Cancer Prevention

... have been personalized by including recipients' demographic characteristics (eg, gender, ethnicity) or other identifying characteristics (eg, the person's name or occupation) in an effort to promote various health ... Health Psychology, 22(1), 60–67. ... The role of self-affirmation in con.

Wstęp: Wobec stałego wzrostu zachorowalności na nowotwory złośliwe - koniecznym stało się opracowanie prostych zaleceń, które wpłyną na kształtowanie motywacji, wiedzy i umiejętności niezbędnych do zdrowego stylu życia. W 1987 roku Komisja Ekspertów sporządziła Europejski Kodeks Walki z Rakiem (Kodeks).
Cel: Europejski Kodeks Walki z Rakiem jako narzędzie służące do obniżenia zachorowalności i umieralności na nowotwory złośliwe.
Materiał i metoda: Autorskie tłumaczenie 4. Edycji Kodeksu wraz z analizą podstawowych wskaźników statystycznych z bazy Globocan i Krajowego Rejestru Nowotworów.
Wyniki: Obserwowany na świecie wzrost liczby zachorowań na nowotwory złośliwe wynika przede wszystkim ze starzenia się społeczeństwa, ekspozycji na czynniki ryzyka oraz postępu w zakresie technik diagnostycznych, zwłaszcza obrazowych (w Polsce dodatkowo z opóźnienia we wprowadzeniu populacyjnych badań przesiewowych i niskiego wskaźnika uczestnictwa w tych badaniach co przekłada się na wyniki leczenia). Badania epidemiologiczne przeprowadzone na świecie dowiodły, że przynajmniej 1/3 zachorowań na nowotwory złośliwe można uniknąć poprzez zdrowy styl życia a kolejnych 1/3 można wcześnie wykryć (tzn. przed wystąpieniem objawów klinicznych) i skutecznie leczyć. Kodeks to 12. zaleceń: Nie pal! Uczyń dom miejscem wolnym od dymu tytoniowego! Dbaj o utrzymanie prawidłowej masy ciała! Bądź aktywny fizycznie! Odżywiaj się zdrowo! Ogranicz spożycie alkoholu! Rozsądnie korzystaj ze słońca! Chroń się przed szkodliwym działaniem substancji rakotwórczych! Chroń się przed szkodliwym promieniowaniem! Staraj się karmić piersią, ogranicz HTZ. Pamiętaj o szczepieniach! Uczestnicz w programach badań przesiewowych w kierunku: wczesnego wykrywania raka piersi, szyjki macicy, jelita grubego!
Wnioski: Jak wykazują badania epidemiologiczne ponad 80% czynników ryzyka zachorowania na nowotwory złośliwe związanych jest z szeroko rozumianym stylem życia. Dane Krajowego Rejestru Nowotworów potwierdzają tezę, iż globalne starzenie się społeczeństwa nie jest jedynym czynnikiem odpowiadającym za wzrost liczby zachorowań na nowotwory i można doprowadzić do zmniejszenia
zachorowalności i umieralności na pewne typy nowotworów. Poprzez budowanie świadomości onkologicznej (m.in. upowszechnianie zaleceń Europejskiego Kodeksu Walki z Rakiem) i dążenie do poprawy jakości życia ludności, stwarzanie warunków do zmiany postaw i kształtowanie odpowiedniej motywacji opartej na wiedzy i umiejętności w zakresie zdrowego stylu życia oraz korzyściach z wczesnego wykrycia choroby można doprowadzić do obniżenia zachorowalności i umieralności Polaków z przyczyn raka piersi-w przeciwnym razie za 20-40 lat nie będzie miał nas kto leczyć i za co leczyć.

