Scientific Program

Conference Series LLC Ltd invites all the participants across the globe to attend 3rd International Conference on Tumor & Cancer Immunology and Immunotherapy San Diego, California, USA.

Day 1 :

Keynote Forum

Colleen Huber

Naturopathic Cancer Society, USA

Keynote: Sugar and cancer: A 7-year, controlled study
Tumor & Cancer Immunology 2018 International Conference Keynote Speaker Colleen Huber photo

Colleen Huber NMD is a Naturopathic Medical Doctor in Tempe, Arizona. She was the Keynote Speaker at the 2015 Euro Cancer Summit, the 2016 World Congress on Cancer Therapy, and a Keynote Speaker at the 2016 and 2017 World Congress on Breast Cancer. She is President of the Naturopathic Cancer Society. She is a Naturopathic Oncologist and Fellow of the Naturopathic Oncology Research Institute. 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 other writing includes her book, choose your foods like your life depends on them, and she has been featured in the books America’s Best Cancer Doctors and Defeat Cancer. Her academic writing has appeared in The Lancet and Cancer Strategies Journal, and other medical journals. Her research interests are in the use of therapeutic approaches targeting metabolic aspects of cancer.



Introduction: Ingestion of glucose and malignant neoplastic growth has been established in animal studies for numerous types of cancer. Such studies examined mice and/or fewer than 20 human subjects and/or were retrospective. This study is a 7-year interventional study of 317 consecutive human cancer patients at one naturopathic cancer clinic, who were treated with cancerdisrupting nutrients and herbs, as well as abstention from sweetened foods as the dietary intervention.

Methods: Survival of sweetened food eaters vs abstainers among cancer patients was examined at one clinic over a sevenyear period. Since 2006, this clinic has recorded data on consumption of sugar and other sweeteners in cancer patients, and has consistently recommended, but never enforced, avoidance of sweetened foods, except with extracts of the plant Stevia rebaudiana, which does not contain saccharides or sugar alcohol. In this controlled interventional study, the diets and outcomes are reported for all 317 patients with a diagnosis of cancer who were treated at the clinic, and who stayed at least two weeks in treatment. All results are reported in this paper.

Results: Achievement of remission was quite different for the following two categories: all patients: 151/317=48% and those who ate sweetened foods: 9/29=31%. The difference between these two groups was much stronger for the cohort of patients who continued treatments until either remission or death. Comparing all patients who were steadfast in the recommended treatments with the sweetened food eaters who were steadfast in all but dietary recommendations, 151/183=83% of all completely steadfast patients achieved remission, but only 9/25=36% of the steadfast sweetened food eaters achieved remission. Remission was defined as no visibly active tumor on MRI imaging of the same area that had previously active tumor growth. Of all patients who were steadfast in the treatments (including the sweetened food eaters), 32/183=17% died while still under the care of the clinic, but considering only the sweetened food eaters who otherwise consistently pursued the recommended treatments, 16/25=64% died. Follow-up studies since 2014 found similar survival differences among the two groups studied.

Conclusion: In this first-ever, long-term, interventional study of glycemic restriction in hundreds of cancer patients, we found that sweetened foods (other than stevia-sweetened foods) were highly correlated with patient mortality across all types and all stages of cancer. Stevia is therefore recommended as the only sweetener to be used by cancer patients.

Keynote Forum

Jie Xu

Anderson Cancer Center, USA

Keynote: Expression of programmed cell death 1 ligands in histiocytic and dendritic cell neoplasms

Time : 09:45-10:15

Tumor & Cancer Immunology 2018 International Conference Keynote Speaker Jie Xu photo

Jie Xu has received her MD from Hubei Medical University and her PhD from the University of Alabama at Birmingham. She is currently an assistant professor in the Department of Hematopathology at the University of Texas MD Anderson Cancer Center. She is board certified by the American Board of Pathology in Anatomic Pathology, Clinical Pathology, and Hematology. she has been actively participating in multiple research projects in tumors of hematopoietic and lymphoid tissue, and cancer, which has led to 48 research papers, 39 presentations at the national and international conferences, and multiple awards. Her major research interests include diagnostic and prognostic factors in lymphoma and leukemia and the potential therapeutic targets for hematopoietic neoplasms.



