory conditions although the results are still controversial. We evaluated CBD as a potential inhibitor of the inflammatory cytokine IL-1β induction of the transition to malignancy and its possible reversion of the cells to a non-invasive phenotype in our in vitro model of breast cancer cells. We found that CBD blocked the progression of the IL-1β-induced signaling pathway and reestablished the epithelial organization lost by dispersion of the cells and re-localized E-cadherin and β-catenin at the adherens junctions. It also prevented β-catenin nuclear translocation causing decreased over-expression of genes of ∆Np63α, BIRC3, and ID1 proteins, all of them effectors in the cytokine signaling by IL-1β and over-expressed for the acquisition of malignant features. Cannabidiol inhibited the protein kinase B (AKT) activation, a crucial effector in the IL-1β/IL-1RI/β-catenin pathway, indicating that at this point there is crosstalk between IL-1β and CBD signaling which results in phenotype reversion. Our 6D cell system allowed step-by-step analysis of the phenotype transition and better understanding of mechanisms by which CBD blocks and reverts the effects of the inflammatory IL-1β. Preliminary results obtained with an in vivo model, using female nu/nu mice, have shown the effect of CBD in reduction of the size of tumors generated after inoculation of 6D cells, showing a potential anti-tumorigenic property of the CBD.

John M. Baust, Ph.D. is the founder of CPSI Biotech.  Dr. Baust completed his studies at Cornell University, Binghamton University and Harvard Medical School. Dr. Baust is a recognized innovator and entrepreneur in cryomedicine and a pioneer in the area of molecular mechanisms of cell death and low temperature stress.  Dr. Baust has been instrumental in the advancement of the field into the molecular biological era focusing on signal transduction and apoptosis and. These efforts have resulted in the identification of a significant molecular stress response component to freezing injury which is responsible for the differential sensitivity of various cancers to ablation. He has led the developed numerous medical devices, including cryoablation devices for the treatment of cancer and cardiac arrhythmias as well as for improved cell and tissue cryopreservation. Dr. Baust has founded 4 companies; published over 100 papers, reviews, book chapters; >75 patents; and serves on several editorial board and reviews for several journals and is a board member for the Society for Cryobiology.

The use of cryotherapy for the treatment of breast cancer has increased over the last several years.  Although successful, one of the challenges in cryoablation is management of cancer destruction in the periphery of the ice ball as the tissue within this outer margin may not experience ablative temperatures.  As such, in this study we investigated the level of cell death at various temperatures associated with the margin of a cryogenic lesion as well as the impact of repetitive freezing and thawing methods on overall efficacy in vitro using a human breast cancer cell line. MCF-7 cells were exposed to temperatures of -5, -10, -15, -20 or -25°C for 5 minute freeze intervals in a single or repeat freeze-thaw cycle.  Samples were thawed with either passive or active warming for 5 or 10 minutes. Samples were assessed at 1, 2 and 3 days post-freeze to assess cell survival, recovery and modes of cell death. Exposure of MCF-7 cells to -5°C and -10°C resulted in minimal cell death regardless of the freeze/thaw conditions.  Freezing to a temperature of -25°C resulted in complete cell death with no recovery in all freeze/thaw scenarios evaluated. Exposure to a single freeze event resulted in a gradual increase in cell death at -15°C and -20°C.  Application of a repeat freeze-thaw cycle (dual 5 min freeze) resulted in an increase in cell death with complete destruction at -20°C and near complete death at -15°C (Day 1 survival: single -15°C freeze/thaw = 20%; repeated -15°C freeze/thaw = 4%).  Analysis of thaw interval time (5 vs. 10 minute) demonstrated that the shorter 5 minute thaw interval between freezes resulted in increased cell destruction.  Further, investigation of thaw rate (active versus passive thawing) demonstrated that active thawing resulted less effective ablation compared to passive thawing (eg. -15°C 5/10/5 procedure survival, Passive Thaw: 4% versus Active Thaw: 29%). In conclusion, these in vitro findings suggest that freezing to temperatures of 25°C results in a high degree of breast cancer cell destruction. The data demonstrate that the application of a repeat freeze procedure with a passive 5 or 10 minute thaw interval between freeze cycles increases the minimal lethal temperature to the -15 to -20°C range whereas active thawing resulted in increased survival. These findings may be important to improving future clinical applications of cryoablation for the treatment of breast cancer.  

