The P53 tumor suppressor gene which has been dubbed both the “Guardian of the Genome” (Lane 1992) and Science “Molecule of the Year”, is directly involved in the initiation of apoptosis and programmed cell death, to prevent an accumulation of abnormal cells. However apoptosis evasion is a characteristic feature of human cancers that promote tumor formation and progression (1). Presently, P53 is known to play a key role in practically all types of human cancers, and the mutation or loss of P53 gene function, can be identified in more than 50% of all human cancer cases worldwide.
This paper was uploaded on behalf of Professor Serge Jurasunas of Lisbon Portugal, www.sergejurasunas.com
The paper goes on to explain the role of the P53 gene and its relationship to Cancer and Apoptosis. It then elaborates on the importance of dietary agents can have a beneficial impact in cancer treatment, and provides a number of case studies. He addresses the importance of the P53 gene and DNA repair, as well as his use of Molecular Markers testing.
Professor Jurasunas believes:
We urgently need to put into clinical practice what we have discovered and learned. Targeting P53 and other genes remain one of the greatest challenges in the treatment of cancer. We have been working now for over 8 years with molecular markers as a diagnostic, prognosis, and follow up to treatment, selected the appropriate bioactive dietary compounds or anticancer agents, exceeding 1000 cases, blood tests, and successes. This may be an incentive for more doctors to venture into this new direction in order to achieve more beneficial results with their patient treatment, especially in cases where we can verify the ones who would be refractory to chemotherapy and have a poor response. It is always best to first check through patient testing, to determine whether or not chemotherapy would be beneficial.
Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
Majority of cancer lead by point mutation in p53 gene. which is also known as "guardian of genome". this mutation leads conversion of normal cell into cancerous cell.
Therapeutic prospects in Cancer Immunotherapy.
Interleukins for Renal Cell Carcinoma.
BCG for Bladder Cancer.
Vaccination Strategies: Oncolytic virus for melanoma, Dendritic Cell therapy for CA Prostate.
Immune Checkpoint inhibitors. PD1 and PD L1 inhibitors.
Adoptive Cell Therpay. CAR T Cell Therapy
Clinical efficacy. Costs.
The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy
Types of immunotherapy
Oncology
cancer vaccines
adoptive T cell transfer
oncolytic viruses
monoclonal antibodies
cytokine
treatment of cancer with immunotherapy
Introduction to Targeted Therapies in OncologyMohamed Abdulla
Describes the molecular background which represents the core for developing targeted therapies against specific biological events in malignant cellular clones.
Cell within a tumor that possess the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor”.
“CSC can thus only be defined experimentally by their ability to recapitulate the generation of a continuously growing tumor”.
p53 has been described as “GUARDIAN ANGEL OF THE GENOME”
because it performs following mechanism:
DNA Repair
Cell growth arrest
Apoptosis (programmed cell death)
P53 is also known as cellular tumour antigen Ag, phosphoprotein
P53 or tumour suppressor p53.
P53 protein is encoded by TP53.
describe the tumor suppressor genes and examples for downloading the presentation, more presentations , infographics and blogs visit :
studyscienceblog.wordpress.com
Therapeutic prospects in Cancer Immunotherapy.
Interleukins for Renal Cell Carcinoma.
BCG for Bladder Cancer.
Vaccination Strategies: Oncolytic virus for melanoma, Dendritic Cell therapy for CA Prostate.
Immune Checkpoint inhibitors. PD1 and PD L1 inhibitors.
Adoptive Cell Therpay. CAR T Cell Therapy
Clinical efficacy. Costs.
The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy
Types of immunotherapy
Oncology
cancer vaccines
adoptive T cell transfer
oncolytic viruses
monoclonal antibodies
cytokine
treatment of cancer with immunotherapy
Introduction to Targeted Therapies in OncologyMohamed Abdulla
Describes the molecular background which represents the core for developing targeted therapies against specific biological events in malignant cellular clones.
Cell within a tumor that possess the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor”.
“CSC can thus only be defined experimentally by their ability to recapitulate the generation of a continuously growing tumor”.
p53 has been described as “GUARDIAN ANGEL OF THE GENOME”
because it performs following mechanism:
DNA Repair
Cell growth arrest
Apoptosis (programmed cell death)
P53 is also known as cellular tumour antigen Ag, phosphoprotein
P53 or tumour suppressor p53.
P53 protein is encoded by TP53.
describe the tumor suppressor genes and examples for downloading the presentation, more presentations , infographics and blogs visit :
studyscienceblog.wordpress.com
Naturopathic Oncology - Nutritional Treatment - Third in a SeriesSheldon Stein
In this workshop given by Professor Serge Jurasunas, N.D., M.D. (Hom.) on Naturopathic Oncology, covering nutrition, diet and lifestyle, especially after remission or cure, as well as dietary prevention. This workshop was given at the 2008 Anti-Aging World Congress in Paris, France. Even more so these nutritional principles hold true today. Please visit: www.sergejurasunas.com , for more information.