Prostate cancer chemoprevention represents a relatively new and promising strategy for reducing the immense public health burden of this devastating cancer of men in the United States and Western societies. Chemoprevention is defined as the administration of agents (drugs, biologics, and natural products) that modulate (inhibit) one or more steps in the multistage carcinogenesis process culminating in invasive adenocarcinoma of the prostate. In 2000, there were an estimated 170,000 new cases of prostate cancer and 31,000 deaths in the United States. During the past decade, the National Cancer Institute (NCI) organized the chemoprevention research program and began testing the first generation of promising agents (eg, 4-(hydroxy)-fenretinide [4-HPR], difluoromethylornithine [DFMO], antiandrogens) in high-risk cohorts and launched the first-large scale US phase 3 primary prevention trial, known as Prostate Cancer Prevention Trial (PCPT-1), in 18,000 average-risk men (age more than 55 years and prostate-specific antigen [PSA] less than 3 ng/mL) treated for 7 years with finasteride or placebo. In the summer of 1998, the NCI Prostate Cancer Progress Review Group (PRG) Report to the director of NCI was published in response to the leadership of the prostate cancer advocacy community in conjunction with Congress. To further elucidate and address critical issues identified in this report and to develop a research agenda for the newly created Prostate and Urologic Cancer Research Group in the Division of Cancer Prevention at NCI, the NCI organized the workshop "New Clinical Trial Strategies for Prostate Cancer Chemoprevention." The major objectives were to promote understanding and cooperation among the NCI, US Food and Drug Administration (FDA), academia, pharmaceutical industry, and the public regarding new opportunities for clinical prevention trials for prostate cancer. The workshop was divided into three concurrent breakout panels and a fourth joint integrative panel. The workshop addressed multiple key areas identified in the PRG report in the following panels: (1) Molecular Targets and Promising Agents in Clinical Development; (2) Intermediate Endpoint Biomarkers for Prevention Trials; (3) High-Risk Study Populations for Prevention Trials, and (4) Preventive Clinical Trial Designs and Regulatory Issues. Expert panelists were drawn from leading academic, pharmaceutical, and government scientists in basic research and clinical investigation. Key pharmaceutical, biotechnology, academic, and National Institutes of Health scientists presented overviews of their new agents and products in clinical development (representing the next generation of promising agents). Senior FDA physicians from the Center for Drugs and Center for Biologics presented on current standards for new drug and biologic approval for chemoprevention efficacy. Some of the key topics included recent advances in the state of knowledge of promising agents in the clinic based on molecular targets as well as bottlenecks in drug development for pharmaceutical sponsors; strategic modulable biomarkers that can serve as primary endpoints in phase 1/2 trials to assess preventive efficacy; high-risk cohorts with precancer (high-grade prostatic intraepithelial neoplasia) and representative clinical trial designs that are ready for immediate translation into efficient prevention trials, such as Bayesian sequential monitoring for early assessment of biologic activity and factorial designs for assessment of multiagent combinations. Finally, each expert panel generated recommendations for areas of future research emphasizing opportunities and infrastructure needs.

This PhD thesis explored the experiences of children whose parent had cancer and their information needs and behaviour to cope with the challenges they faced as dependent children and care-givers. The aim of the thesis was to understand children’s information experience including their perception of cancer and information culture; information needs, information seeking behaviour, barriers and enablers.

The research used a six-stage process. This study was informed by an extensive literature review and discussions with cancer specialists, psychologists and researchers from United Kingdom, United States, Australia and Malaysia. This study used a three-cycle, eight-step process of Participative Action Research (PAR) with data on the experiences of ten Malay families; ten breast cancer patients and 22 dependent children.

Three instruments were developed for this thesis. First was the Inquiry to Participate Form (InqFE-v.04 and InqFBM-v.02), an instrument to help in selecting potential participants who had dependent children and were willing to participate. The second instrument was a set of three questions that were opened-ended and formed a line of inquiry to obtain children’s cancer experience and information needs. Drawing as a communication and narrative tool was used to encourage children’s responses. The third instrument was a 15-question questionnaire (CQ1) to understand children’s experience and preference in obtaining information. All instruments were translated into Bahasa Malaysia for use in Malaysia.

A total of 205 respondents were collected from the selection process from activities held at the National Cancer Society Malaysia. A total of 30 families volunteered to participate, however, only ten families could commit to the study.

It was found that cancer affected parenting abilities and the challenging experiences identified that a lack of culturally relevant information and the shift in caregiving responsibilities to dependent children necessitated a more assessable, supportive and sensitive information system.

It was also found that children’s understanding of cancer was influenced by their experiences and observations, many of which resulted in misconceptions about cancer, its causes, treatment and preventative measures. It seemed that children participant’s reaction to a health situation triggered their information behaviour. Children had more dimensions of concern and their cancer experience highlighted the myriad challenges they faced. The affects of cancer to children for this ethnic group were not previously documented and an assessment found that the burden of caregiving and the consequences of a lack of information were greater than anticipated. Children’s experiences identified that a lack of children-centric information about the affect of cancer to them and, parental expectations in the face of illness necessitated a more assessable, attractive and sensitive information system.

A synthesis of the data contributed to the development of a “Children’s Reactive Information Seeking Behaviour – An Integrated Model” that seeks to explain the relationship between children participants’ reaction to a health situation and the subsequent processes they undergo to resolve the their state of information need.