Dr. Marcato obtained her BSc (Cell Biotechnology) and PhD (Medical Microbiology and Immunology) from the University of Alberta. Dr. Marcato went on to complete postdoctoral training on cancer research with Dr. Patrick Lee at Dalhousie University. In 2012, Dr. Marcato started a breast cancer research laboratory at Dalhousie University.  The research projects in Dr. Marcato’s laboratory have the long-term goal of developing improved therapeutic strategies for breast cancer based on a precision medicine approach. They use transcriptome and genome-wide functional assays, cell lines, patient-derived xenografts (PDXs), mouse tumor models, and analysis of published patient datasets to identify biomarkers, study breast cancer stem cells (CSCs) and understand factors important in breast cancer progression. These factors include epigenetic modifications such as DNA methylation and long non-coding RNA

Fabienne Lamballe got her PhD in France, then went to the US for a 4-year post-doc in Dr Barbacid’s lab where she uncovered TrkC, the high affinity receptor for neurotrophin-3. In 1994, she got a permanent researcher position in Paris, at the INSERM, the French National Institute of Health and Medical Research. Then moved in 2001 to the IBDM in Marseille to join Flavio Maina’s team.  She has a long-lasting experience in neurobiology and signaling during development and in pathologies. Since 2014, her research focusses on signaling mechanisms implicated in tumorigenesis. The overall goal of her current work is to identify signaling vulnerabilities in TNBC, the very aggressive triple-negative breast cancer subtype, to ultimately propose new therapeutic approaches.

Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype characterized by a remarkable molecular heterogeneity. Currently, there are no effective druggable targets and advanced preclinical models of the human disease. We generated a unique mouse model (MMTV-R26Met mice) of mammary tumors driven by a subtle increase in the expression of the wild-type MET receptor. MMTV-R26Met mice develop spontaneous, exclusive TNBC tumors, recapitulating primary resistance to treatment of patients. Proteomic profiling of MMTV-R26Met tumors and machine learning approach showed that the model faithfully recapitulates intertumoral heterogeneity of human TNBC. Further signaling network analysis highlighted potential druggable targets, of which co-targeting of WEE1 and BCL-XL synergistically killed TNBC cells and efficiently induced tumor regression. Mechanistically, BCL-XL inhibition exacerbates the dependency of TNBC cells on WEE1 function, leading to Histone H3 and phosphoS33RPA32 upregulation, RRM2 downregulation, cell cycle perturbation, mitotic catastrophe and apoptosis. Our study introduces a unique, powerful mouse model for studying TNBC formation and evolution, its heterogeneity, and for identifying efficient therapeutic targets.

Dr. Craig Kukard is the head of the department of medical oncology and senior staff specialist at the Central Coast Cancer Centre on the Central Coast in New South Wales, Australia. He is a fellow of the Royal Australasian College of Physicians (FRACP). He is actively involved in research and his main research interests include breast, urological, gynaecological, and head, and neck cancers. He is a member of the Central Coast Local Health District (CCLHD) operational research committee and the Central Coast Cancer Services research executive committee.

We reviewed the research into the mechanisms of growth of triple negative breast cancer (TNBC) based on laboratory pre-clinical studies that have shaped understanding of the disease over the past decade. In response to these findings,

We propose an approach to potentially prevent cancer metabolic adaptation and recurrence. This paper collates preclinical results, first to determine the tumour’s mechanisms of growth and then to source natural substances that could potentially suppress those mechanisms. The results from in vivo and in vitro studies of TNBC were combined first to select 10 primary mechanisms (Hypoxia-inducible factor 1α, Hedgehog, MAPK, MTAP, NF-κ B, Notch, P13K, STAT3, and Wnt signalling pathways plus p53 and POL2A gene expression) that promote TNBC growth, and second to propose a treatment array of 21 natural compounds that suppress laboratory models of TNBC via these mechanisms.

We included BRCA mutations in the review process, but only pathways with the most preclinical studies utilizing natural products were included. Then we outlined potential biomarkers to assess the changes in the micro-environment and monitor biochemical pathway suppression.

This suppression-centric aim targets these mechanisms of growth with the goal of potentially halting

tumour growth and preventing cancer cell metabolic adaptation.

We chose TNBC to demonstrate this 5-step strategy of supplementary therapy, which may be replicated for other tumour types.

Dr. Suad Shamis obtained her BSc (Medicine) from Tripoli University and her MRes (Medicine) from the University of Glasgow. She worked as a dermatologist in Gharyan Hospital in Libya. Her Ph.D. research is based on studying hypoxic markers in breast cancer patients.