Naturopathic Oncology - Anti-Oxidants - Second in a SeriesSheldon Stein
Professor Serge Jurasunas N.D., M.D. (Hon.) addresses the use of antioxidants in the treatment of cancer, given in Paris, France 2008, at the Anti-Aging Medicine World Congress. This was a workshop for the participants. For further information: www.sergejurasusas .com
Activation of p53 mediated glycolytic inhibition-oxidative stressapoptosis pa...rkkoiri
There is a general agreement that most of the cancer cells switch over to aerobic glycolysis (Warburg
effect) and upregulate antioxidant enzymes to prevent oxidative stress induced apoptosis. Thus, there is
an evolving view to target these metabolic alterations by novel anticancer agents to restrict tumor
progression in vivo. Previously we have reported that when a non toxic dose (10 mg/kg bw i.p.) of a novel
anticancer ruthenium(II)-complex containing 4-carboxy N-ethylbenzamide; Ru(II)-CNEB, was administered
to the Dalton's lymphoma (DL) bearing mice, it regressed DL growth by inducing apoptosis in the
DL cells. It also inactivated M4-LDH (M4-lactate dehydrogenase), an enzyme that drives anaerobic
glycolysis in the tumor cells. In the present study we have investigated whether this compound is able to
modulate regulation of glycolytic inhibition-apoptosis pathway in the DL cells in vivo. We observed that
Ru(II)-CNEB could decline expression of the inducible form of 6-phosphofructo-2-kinase (iPFK2:
PFKFB3), the master regulator of glycolysis in the DL cells. The complex also activated superoxide dismutase
(the H2O2 producing enzyme) but declined the levels of catalase and glutathione peroxidase (the
two H2O2 degrading enzymes) to impose oxidative stress in the DL cells. This was consistent with the
enhanced p53 level, decline in Bcl2/Bax ratio and activation of caspase 9 in those DL cells. The findings
suggest that Ru(II)-CNEB is able to activate oxidative stress-apoptosis pathway via p53 (a tumor
supressor protein) mediated repression of iPFK2, a key glycolytic regulator, in the DL cells in vivo.
Protocol for the Treatment of Prostate CancerSheldon Stein
Professor of Naturopathic Oncology, Serge Jurasunas explains the nature of prostate cancer and outlines the unique protocols he utilizes at his Lisbon clinic. Additional information is available on his website: www.sergejurasunas.com
Esta presentación es producto de una investigación que he realizado sobre las proteínas p53 y pRb así como la enfermedad ataxia telangiectasia. Considero que es una forma sencilla y practica de distribuir mi proyecto.
Presentation given by Dr. Wayne Danter at the 16th International p53 Workshop in Stockholm Sweden on June 16, 2014. This presentation provides an overview of Critical Outcome Technologies' lead cancer drug candidate, COTI-2, and outlines its p53-dependent mechanism of action.
p53 Protein: Master Regulator of Apoptosis and its Application in Cancer TherapyBRNSS Publication Hub
Cancer is characterized by uncontrolled and abnormal cells growth. In the body, the cell growth and cell
division are governing by apoptosis. The process of apoptosis is mainly regulated by the p53 protein. p53
is a tumor suppressor protein. The amount of p53 in a cell is mainly controlled by the negative regulator
murine double minute 2 (MDM2), which on complex formation with p53 leads to an overall reduction
of the p53 level. Inhibition of p53 function will inhibit the apoptosis and leads to cancer. Consequently,
inhibition of the MDM2/p53 interaction using the small molecules activates the p53 function and apoptosis
in the cells which contain the wild-type p53. It is a promising new therapeutic strategy for the treatment
of cancers retaining wild-type p53. However, the safety window of this class of compounds must be
evaluated. Moreover, it has to require the development of compounds, which can also be able to target the
cells which contain the mutated or deleted p53.
How to Understand and Treat Cancer with Molecular MarkersSheldon Stein
How to Understand and Treat Cancer with Molecular Markers by Professor Serge Jurasunas, N.D., M.D. (Hom)
This is the first in a series of presentations on Naturopathic Oncology.
For More Information Visit: www.sergejurasunas.com
Annals of Mutagenesis is an open access, peer reviewed, scholarly journal dedicated to publish articles covering all areas of Mutagenesis.
The journal aims to promote research communications and provide a forum for doctors, researchers, physicians and healthcare professionals to find most recent advances in all areas of Mutagenesis. Annals of Mutagenesis accepts original research articles, reviews, mini reviews, case reports and rapid communication covering all aspects of mutagenesis.
Annals of Mutagenesis strongly supports the scientific up gradation and fortification in related scientific research community by enhancing access to peer reviewed scientific literary works. Austin Publishing Group brings universally peer reviewed journals under one roof thereby promoting knowledge sharing, mutual promotion of multidisciplinary science.
Prof. Serge Jurasunas Biological Aging vs. Chronological Aging Part 1.pdfSheldon Stein
Biological Aging VS. Chronological Aging - How to Build a Healthy Longevity - An Important Role for the Mitochondria
Part I
Professor Serge Jurasunas, M.D. (hc) N.D. M.D (Hom)
Topics in Part 1:
A Longer Lifespan No Longer Means a Healthier Lifespan
What are the Causes of Normal Aging or Premature Aging?
Mitochondria, Oxidative Stress, and Premature Aging
What are Mitochondria?
Brain Neurons
The Brain and Alzheimer’s
Prof. Serge Jurasunas Biological Aging vs. Chronobiological Aging Part 2.pdfSheldon Stein
Prof. Serge Jurasunas Biological Aging vs. Chronobiological Aging Part 2.pdf
Topics in Part 2:
Food Diet and Healthy Lifespan
The Okinawa Food Model
List of the Best Anti-Aging Foods
Supplements that enhance Anti-Aging and Mitochondria
Professor Serge Jurasunas' upcoming presentation: "A New Way to Approach Cancer". This presentation is for the Medicine Week Congress in Baden Baden Germany, October 30 thru November 3rd, 2019.