PD-1 (programmed cell death protein 1) is expressed on activated T cells. The ligands (PD-L1 or PD-L2) on tumor cells or antigen presenting cells bind to PD-1 and results in reduced T cell activation and inhibited immune responses. Antibodies targeting PD-1 or PD-L1 elicit antitumor immunity in a subset of patients with solid tumors including melanoma, renal cell carcinoma, non-small cell lung cancer and hematopoietic tumors such as classical Hodgkin lymphoma, and clinical response correlates with PD-1 ligand expression by malignant or immune cells within the tumor microenvironment. Histiocytic and dendritic cell sarcomas are malignant neoplasms with high morbidity and mortality; they are rare and can be difficult to diagnose. We examined the expression of PD-1 ligands on histiocytic and dendritic cell sarcomas. Seven of 14 histiocytic sarcomas (HS) (50%), 2 of 5 interdigitating dendritic cell sarcomas (IDS) (40%), 10 of 20 follicular dendritic cell sarcomas (FDS) (50%), and none of 9 blastic plasmacytoid dendritic cell neoplasms (BPDCN) were positive for PD-L1. Eleven of 20 (55%) follicular dendritic cell sarcomas were also positive for PD-L2. Our results suggest that PD-L1 and PD-L2 IHC may prove useful in establishing or confirming the diagnosis of histiocytic and dendritic cell sarcomas. Given that patients with histiocytic and dendritic cell sarcomas are generally resistant to conventional chemotherapy, checkpoint blockade may prove a more effective alternative. In summary, PD-L1 and PD-L2 are useful new markers for identifying select histiocyte and dendritic cell neoplasms and reveal novel patient populations as rational candidates for immunotherapy.


Keynote Forum

Andrei L Gartel

University of Illinois at Chicago, USA

Keynote: FOX(M1) and cancer

Time : 10:15-10:45

Tumor & Cancer Immunology 2018 International Conference Keynote Speaker Andrei L Gartel photo

Andrei L Gartel, PhD, is an Associate Professor in the Department of Medicine at the University of Illinois at Chicago and is the academic editor of PLOS ONE. He is the author of 90 peer-review publications that include more than 25 reviews. He has more than 11,000 citations and his h-index is 41. His scientific interests include cancer, regulation of oncogenic transcription factors FOXM1, protein-protein interactions; cell cycle and regulation of CDK inhibitor p21. Specifically, his lab is interested in the identification of new FOXM1 inhibitors. He received his funding from NIH, DOD and private companies/foundations.



FOXM1 is an oncogenic transcription factor that is overexpressed in the majority of human cancers and is a potential target for anticancer drugs. We identified proteasome inhibitors as the first type of drugs that target FOXM1 in cancer cells. Moreover, we found that HSP90 inhibitor PF-4942847 that does not act as proteasome inhibitor also suppresses FOXM1. Chaperone HSP70 is induced after treatment with both proteasome/HSP90 inhibitors and after heat-shock stress and we identified this chaperone as a novel negative regulator of FOXM1 after proteotoxic stress. We showed that FOXM1 and HSP70 interact in cancer cells following proteotoxic stress and FOXM1/HSP70 interaction led to inhibition of FOXM1. We have previously shown that FOXM1 interacts with nucleophosmin (NPM) in cancer cells and NPM determines the cellular localization of FOXM1. Mutations in NPM1 result in cytoplasmic re-localization of NPM (NPM1mut) and favorable outcome for the patients. We found the evidence that improved outcomes in the subset of NPM1mut AML may be partially explained by the cytoplasmic re-localization and consequent functional inactivation of FOXM1. First, we confirmed the co-localization of FOXM1 and NPMmut in the cytoplasm of AML patients bone marrow biopsies and determined a strong cytoplasmic expression of FOXM1 only in NPM1mut AML cells. We also showed an important role of FOXM1 in chemo-resistance in leukemia cell lines with nuclear, but not cytoplasmic FOXM1. These data imply that suppressing of FOXM1 in AML could increase sensitivity to standard chemotherapy.


Break: Networking & Refreshment Break 10:45-11:00 @ Foyer

Keynote Forum

Marja T Nevalainen

Medical College of Wisconsin Cancer Center, USA

Keynote: Novel small-molecule Stat5 Inhibitor for further optimization and clinical development for cancer therapy

Time : 11:00-11:30

Tumor & Cancer Immunology 2018 International Conference Keynote Speaker Marja T Nevalainen photo

Marja Nevalainen, MD, PhD is an internationally recognized leader in the field of cytokine and steroid hormone signaling in prostate cancer. Dr Nevalainen holds the title of Eminent Scholar at MCW. She is also Director of Prostate Cancer Center of Excellence at MCW Cancer Center, which is a multi-disciplinary hub for prostate cancer research with an international collaborative network. Dr Nevalainen serves as Assistant Dean for Research at MCW, and Associate Director of Education for the MCW Cancer Center. Her primary appointment is in the Department of Pathology, and a secondary appointment in the Department of Pharmacology and Toxicology.