This study examined relationships between hypoxic markers, clinicopathological features, and survival in breast cancer patients. Immunohistochemistry for HIF-1α and CAIX was performed on a tissue microarray of 581 patients. Marker expression was assessed using the weighted histoscore method and analysed for association with cancer-specific survival (CSS), overall survival (OS) and clinicopathological parameters.

575 cases were included in the analysis. They had ductal carcinoma, with 70% of patients being over 50 years, 57% tumours size ≤ 20 mm, 41% of tumours were grade II and 43% were grade III. Additionally, 65%, 45%, and 19% of tumours were ER positive, PR positive and Her-2 positive, respectively.

HIF-1α cytoplasmic expression was associated with poorer CSS (P=0.043). High cytoplasmic CAIX expression was associated with worse CSS (P<0.001), OS (P=0.001), small tumour size (P=0.01), high tumour grade (P< 0.001), ER negativity (P< 0.001), PR negativity (P< 0.001), Her-2 negativity (P=0.005), low proliferative index (P=0.003) and increased tumour necrosis (P<0.001). Furthermore, high membrane CAIX expression was associated with worse CSS (P<0.001), OS (P=0.041), small tumour size (P=0.018), high tumour grade (P<0.001), ER negativity (P<0.001), PR negativity (P<0.001), Her-2 negativity (P=0.005), low proliferative index (P<0.001), increased tumour necrosis (P<0.001), and low tumour budding (P=0.001). Multivariate analysis with known clinical parameters showed only cytoplasmic HIF-1α (P=0.005), and cytoplasmic CAIX (P=0.024) were independently associated with poorer CSS.

HIF-1α and CAIX were associated with poor prognosis in the ductal cell carcinomas and were independent prognostic factors, warranting further investigation of their value as a biomarker of hypoxia in breast cancer.

Shadi Momtahen obtained her BSc (Computer Science) from Simon Fraser University (SFU), Canada, and is currently working as a Ph.D. candidate (Mechatronic Systems Engineering) at SFU and as a research assistant at BC Cancer, in Abbotsford, Canada. Her Ph.D. research is based on the multi-modality breast cancer assessment tools using diffuse optical tomography.

The diffusion approximation of the photon transport equation is frequently used to determine breast tissue’s optical properties. However, the applicability of the diffusion equation is limited. We have utilized an optimized diffusion equation using a unique scaling method to address this issue. The proposed model is evaluated using different phantoms from experimental measurements of spatially resolved diffuse reflectance. The results show that the optimized diffusion equation is more advantageous than the diffusion equation model for the diffuse reflectance estimation.

Dr. Monther AlAlwan is a senior scientist at the Stem Cell and Tissue Re-engineering Program (SCTRP), King Faisal Specialist Hospital and Research Centre, as well as an Adjunct Professor at Alfaisal University, Riyadh Saudi Arabia. He holds M.Sc. and Ph.D. in Immunology from Dalhousie University (Halifax, Canada). Dr. AlAlwan conducted a 3-years postdoctoral fellowship studying signaling in immune cells at the University of Manitoba, Canada. During his graduate studies and postdoctoral fellowship, Dr. AlAlwan made substantial contribution in the immunology field, particularly his groundbreaking discovery that highlighted the significance of the dendritic cells in the immunological synapse. After joining the SCTRP in 2007, he shifted gear to study cancer, where he identified novel mechanisms that regulate cancer metastasis and chemoresistance. Currently, he is actively involved in dissecting the molecular pathways that regulate the function of cancer stem cells and how this is related to chemoresistance and metastasis.

Using targeted therapies in combination with surgery and chemotherapy have significantly improved the clinical outcomes of breast cancer. Nonetheless, tumor-related mortality remained a major challenge mainly due to chemoresistance-mediated tumor relapse and metastasis. Cancer stem cells (CSCs), a small subpopulation of the tumor bulk that possess stem cell-like features, were reported to be resistant to chemotherapy and main mediator of tumor recurrence and metastasis. We have shown significant association between expression of the actin-bundling protein (fascin) in breast cancer patients and worse clinical outcome, including chemoresistance, metastasis and shorter survival. Fascin regulates stemness of breast cancer cells via promoting the Notch signaling pathway. More recently, we have demonstrated a direct effect of fascin on β1 integrin expression in breast cancer cells. Fascin-mediated β1 integrin expression stabilizes focal adhesion kinase (FAK) activation and enhances β-catenin signaling to promote CSC functions. Collectively, the data presented in this study offer a viable strategy to eliminate CSCs, the tumor seed that fuel chemoresistance, via therapeutic targeting of the fascin/β1 integrin/FAK axis of evil.