How to Understand and Treat Cancer with Modern Methods. Public Presentation B...Sheldon Stein
Professor Serge Jurasunas' Public Presentation on the New Modern Way to Treat Cancer - Strategic Immunotherapy, Apoptosis, Angiogenesis at the Biobran Workshop in Zagreb, Croatia, 2-27-2018.
Professor Serge Jurasunas - New Modern Way to Approach Cancer - Biobran Works...Sheldon Stein
How to Treat Cancer with Immunotherapy Utilizing Biobran through the Microbiome. Professional Presentation for Medical Practitioners with Clinical Cases By Professor Serge Jurasunas.
Can Food Diet Prevent and Be Efficient In Cancer Treatment?Sheldon Stein
In this paper Professor Jurasunas writes about food diet and nutrition in cancer prevention and treatment. He shares his knowledge about what he has learned about the role of food diet from his 50 years of clinical experience in cancer treatment, emphasizing the role of diet, nutrition, and antioxidants in naturopathic oncology. He also gives recipes for a juice cocktail, special soup and an energy drink. Good nutrition and a healthy food diet a useful adjunct and foundation for cancer prevention and treatment.
New Modern Way to Approach Cancer - 5th International Biobran WorkshopSheldon Stein
New Modern Way to Approach Cancer - 5th International Biobran Workshop Krakow , Poland June 9-11, 2017. Professor Jurasunas discusses the problems of conventional oncology and offers insight into less toxic and more efficient methods of cancer treatment. He offers case histories and reviews protocols
using Biobran and other modern methods against cancer, focusing on Strategic Immunotherapy, Apoptosis and Angiogenesis. He shows how Biobran improves cancer survival rates and metastases prevention and disease recurrence.
Protocol for the Treatment Prostate Cancer - Dr Serge JurasunasSheldon Stein
Dr. Serge Jurasunas shares his Prostate Cancer Protocol in this paper, explaining the nature and treatment of Prostate Cancer from a Naturopathic Oncology Perspective. Professor Jurasunas is located in Lisbon Portugal and has lectured worldwide throughout his 50 years as a clinician.
He explains what can be done about the #1 cause of death in males even before lung cancer and what can be done, from the new perspective of Naturopathic Oncology.He offers an example, explains diagnostic procedures with Molecular markers and addresses detox, supplements and treatment.
Further information may be found in his new book, Health and Disease Begin in the Colon" and in his Blog: Naturopathiconcology.blogspot.com .
Professor Jurasunas explains what is cancer and how it develops. He explains the nature of this disease, and why cells mutate, elaborating on P53 and apoptosis. He explains why Cancer is a silent killer, while addressing the cellular cycle.
Health and Disease by Iridology Examination - Professor Serge JurasunasSheldon Stein
Professor Jurasunas offers an introductory overview to the history and practice of Iridology. He draws from his 50 years of clinical practice and offers real life cases, emphasizing the value of Iridology as a diagnostic tool, explaining the relationship between the iris, nervous system, and body's organs, as well as embryological development.
Preview - Health and Disease Begin in the ColonSheldon Stein
Health and Disease Begin in the Colon A preview of Professor Serge Jurasunas' new book, now available on Amazon in eBook and paperback formats. www.sergejurasunas.com
Inquiries: sergejurasunas@hotmail.com
IRIDOLOGY RESEARCH BY GAEL RIVERZ N.D., IRIDOLOGISTSheldon Stein
A Presentation of the Work of Professor Serge Jurasunas in the Field of Cancer Detection through Iridology Profiling
(As Described his Last Important Book "Health and Disease Begin in the Colon, Featuring Prof. Serge Jurasunas’ Natural Medicine)
Breast Cancer Theory, Profiling Through Iridology & TherapiesSheldon Stein
Professor Serge Jurasunas offers an in-depth understanding of breast cancer theory, its development, history and treatment. He discusses environmental factors, risk evaluation, genetics and family risk, cellular respiration and treatment innovations back in 2003. You can ask yourself what has happened over the past 13 years since then?
He offers detoxification drinks and formulas, discusses the reversal of mitochondrial damage as well as the need for psychological counseling and support. He then offers several cases.
Please note his new address:
Professor Serge Jurasunas
R.coelho 93 QTA Marinha
2750-008 Cascais
Portugal
Sergejurasunas@hotmail.com
Serge Jurasunas: A Complementary Approach to Breast Cancer - A Case with Mult...Sheldon Stein
A Complementary Approach to Breast Cancer - A Case with Multiple Liver Metastases is Free from Disease . In this paper Professor Jurasunas explains breast cancer, it's development
and treatment. He offers illustrations with Live Blood Microscopy, Oxidative Dried Layer Blood Testing, and his protocol for a successful outcome.
Serge Jurasunas: Oxygen, Mitochondria and CancerSheldon Stein
Oxygen, Mitochondria and Cancer - In this well documented paper Professor Jurasunas explains the role of Mitochondria and Oxygen play in cancer development and treatment, discussing ATP, genetic mutation, treatment protocol and nutrition.