Jak2-Stat5 signaling plays a significant role in promoting growth and progression of Bcr-Abl-driven hematological malignancies as well as prostate cancer. Bypassing tyrosine kinases compelled for Stat5a/b phosphorylation would be favourable for therapy development for Stat5a/b- controlled cancers. To identify small-molecule inhibitors of Stat5a/b for lead optimization and therapy development, in silico screening of chemical structure databases combined with medicinal chemistry was used for identification of a group of small-molecule forestalling to block SH2-domain-mediated docking of Stat5a/b to the receptor-kinase complex and subsequent phosphorylation and dimerization. The lead compound Inhibitor of Stat5, IST5-002, (IST5) binds directly to the SH2-domain of Stat5 in fluorescence polarization assays. We additionally tried the viability of the lead-compound IST5 in exploratory models and patient examples of two best-known Stat5a/b-driven tumors, prostate cancer (PC) and interminable myeloid leukemia (CML). IST5 forestalled both Jak2 and Bcr-Abl-interceded phosphorylation and dimerization of Stat5a/b, and specifically hindered the transcriptional action of Stat5a (IC50 1.5μM) and Stat5b (IC50 3.5μM). IST5 suppressed nuclear translocation of Stat5a/b, binding to DNA and Stat5a/b target gene expression. IST5 had no significant inhibitory activity on a panel of 52 kinases, including Jak2 and Abl. Importantly, no signs of toxicity were noted at the dose of 100 mg/kg in acute or chronic toxicity studies conducted in mice. IST5 incited broad apoptosis of PC cells, weakened development of PC xenograft tumors and prompted cell demise in quiet inferred PCs when tried ex vivo in explant organ societies. Critically, IST5 initiated hearty apoptotic passing of imatinib-delicate as well as imatinib-safe unending myeloid leukemia (CML) cell lines and essential CML cells from patients. IST5 gives a lead structure to advance synthetic alterations for clinical improvement for Stat5a/b-driven strong tumors and hematological malignancies.


Tumor & Cancer Immunology 2018 International Conference Keynote Speaker Magnus S Magnusson photo

Magnus S Magnusson, Research Professor, PhD in 1983, University of Copenhagen. Author of the T-pattern model initially focused on the real-time organization of behavior and has co-directed DNA analysis. Numerous papers and invited talks at international mathematical, neuroscience, proteomics, bioinformatics and science of religion conferences and at leading universities in Europe, USA and Japan. Deputy Director 1983-1988, Anthropology Laboratory, National Museum of Natural History, Paris. Then repeatedly invited temporary Professor in psychology and ethology (biology of behavior) at the University of Paris (V, VIII & XIII). Since 1991, Founder and Director of the Human Behavior Laboratory, University of Iceland. Works in formalized collaboration between now 32 European and American universities based on “Magnusson’s analytical model” initiated at University René Descartes Paris V, Sorbonne, in 1995.



This talk concerns spatial and temporal self-similarity across more than nine orders of magnitude, implicating a self-similar fractal-like pattern, called T-pattern, a natural or pseudo-fractal pattern, recurring with statistically significant translation symmetry (Magnusson et al. eds. 2016). It is here presented in the order realized within a longstanding primarily ethological (i.e. biology of behavior) project beginning in the early 1970’s concerning social interaction and organization in social insects and primates including humans and inspired mainly by the work of Lorenz, von Frisch and Tinbergen for which they shared a Nobel Prize in Medicine or Physiology in 1973. The smallest animals concerned in their ethological work were social insects and there was no implication of self-similarity. The present project has focused on developing time pattern definitions and corresponding detection tools resulting in the T-pattern type and corresponding detection algorithms implemented as the THEME software, which has allowed their abundant detection (Casarrubea et al., 2015), in many kinds of animal and human behavior and interactions and later in neuronal interactions within living brains (Nicol et al.), thus showing T-patterned self-similarity of temporal interaction between and within brains. Apparently, the RNA world invented its evolving external memory as the purely informational T-patterned DNA strings and now there is only a DNA world. Similarly, humans invented their evolving external memory as the purely informational T-patterned strings of written language making possible very recently and in a biological eye-blink the development of modern science and technology and the creation of extremely populous and complex human mass-societies, the only mass-societies among large-brained animals and now all based on T-patterned text strings. Protein and human mass-societies seem to be the only ones using such durable long memory strings external to their citizens. Strings that are highly standardized with parts being massively copied, distributed, promoted and even enforced such as those among humans called legal or holy. Both Human and protein mass-societies create their specialized citizens using various sub-sections of the external T-patterned memory strings. Extensive temporal and spatial self-similar patterning thus seems to exist in form and function from nano to human temporal and spatial scales regarding transient nonverbal behavior and its more durable spatial traces or products such as texts, all patterned in a way reflecting the fundamental and extremely ancient molecular structure of their creators.