Dr. Mintu Pal is now working as Senior Associate Professor, University of Petroleum and Energy Studies (UPES), Energy Acres, 248007, Dehradun, India. Prior to that Dr. Pal was Assistant Professor, Academy of Scientific & Innovative Research (AcSIR) and SERB-Department of Science and Technology Ramanujan Fellow in CSIR-North East Institute of Science and Technology, Jorhat, Assam, India. He has obtained PhD from Nanyang Technological University (NTU), Singapore. His major interest of research includes multidisciplinary project on the interface between biology and chemistry with a wide variety of state-of-the-art technologies on stem cell and cancer research.

Epithelial-Mesenchymal Transition (EMT) intrinsically linked to dynamic changes of cellular organization from epithelial to mesenchymal phenotypes that result in functional changes of cell migration and invasion. This EMT transdifferentiation process is well associated with breast cancer progression & metastasis and is driven by a conserved set of transcriptional regulators. Recent evidences also suggest that cancer cells undergoing EMT acquire stem cell-like phenotype associated with malignant behaviour, chemoresistance, and relapse. Current two-dimensional (2D) in-vitro culture models of tumorigenesis are inadequate to replicate the complexity of in-vivo microenvironment. Therefore, the generation of functional three-dimensional (3D) constructs is a fundamental prerequisite to form multi-cellular tumour spheroids for studying basic pathological mechanisms. We focused herein on two major points: designing & fabrication of 3D hybrid scaffolds comprising electrospun fibers with cancer cells embedded within hydrogels, and determining the potential roles of 3D hybrid scaffolds associated with EMT in cancer progression and metastasis. Our findings revealed that 3D hybrid scaffold enhances cell proliferation and induces cancer cells to undergo EMT, as demonstrated by significant up-regulation of EMT associated transcriptional factors including Snail1, Zeb1, and Twist2; and mesenchymal markers whereas epithelial marker, E-Cadherin was downregulated. Remarkably, this induction is independent of cancer cell-type as similar results were obtained for breast cancer cells, MDA-MB-231 and gastric cancer cells, MKN74. Moreover, the hybrid scaffolds enrich aggressive cancer cells with stem cell properties. We showed that our 3D scaffolds could trigger EMT of cancer cells which could provide a useful model for studying anticancer therapeutics against metastasis (Pal et al., 2019).

Vitor Alves Marques is physical education by profession, he holds licenciaded in Physical Education and currently pursuing a doctor in Health Science at the Federal University of Goias. Vitor is master in Health Science at the Federal University of Goias, and its dissertation is about the effects of chemotherapy treatment on muscle performance in women with breast cancer in the year 2018. He is member the Laboratory of Physiology of the Exercise and Nutrition and Healthy at the Federal University of Goias (LAFINS/UFG) and also is member the Laboratory of Analyzes of Human Moviment (LAMOVH/UFG

Associate Professor of General Surgery – Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Catholic University, Rome - Italy. Coordinator of integrated therapies for breast cancer at the Department of Women’ and Children’s Health, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome - Italy. Senior Staff Surgeon- Breast Unit, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome - Italy. Breast Surgeon with expertise in the surgical treatment of breast tumors and oncoplastic techniques; over 4.000 surgical procedures for breast cancer from 1 January 2010 to 31 October 2020. Author of over 200 scientific papers in international journals and 15 textbook chapters (Orcid ID 0000-0002-2950-339; Scopus Author ID 23027478400). Professor at the School of Specialization in General Surgery, Plastic Surgery and Oncology at the Catholic University of Rome, Italy, from 2013.

Nipple-sparing mastectomy (NSM) with immediate prosthetic breast reconstruction (IPBR) is an oncologically accepted technique for selected breast cancer patients that allows to improve aesthetic outcomes and patient quality of life. IBPR has a positive effect on psychological health, sexuality, body image, and self-esteem of breast cancer survivors and permits them to avoid further surgical procedures. Traditionally, prosthesis has been placed into the submuscular (SM) pocket behind the pectoralis major muscle (PMM) that protects implant and reduces its visibility, palpability and ripple. More recently, thanks to introduction of more conservative mastectomies, newer generations of implants and especially acellular dermal matrices (ADMs), a muscle-sparing placement of prosthesis in a prepectoral (PP) plane is increasingly used; when this technique is performed, a coverage of the implant with ADMs is usually used in order to secure and shield the implant underneath skin flaps in the subcutaneous space. ADMs-assisted PP-IPBR seems to improve aesthetic outcomes and minimize complications related to manipulation of the PMM such as breast animation deformity, postoperative pain and injuryinduced muscular deficit; however, an increased risk of seromas, infections and skin/nipple-areola complex (NAC) necrosis and higher medical costs due to use of ADMs were hypothesized. To date, there is paucity of trial data on PP-IPBR using only definitive implants without coverage with ADMs. We present a personalized PP-IPBR using implants with micropolyurethane foam coated shell surface (microthane) without ADMs after NSM. Our preliminary experience shows that PP-IPBR using polyurethane-coated implant after NSM is a safe, reliable and effective alternative to traditional IPBR with excellent aesthetic outcomes and high patient quality of life; it is easy to perform, minimizes complications related to manipolation of PPM and reduces operative time while resulting also in a cost-effective technique. 