Serge Jurasunas: Clinical Evidence of Cellular Respiration to Target CancerSheldon Stein
In this paper, Professor Jurasunas discusses clinical evidence on cellular respiration and its use in treating cancer. He offers documentation, dietary advice and documentation, along with protocols.
Integrative Cancer - New theories and Advances in Treatment From Hippocrates ...Sheldon Stein
Professor Serge Jurasunsas' recent paper on Integrative Cancer, From Hippocrates to the Human Genome - posted on his behalf. Discusses testing, protocols and case discussion.
Naturopathic Oncology-Health Begins In The Colon As Seen through Iridology-Ho...Sheldon Stein
Naturopathic Oncology-Health Begins In The Colon As Seen through Iridology - How To Detoxify - Professor Serge Jurasunas
Professor Serge Jurasunas' Presentation for the International Physician Round Table in Tampa Fl. , January 2016
www.sergejurasunas.com
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
P53 Tumor Suppressor Gene: Understanding P53 Based Dietary Anti Cancer Therapies Utilizing Dietary Agents
1. P53 – Tumor Suppressor Gene:
Understanding P53 – Based
Anticancer Therapies Utilizing
Dietary Agents
by Serge Jurasunas,N.D., M.D. (Hom)
www.sergejurasunas.com
Lisbon, Portugal
1
2. P53 – Tumor Suppressor Gene: Understanding P53 –
Based Anticancer Therapies Utilizing Dietary Agents
(At the end of this paper we made an announcement
concerning the “20th
World Congress on Advances in
Oncology – 18th
International Symposium of Molecular
Medicine”, featuring a program presenting several topics
related to our therapies.)
Abstract
The P53 tumor suppressor gene which has been dubbed both the “Guardian of
the Genome” (Lane 1992) and Science “Molecule of the Year”, is directly
involved in the initiation of apoptosis and programmed cell death, to prevent
an accumulation of abnormal cells. However apoptosis evasion is a
characteristic feature of human cancers that promote tumor formation and
progression (1). Presently, P53 is known to play a key role in practically all
types of human cancers, and the mutation or loss of P53 gene function, can
be identified in more than 50% of all human cancer cases worldwide (2).
Frequency of P53 mutations
70% in lung cancer
60% in cancers of colon, head, neck, ovary, bladder
45% in stomach cancer
35% - 40% in breast cancer
Recent data has shown in addition to losing transcriptional function, mutant
P53 gains oncogenic functions termed GOF (Gain of Function) that drive cell
migration, invasion, and metastases (3-4). The notion for mutant P53 GOF
theory is supported by recent studies using mutated P53-blocked mice which
display a broader tumor spectrum, increased aggressiveness and metastatic
potential as compared with their P53–null counterparts (5-6). Similarly in
human cancers mutant P53 expression has been linked with a poor prognosis
(7).
Therefore mutant P53 function raises the possibility that the mutant protein
may be a good target for designing novel therapies.
The P53 pathway seems to play a critical role in therapeutic response and
both as a diagnostic and marker in the prognosis of therapeutic treatment
effects.
The inability of most cancers to undergo apoptosis in response to appropriate
stimuli is a key cause of treatment failure, presenting one of the major, yet
unsolved problems in Oncology (8).
2
3. Introduction
Programmed cell death, called apoptosis is a fundamentally important process
that prevents an accumulation of genetically abnormal cells. Apoptosis
Induction often appears to be related to the production process of P53
protein. This follows the activation of the tumor suppressor gene as a stress
response to any DNA damage within a cell nucleus (9). In normal, unstressed
cells, P53 is expressed at a very low level; the half-life of the protein does not
exceed 20 minutes.
Active P53 binds to target DNA and determines the choice between trigger cell
cycle arrests at a check point to allow DNA repair or can activate a special
molecular pathway leading to the self-destruction of a cell through apoptosis.
Both alternatives provide any organism with genetic stability.
P53 – Apoptosis pathway
Transcriptional upregulation of pro-
apoptotic genes.
Pro-apoptotic BCL-2 members
BAX, Puma, Noxa
Initiating cyto C Release.
P53 expressed at very low levels in
normal cells
accumulated if cell is damaged by
genotoxic stress
Oren M. (2003) decision making by P53 – Life, death and cancer – Cell death Differ 10 – 431-442
Stress
Damaged
Chemotherapy
P53
P21
Cell cycle
arrest
Apoptosis
DNA repair
Angiogenesis
inhibition
Tumor inhibition
Loss of P53 pathway function can contribute not only to
aggressive tumor behaviour but also to therapeutic
resistance
Figure 1
The critical role of P53 is made evident by the fact that it is mutated in
approximately 50% to 70% of all human cancers. In fact, P53 is the most
commonly mutated gene in human cancer. In human malignancies, very often
there are mutations or a loss of alleles in the gene located on the
chromosome 17P. More than 500 mutations in the P53 gene have been
discovered, although they are not equal in terms of biological activity.
The mutated gene in transformed cells leads to protein confirmation changes
and the accumulation of very stable mutant forms of P53 in the nucleus. All
3
4. types of mutated P53 are likely to be ineffective in maintaining a non-
tumorigenic cellular phenotype when compared to a wild type P53.
Wild Type P53, which is a nuclear phosphoprotein, has been shown to be a
sequence specific transcription factor which induces the expression of P21,
WAF1/C1P1/Sdi-1, leading to a G1 arrest checkpoint to step up repair before
DNA replication and contributes to normal cell proliferation (10) unless DNA
replication is successful, the cells will be induced to undergo apoptosis.
However during a stress response from its P53 gene to any damage, recent
findings suggest that P53 induces apoptosis by trans-activating expression of
the BAX gene MRna (11) to increase BAX protein and simultaneously inhibit the
function of BCL2. RNA proteins are homologs, through BAX acts as an
accelerator of apoptosis while BCL2 serves to prolong life survival (12).
This suggests that P53 mutation not only serves to inactivate the pro-
apoptotic P53 pathway, but that may also play an additional role in tumor
progression. Mutant P53 itself provides a selective advantage to tumor cells
and promotes tumor growth. Recent data suggests that expression of mutant
P53 is not the equivalent of P53 loss, where mutant P53 can acquire new
functions.
BCL2 activity up-regulates in many types of cancer and correlates with cancer
cell resistance to a wide spectrum of chemotherapy agents (13). Over-
expression of the anti-apoptotic BCL2 proteins blocks cytochrome C release in
mitochondria in response to a variety of stimuli, whereas the pro-apoptotic
BAX protein releases cytochrome C that in turn activates an apoptotic
cascade, while the loss of BAX associates with tumor progression and with
shorter survival in metastatic breast cancer (14).
Figure 2
4
5. BAX was the first identified P53–regulated, pro-apoptotic BCL2 family
member. P53–responsive elements have been unequivocally identified in the
BAX gene (15). BAX is specifically required for Puma mediated apoptosis, and
it also participates in the death response as an indirect target of P53 through
Puma (16) and Noxa, both implicated in P53–dependent apoptosis.
Some studies show that the loss of BAX is responsible for nearly half of the
accelerated tumor growth in brain tumors that are related to loss of P53
function (17). BAX is inactive in approximately one third of invasive breast
cancers, where in a study of 119 women with metastatic breast cancer, it was
found that patients whose tumors had lost BAX activity, had poor responses to
combination chemotherapy, faster time to tumor progression, and shorter
overall survival (18).
This may suggest that turning on this pro-apoptotic gene may be important for
chemotherapy response, where one of the factors that can regulate BAX gene
activity is the P53 tumor suppressor gene, which also simultaneously inhibits
BCL2 during the process of apoptosis. Nevertheless because BAX proteins
antagonize BCL2 anti-apoptotic function, it is likely that the BCL2/BAX
balance ratio determines both the susceptibility of a cell to apoptosis as well
as therapeutic response to apoptosis stimuli (19).
If apoptosis signaling is not initiated by nuclear P53 and/or the presence of a
mutated P53 gene, loss of BAX and over-expressed BCL2, this allows some
cancer cells to divide unchecked after radiation or chemotherapy treatment;
associating with cancer cell resistance, increased rate of tumor recurrence,
and shorter patient survival (20).
5
6. Figure 3
Another profound feature of malignant cells is their ability to induce
angiogenesis necessary for tumor growth. Again, there is a clear correlation
between mutant P53 GOF that facilitates angiogenesis by increasing the
expression of VEGF (21), via interaction with E2F1 that induces the expression
of ID4, which in turn promotes the expression of pro-angiogenic factors such
IL and GROa, thus eventually leading to increasing angiogenesis in cancerous
tissues (22). Other novel functions of mutant P53 GOF are shown through the
activation of specific target genes EGFR/1, RAS, Myc, and interference with
the TGFB growth arrest control pathway, down-regulation of the E-Cadherin
cell-cell adhesion molecules to enhance motility and tumor cell migration and
invasion (23).
We have new clues and important conceptualizations that indicate tumors
cannot be viewed simply as an uncontrolled proliferative mass, but rather as a
cellular community, interacting with a microenvironment (24-25). This is why
targeting mutant P53 remains an urgent need to improve cancer treatment by
increasing a cancer cell’s sensitivity to apoptosis.
Therapeutic Strategy
Targeting mutant P53 and restoring the wild type function of P53 tumor
suppressor gene in tumor cells would be of potential therapeutic benefit and
an attractive strategy for anticancer treatments (26-27). Upon restoration of
P53 transcriptional activity, the apoptosis pathway would predominate.
Many cancer cells escape apoptosis and become resistant to chemotherapy
radiation or from destruction by the immune cells by endogenous cytotoxic T-
cells and natural killer cells (NK). If the oncogene BCL2 is highly expressed it
confers greater resistance to cancer cells from attacking immune cells,
increasing the urgent need for effective cancer therapies.
Furthermore some of the P53 apoptosis targets such as BAX, Puma, Noxa, and
P21 could potentially be used as targets for gene therapy to increase the
effectiveness of chemotherapy.
Dietary Agents that Induce Apoptosis with Chemo
Preventive Effects
A large number of dietary agents can exert effects on the human genome
either directly or indirectly to modulate gene expression. Extensive research
during the last half century demonstrated that numerous agents identified
from fruits and vegetables can interfere with several signaling pathways, and
were validated as apoptosis inducers in research experiments.
6
7. Figure 4
These dietary agents include well known, well documented substances
recommended for cancer prevention and therapy, such as curcumin (tumeric)
(28-29) resveratrol (grapes) (30) genistan (soybean) (31) capsaicin (red chili)
(32) ellagic acid (pomegranate) (33) caffeic acid and phenyl ester (propolis),
polyphenols (green tea), (34) catechin (green tea) (35), and índole-3-carbinol
(cruciferous vegetables) (36).