Dr. Yutaka Tsutsumi was born on September 9, 1951, in Yokohama, Japan. He graduated from Keio University School of Medicine, Tokyo, and obtained a national medical license in 1976. He continued to study as a pathologist in the Postgraduate School of Keio University. In 1982, he received a diploma of Doctor of Medical Science in the field of malignant lymphoma.

Triple-negative breast cancer (TNBC) encompasses heterogeneous subtypes.  Neoadjuvant chemotherapy (NAC) is ineffective against some TNBCs, while others show a favorable prognosis despite chemoresistance. [Cases] Fifty-one cases with Stages I and II TNBC were analyzed.  Thirty-four TNBCs treated with NAC were divided into “good responders” (n=22) showing therapeutic effect G2b or G3 in surgical specimens and “poor responders” with therapeutic effect G0, G1a, G1b and G2a (n=12).  NAC was spared in 17 cases (non-NAC group).  Apocrine-type TNBC was defined as TNBC immunoreactive for both androgen receptor and forkhead-box protein A1.  TNBC other than apocrine-type (n=16) and special types (myoepithelial, medullary, adenoid cystic and spindle cell carcinomas, n=6) was categorized as basal-like subtype (n=29).  The prognosis was evaluated in each category.  [Results] NAC showed significant effects against basal-like TNBC with high Ki-67 labeling (≧50%), and tumor-infiltrating lymphocytes predicted high chemosensitivity.  NAC was ineffective and avoidable in TNBC of apocrine- and special types showing low (<50%) Ki-67 labeling.  Ten (59%) lesions in the non-NAC group belonged to the apocrine-type.  When clinical complete remission shown by contrast-enhanced magnetic resonance imaging was reached in the course of NAC against basal-like TNBC, the NAC period was shortened in 14 (64%) of 22 good responders.  Disease-free and overall survival was excellent in all groups.  [Conclusions] The following two hypothetical proposals should be proven by large-scale clinical trials.  Immunohistochemical recognition of apocrine-type TNBC with low Ki-67 labeling is important for avoiding ineffective/unnecessary NAC.  By employing appropriate clinical imaging, period-shortening is achievable in basal-like TNBC with high Ki-67 labeling.

Roma Ghai has been working in KIET School Of Pharmacy, KIET Group of Institutions, Ghaziabad, India since 2009. Have in total 15 years of teaching experience and also have been guiding M.Pharm students in their research projects. Have 3 patent publications to her credit. Have written two books; one on “Pharmacological & Toxicological screening for B.Pharm and M.Pharm students’ as per PCI curriculum and second book on “Text book of Pharmacovigilance” as per PCI curriculum for 8th B.Pharm semester students. Have given training in DST programmes. Have developed a virtual lab experiment for AKTU for Human Anatomy and Physiology. Have in total 20 publications in national and international journals. Have participated in more than 18 conferences and seminars

According to the American Institute of Cancer Research, if breast cancer is not detected early enough, it is the second largest cause of death among women. Breast cancer death rates have decreased by 40% in recent decades as a result of increased awareness and advancements in screening and treatment. However, medications used to treat breast cancer can have adverse effects. Efforts are being made all around the world to detect and counter these negative consequences. As a result, it is necessary to bring it to the attention of physicians through anticancer medication adverse drug response monitoring. This study explores the possible ADRs in individual case reports compiled from reputable journal databases such as Google Scholar, Science Direct, Cochrane Library, and PubMed. Breast cancer drugs such as 5-fluorouracil, cisplatin, sunitinib, doxorubicin, cyclophosphamide, and topotecan are commonly used to treat the disease. A specific approach to monitor the ADR is necessary to deal with them. This study looks at the complexities of ADRs caused by anti-cancer medicines and how that data can subsequently be used by the clinicians who are serving in the tertiary health care system

Viji Remadevi is a second year PhD student in Cancer Biology, working under the guidance of Dr S Sreeja, Rajiv Gandhi Centre for Biotechnology, India. Her main research centers on identifying the genes that are differentially expressed in oral cancer that can lead to a better understanding of the disease.  She is also concerned about the potent active molecule in the ficus extract against its crude extract, which will further aid in designing and conceptualizing new and better therapeutic interventions for breast cancer. Indian Council for Medial Research, ICMR, funds her research.