They have all clearly accumulated evidence demonstrating their efficacy to
induce apoptosis by modulation of the P53 independent pathway, BAX, BAK,
targeting the anti-apoptotic proteins, BCL2, and Survivin gene so as to
potentialize a chemotherapy/radiation regimen. Curcumin, for instance, has
been found to inhibit the activity of NF-KB, BCL2, and increase P53 activity as
well as sensitize cancer cells to Cisplatin and Taxol–induced apoptosis (37).
The combination of 5-Fu and genistein enhances therapeutic effects in colon
cancer through the COX2 pathway (38). Genistein combined with docetaxel or
Gemicitabine significantly inhibited BCL2 – BCL–XL, Survivin and induced P21
WAF1, suggesting that combination treatment regulates the important
molecules in the apoptotic pathway (39-40). Green tea and black tea cause
induction of apoptosis accompanied with up regulation in BAX and a decrease
in BCL2 proteins in prostate cancer cells (41). Capsaicin caused apoptosis in
prostate cancer cells show an increase of P53, P21 and BAX (42). Curcumin
down-regulates the apoptosis suppressor proteins BCL2 and BCL–XL in several
cancer cell lines, thus increasing apoptosis overall. (43).
7
8. In human breast cancer cells curcumin, induces apoptosis through P53
dependent BAX induction (44) curcumin resveratrol and green tea polyphenols
are also known to down-regulate the expression of apoptosis suppressor
proteins, such as BCL2 and BCL-X in several cancer cell lines.
In human prostate carcinoma, LNCaP cells, treatment with EGGG induced
apoptosis, was associated with stabilization of P53, with an accompanying
down regulation of NF.KB activity resulting in a decreased expression of the
anti-apoptotic BCL2. Overall dietary agents synergise with chemotherapeutic
drugs, thereby reducing the toxicity of chemotherapeutic agents. (45)
Numerous studies continue to report that resveratrol exerts its anticancer
effects by causing cell cycle arrest and inducing apoptosis in many different
cancers (46). These include colon adenocarcinoma cells (Caco-2), esophageal
carcinoma cells, medulloblastoma cells, the highly invasive and metastatic
breast cancer cell line MDA-MB-231, melanoma cells, pancreatic carcinoma
cells, esophageal squamous carcinoma cells, as well as lung cancer cells.
A complete document concerning the modulation of apoptosis by active
compounds for cancer therapy and their synergy with chemotherapeutic agent
is available at www.sergejurasunas.com .
Conclusion
Deregulation of P53 has enormous influence on carcinogenesis as mutant P53,
which can induce an increased epigenetic instability of tumor cells,
facilitating and accelerating tumor evolution.
Increasing body of investigation has shown that inhibitor of apoptosis protein
(IAP’s) as BCL2, Survivin, etc. is now seen as diagnostic markers for early-
stage malignancy and novel prognostic markers (47). In addition these
molecules have been validated as therapeutic targets. Accumulated evidence
clearly indicates that dietary agents may play a critical role by targeting P53
and IAP’s and improve chemotherapy regimen. Despite significant advances in
cancer diagnosis and therapy, there is still little progress in the treatment of
advanced disease.
Most modern medicines currently available for treating cancer are very
expensive, toxic, and less effective in treating the disease. Therefore new
effective ways to treat cancer have become a priority. Thus, one must
investigate further in detail, dietary agents derived from natural sources
without toxicity. Hopefully they will find a place in the clinical management
of patients with malignancy.
Case Reports
We have been measuring the activity of P53 pathway, BAX, BCL2, Survivin and
P21 gene expression with a large number, variety, and grades of cancer
patients, developing a targeting therapy that could restore mutant P53 to a
normal wild type function as a first step after gaining results to modulate
8
9. BAX, inhibit the BCL-2 and Survivin anti-apoptotic proteins. The targeting
therapy includes dietary agents such as curcumin and other compounds
empirically experimented upon by the author. It includes an extract of fish
oils rich in oligopeptide, that contain short-chain of amino acids shown to
have efficiency to target mutant P53 (48), fermented chlorella in tablets rich
in vitamins, minerals and nucleic acids. The fermenting process increases the
level of nutrients and absorptive power. Finally an antioxidant compound was
derived from modified vegetables and seeds, with low molecular weight
having an S.O.D. - like activity (49).
This targeting therapy is known as PSJ-53 therapy, had been first utilized in
experiments to restore mutant P53, and were proven by P53 gene expression
and P53 protein testing. Later experimentation in modulating BAX gene
expression and targeting BCL2 and Survivin anti-apoptotic proteins (50), were
shown to potentialize the efficiency of chemotherapy and radiation. Survivin,
a unique member of the IAP’S inhibits Caspase 7-9 and promotes both cell
proliferation and angiogenesis (51). Measuring and targeting Survivin remains
a major goal in response to antineoplasic agents (52).
We present three cancer cases with blood analysis reports of P53 gene
expression and mutated protein levels before and after the treatment, along
with two cases with complete figures of the pro-apoptotic and anti-apoptotic
genes before and after treatment.
1 – A case of multi-cancer recurrence.
2 – Remission of breast cancer
3 – Pancreatic cancer
4 – Recurrence of colon cancer
5 – Lung cancer
6 - Glioma
Methodology
P53 pathway activity and other pro-apoptotic and anti-apoptotic genes were
evaluated by measuring protein concentration and the level of P53 gene
expression, BCL2, BAX, Survivin , and P21 in the same peripheral venous blood
obtained from patients in the clinic.
The enzyme-link immunosorbent assay (Elisa) was used together with the
Polymer chain reaction (PCR) for the evaluation of the level of P53, BAX,
Survivin, P21 gene expression and for the qualitative detection of P53 protein.
Blood samples were collected in sterile tubes and sent to a laboratory
specializing in molecular marker tests, which offers complete reports and
discussion about each test.
9
10. Table 1 - Effects of PSJ-53 Therapy on the Tumor Suppressor P53 Pathway
M – Case of Multiple Cancer Recurrence
P53 protein level units/ml
of plasma
No
Date of
blood
sample
collection
Wild P53
Ref.range*
<0.33
units/ml of
plasma
Mutated P53
Ref.range
N.D.**
P53 gene (wild
expression level
Ref.range * <106
copies/ml of
plasma
Comments
1 2 Feb 2009 N.D.** 26.1 2.7 x 105
The blood sample was
collected prior to PSJ-53
therapy
2 18 May 2009 16.8 N.D.** 8.9 x 1011
The blood sample was
collected after a 3 month
course of PSJ-53 therapy
3 21 Sep 2009 156.0 N.D.** 1.5 x 1013
The blood sample was
collected 4 months after
completion of the PSJ-53
therapy during which time no
further treatment was given.
Table 2 – F – 48 years old: Breast Cancer – Breast Cancer in Remission 2009
P53 protein level units/ml
of plasma
No
Date of
blood
sample
collection
Wild P53
Ref.range*
<0.33
units/ml of
plasma
Mutated P53
Ref.range
N.D.**
P53 gene (wild
expression level
Ref.range * <106
copies/ml of
plasma
Comments
1 2 Feb 2010 N.D.** 52.5 52.245 The blood sample was
collected prior to PSJ-53
therapy
2 19 Apr 2010 10.99 N.D.** 170.000 The blood sample was
collected after a 2 month after
completion of the PSJ-53
therapy
The results clearly show the presence of mutated P53 prior to PSJ-53 therapy.
However after 2 months of the treatment we reversed the mutant P53 to a
normal wild type function, associated with an increase of the P53 gene
expression and protein level during this period of time.
10
11. Table 3 – F – 56 years old – Pancreatic Cancer – 5 Years of Remission
P53 protein level units/ml
of plasma
No
Date of
blood
sample
collection
Wild P53
Ref.range*
<0.33
units/ml of
plasma
Mutated P53
Ref.range
N.D.**
P53 gene (wild
expression level
Ref.range * <106
copies/ml of
plasma
Comments
1 4 May 2009 N.D.** 52.5 52.245 The blood sample was
collected prior to PSJ-53
therapy
2 4 July 2009 10.99 N.D.** 170.000 The blood sample was
collected after a 2 month
after completion of the
PSJ-53 therapy
3 17 Nov 2009 67.4 N.D.** 1.2 x 106
The blood sample was
collected after a 4 month
after completion of the
PSJ-53 therapy
The results clearly show the presence of mutated P53 prior to the PSJ-53
therapy. However after 2 months of therapy followed by 4 months of
treatment, we reversed the mutant P53 to a normal wild type function and
gradually the P53 wild protein production had risen to a high level leading to
increased self-destruction of cancer cells.
Table 4 – M – 81 years old – Recurrence of Colon Cancer – Liver Metastases
The patient refused chemotherapy but agreed to take some radiation therapy.
He was sent by his medical doctor to take molecular markers testing to first
check if radiotherapy will be efficient or not. P53, BAX or either P21 should
be active, sensitive to radiation and increase self-destruction of cancer cells.
New Reference range: P53 protein level wild – 0.10 – 1.00 units/ml of plasma
P53 gene expression – 10-50 units/ml of plasma
BCL2 gene expression - 10 units
BAX gene expression - 10 – 100 units
Survivin gene expression - 10 units
P21 gene expression - 10 – 50 units
11
12. P53 protein level
units/ml of plasma
No
Date of
blood
sample
collection
Wild P53
Ref.range*
<0.33
units/ml of
plasma
Mutated
P53
Ref.range
N.D.**
P53 gene
(wild
expression
level
Ref.range *
<106
copies/ml of
plasma
BCL-2 BAX Survivin P21
1 1 Mar 2011 N.D.** 10.88 N.D.** 390 N.D.** 129 N.D.**
2 11Jul 2011 N.D.** N.D.** 1.180 N.D.** 409 N.D.** N.D.**
The results clearly show after 4 months of treatment a significant
improvement and reversal of the mutant P-53 tumor suppressor gene.
However the P53 gene didn’t induce the level of normal protein (Often
because of a blockage of Puma). BAX gene expression is now active as a
pathway to destroy cancer cells and the Oncogene BCL2 and Survivin are not
active due to the applied treatment. Therefore the new pattern showed that
cancer cells were destroyed and that radiotherapy would be efficient,
increasing the destruction of cancer cells. The first report showed BCL2 and
Survivin were slightly active (at risk) but after the treatment, were totally
inhibited which contributed to increase the efficiency of
chemotherapy/radiation regimen.