Ficus extract have been shown to exert anticancer effect in many cancers especially in breast cancer. It mainly functions by alleviating cell proliferation, invasion and metastasis. In particular its propensity to subjugate the main characteristic of cancer potentiates its therapeutic interventions. From our previous studies its evident that ficus extract induced apoptosis via ROS mediated Bax induction. Along with its strong photosensitizing effect ensues rapid mitochondrial transmembrane potential collapse initiating partial caspase mediated apoptosis. Collectively, its dynamic action in compacting breast cancer substantiates its clinical relevance. Nevertheless, the underlying molecular mechanism involved in this process remains elusive. Research attempts should be made to elucidate the mechanisms of action and its active molecule at the cellular and molecular levels. Likewise a contrast study on efficacy of crude extract and its potent active molecule will further assist in designing and conceptualizing new and better therapeutic treatment or prevention for breast cancer.

Luiza Kuhnen Reitz is a PhD student in Nutrition at Federal University of Santa Catarina (UFSC) and obtained her BSc (Nutrition) from the same institution (UFSC). She has previously worked in nutrition clinic and home care assistance for oncology and cardiopathy patients. She is professor at Post Graduation in Advanced Clinical Nutrition at Catholic University Center of Santa Catarina, teaching the subjects of gastrointestinal diseases, cancer, and home care assistance. Her PhD research is based on the associations between Diet quality, Dietary antioxidant capacity and oxidative stress biomarkers in women submitted to adjuvant treatment for breast cancer.

 

Oxidative stress produced by adjuvant treatments is associated with cell injury; however, a healthy diet can help mitigate it. The aim of this study is to investigate the association between diet quality and oxidative stress parameters in women subjected to adjuvant treatment for breast cancer. The sample comprised 70 women. Oxidative stress biomarkers and diet quality parameters based on the Brazilian Healthy Eating Index—Revised (BHEI-R)—were evaluated at baseline (p0) and after adjuvant treatment (p1). Ferric reducing antioxidant potential (FRAP) was associated with diet quality at p0. BHEI-R scores were not different between p0 and p1; however, scores from total vegetables, total fruits, milk and dairy products, and meat, eggs and legumes were lower during treatment. On the other hand, lower sodium and saturated fat intake observed at p1 counterbalanced the BHEI-R score. Oxidative stress parameters have increased at p1, but they were not associated with diet quality; thus, changes in component intake were not enough to promote changes in oxidative stress during treatment. It appears that diet can enhance patients’ antioxidant defense before treatment, which could lead to better outcomes in the long term. Further investigations may help to clarify the association between diet and oxidative stress in women with breast cancer.

Anna Pogorzelska obtained her BCs (Biochemistry) from the Jagiellonian University in Cracow. She is conducting a research on the new therapeutical strategies of breast cancer for the PhD thesis in Laboratory of Biomacromolecular Interactions at the department of Biotechnology of Medicines and Bioinformatics in the National Medicines Institute in Warsaw.

This study presents the anticancer effectiveness of a novel formulation of isothiocyjanate - sulforaphane (SFN) with an cytostatic - doxorubicin (DOX) together encapsulated in liposomes. The safety and cardiotoxicity of this novel formulation was evaluated in vivo, the anticancer effectiveness was determined in vitro. As an in vivo model Balb/c mouse was used, the in vitro experiments was performed using triple negative breast cancer cell line MDA-MB-231 and nontumorigenic MCF-10A cell line as a healthy breast tissue control. Results showed that tested formulations are safe and characterize lower cardiotoxicity that DOX alone. The anticancer effectiveness showed that the novel formulation is effective on TNBC cell line and safe for the healthy breast cell line. DOX and SFN acts synergistic and dose reduction of DOX is possible when combined with SFN. These results indicate a lower toxicity of (DOX+SFN)-lip. administration for normal cells, but a stronger effect in cancer cells than the administration of DOX-lip. separately.