After radiation therapy and further treatment with natural compounds, the
patient was free from liver metastases.
Table 5 – M – 50 years old – Lung Cancer
P53 protein level
units/ml of plasma
No
Date of
blood
sample
collection
Wild P53
Ref.range*
<0.33
units/ml of
plasma
Mutated
P53
Ref.range
N.D.**
P53 gene
(wild
expression
level
Ref.range *
<106
copies/ml of
plasma
BCL-2 BAX Survivin P21
1 7Jan 2013 N.D.** 16.26 N.D.** 340 330 1.028 552
2 11Mar2013 0.1 N.D.** 3 2 5 5 4.527
12
13. Ratio of the 1st
Analysis – BCL/BAX - 0.89
- Survivin/P21 – 0.53
Ratio of the 2nd Analysis – BCL/BAX – 2.5
- Survivin/P21 – 905.4 – Too high to make a ratio
The results clearly show after 2 months with PSJ-53 therapy that we reversed
mutant P53 to a wild type function, however P53 protein was produced only
to a certain extent. However we have targeted BCL2 and especially the high
expression of Survivin to a normal range and eliminated resistance in some
population of cancer cells and increased the self-destruction of cancer cells
through chemotherapy/radiation with a resultant decrease in lung nodule
size. P21 gene expression is very highly active (4.527) and promotes the self-
destruction of cancer cells. P21 is a P53-independent channel to apoptosis and
can be independent of P53 activated by another channel such as the TGF-B.
P21 is very sensitive to radiation in destroying cancer cells.
Table 6 – F – 8 years old – Glioma
Postponed Chemotherapy after 3 surgeries with poor results.
P53 protein level
units/ml of plasma
No
Date of
blood
sample
collection
Wild P53
Ref.range*
<0.33
units/ml of
plasma
Mutated
P53
Ref.range
N.D.**
P53 gene
(wild
expression
level
Ref.range *
<106
copies/ml of
plasma
BCL-2 BAX Survivin P21
1 6Jan 2013 0.2 N.D.** 1.344 2.066 1.714 1.734 2.192
2 11Mar2013 16.4 N.D.** 820 131 N.D.** N.D.** 229
We have clearly demonstrated that mutant P53 can be targeted together with
other pro-apoptotic and anti-apoptotic genes using dietary compounds, which
for many patients has been proven with many scientific examples. This is only
one example and not the publication of cancer cases followed under 1 or 2
year period as we have done with many patients (This child has now been
treated for over 2 years with excellent results, and has taken 5 blood
analyses,
Which each time indicated what treatment should be done. However, my last
article in the Townsend Letter 2014 (p.68-74) showed complete cases relative
to breast cancer with molecular markers testing done over a one year period
13
14. and more. Step by step it showed improvement and the normal balance
between the pro-apoptotic and anti-apoptotic genes (pp.68-74).
New avenues are now focusing on targeting apoptosis in cancer, which include
Oncogenes, BCL2, and Survivin that increases cancer cell resistance to
chemotherapy/radiation regimen while scientific literature today has already
accumulated thousands of articles on laboratory reports, theories, and
studies.
We urgently need to put into clinical practice what we have discovered and
learned. Targeting P53 and other genes remain one of the greatest challenges
in the treatment of cancer. We have been working now for over 8 years with
molecular markers as a diagnostic, prognosis, and follow up to treatment,
selected the appropriate bioactive dietary compounds or anticancer agents,
exceeding 1000 cases, blood tests, and successes. This may be an incentive
for more doctors to venture into this new direction in order to achieve more
beneficial results with their patient treatment, especially in cases where we
can verify the ones who would be refractory to chemotherapy and have a poor
response. It is always best to first check through patient testing, to determine
whether or not chemotherapy would be beneficial.
20th
World Congress on Advances in Oncology
18th
International Symposium of Molecular Medicine – October 8-10, 2015
Metropolitan Hotel – Athens – Greece
Participants from nearly 36 countries
In October we will participate in this important event that focuses on
molecular medicine and opens the door to a new conception of future
diagnostics and personalized treatment that predicts outcome in advance. The
purpose of the Congress is to offer a significant opportunity to share the
knowledge that cancer cells are “addicted” to certain altered genes, a
vulnerability that can be exploited therapeutically. These driver genes
correspond to Oncogenes or tumor suppressor genes causing the tumor to
grow and proliferate. Oncogenes as BCL2 or Survivin are two anti-apoptotic
genes mostly expressed in cancer. The program includes at least 2 lectures on
BCL-2.
The preliminary presentation includes new Biomarkers for molecular
medicine, the role of angiogenesis, the Japanese Kampa Medicine, lecture on
herbal extract including curcuma which is a real opening in a Congress of
Oncology.
It is now more than 8 years since I have been involved with the study and
clinical practice of Molecular Markers and cancer, including P53 mutation and
we are able to modulate treatment of patients according to the results of the
test and predict better how patients react to chemotherapy.
14
15. This Congress is a real opportunity for M.D., N.D.'s that are looking for a
better way to treat patients and enter now in the future which has now
arrived.
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Author Contact Information:
Professor Serge Jurasunas, N.D., M.D. (Hom)
Holiterapias
Rua da Misericordia, 137 – 1º
1200-272 Lisboa -Portugal
Email: info@sergejurasunas.com
www.sergejurasunas.com
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