The past decade has seen rapid progress in our understanding of cancer, although many mechanisms by which genomic and non-genomic factors contribute and interact to initiate carcinogenesis, drive invasion and metas-tasis, and enable the favourable conditions that facilitate cancer progression remain to be elucidated. Large international initiatives have been created to interrogate whole genomes, including those of many thousands of tumours from patients worldwide, in order to identify specific mutation patterns associated with particular causes of cancer (commonly referred to as 'mutational signatures'). Prime examples of such efforts include the Mutographs study funded through the Cancer Research UK (CRUK) Grand Challenges initiative with a focus on five cancer types, and the Sherlock initiative led by the US National Cancer Institute (NCI) with a focus on lung cancer among never smokers. Such global collabo-rative efforts have driven the science forward to identify and better understand causal factors, and to shed light on new opportunities to prevent cancer. As a result of these efforts, our understanding of the risk of developing cancer that is attributable to moderately and highly penetrant mutations in cancer susceptibility genes across different populations has also improved 1. In addition, genome-wide association studies (GWAS) have led to the identification of single nucleotide polymorphisms that individually confer a small cancer risk but in combination are associated with clinically relevant effects on cancer risk 2-4. These discoveries can provide actionable information by enabling estimation of an individual's risk of developing specific cancers with improved accuracy and, with important caveats, by offering oppor tunities to tailor (or 'personalize') guidance on how to reduce the cancer risk. As the science of cancer genomics evolves and, with it, the potential to inform prevention practices, such as risk-reduction mastectomy for BRCA1 or BRCA2 (BRCA1/2) carriers (primary prevention) and enhanced breast screening with MRI (secondary prevention), the effect that this information can have in reducing preventable cancer deaths globally is important to consider. Nevertheless, with limited exceptions outside of the research setting, the clinical applications of these discoveries are available only in high-income countries (HICs) in which robust health care systems and financing can support the implementation of 'precision pre-vention'. Even in HICs, gross inequities exist in access to and use of clinical cancer genetics services, including tailored risk assessment and risk reduction strategies. Moreover, genomic medicine continues to suffer from Abstract | Despite improvements in the understanding of cancer causation, much remains unknown regarding the mechanisms by which genomic and non-genomic factors initiate carcinogenesis, drive cell invasion and metastasis, and enable cancer to develop. Technological advances have enabled the analysis of whole genomes, comprising thousands of tumours across populations worldwide, with the aim of identifying mutation signatures associated with particular tumour types. Large collaborative efforts have resulted in the identification and improved understanding of causal factors, and have shed light on new opportunities to prevent cancer. In this new era in cancer genomics, discoveries from studies conducted on an international scale can inform evidence-based strategies in cancer control along the cancer care continuum, from prevention to treatment. In this Review, we present the relevant history and emerging frontiers of cancer genetics and genomics from the perspective of global cancer prevention. We highlight the importance of local context in the adoption of new technologies and emergent evidence, with illustrative examples from worldwide. We emphasize the challenges in implementing important genomic findings in clinical settings with disparate resource availability and present a conceptual framework for the translation of such findings into clinical practice, and evidence-based policies in order to maximize the utility for a population.

REVIEWS:
In Medicine, Health Care and Philosophy: http://www.springerlink.com/content/44275q410286r7q1/

ABSTRACT
Medical or health-oriented screening programs are amongst the most debated aspects of health care and public health practices in health care and public health ethics, as well as health policy discussions. In spite of this, most treatments of screening in the research literature restrict themselves to isolated scientific aspects, sometimes complemented by economic analyses or loose speculations regarding policy aspects. At the same time, recent advances in medical genetics and technology, as well as a rapidly growing societal focus on public health concerns, inspires an increase in suggested or recently started screening programs.


This book involves an in-depth analysis of the ethical, political and philosophical issues related to health-oriented screening programs. It explores the considerations that arise when heath care interacts with other societal institutions on a large scale, as is the case with screening: What values may be promoted or compromised by screening programs? What conflicts of values do typically arise – both internally and in relation to the goals of health care, on the one hand, and the goals of public health and the general society, on the other? What aspects of screening are relevant for determining whether it should be undertaken or not and how it should be organised in order to remain defensible? What implications does the ethics of screening have for health care ethics as a whole?

These questions are addressed by applying philosophical methods of conceptual analysis, as well as models and theories from moral and political philosophy, medical ethics, and public health ethics, to a large number of ongoing and proposed screening programs which makes this book the first comprehensive work on the ethics of screening. Analyses and suggestions are made that are of potential interest to health care staff, medical researchers, policy makers and the general public.

CONTENTS
Acknowledgements

Chapter 1: Introduction

1.1 The Wilson and Jungner Criteria
1.2 Point and Plan
1.3 The Concept of Screening

Chapter 2: Why Screening?

2.1 Screening, Treatment and Prevention: Preliminary Remarks
2.2 Health: Life and Well-being
2.2.1 Health and Counselling
2.2.2 The Good of People and of the Population
2.3 Autonomy
2.3.1 Respecting and Promoting Autonomy
2.3.2 Promoting Autonomy through Screening
2.4 Justice
2.5 Summary

Chapter 3: Screening – What, When and Whom?

3.1 Diseases and Groups
3.1.1 Prenatal Screening
3.1.2 Neonatal Screening
3.1.2.1 Reasons for Screening in the Neonatal Period
3.1.2.2 Neonatal Screening and Parental Informed Consent
3.1.2.3 Expanding Neonatal Screening – How Far?
3.1.3 Child and Adolescent Screening
3.1.3.1 Stigmatisation
3.1.3.2 The Child as Decision Maker
3.1.4 Adult Screening

3.2 Testing and Analysis
3.2.1 Safety
3.2.2 Validity
3.2.3 Predictive Value

3.3 Treatments
3.3.1 Abortion as Treatment
3.3.2 Counselling as Treatment

3.4 Summary

Chapter 4: Screening – How?

4.1 Informed Consent
4.2 Counselling
4.2.1 Genetic Counselling as a Template
4.2.2 Expansion: Shared Decision Making

4.3 Funding and Participation
4.4 Summary

Chapter 5: Case Studies

5.1 Non-Invasive Prenatal Diagnosis
5.2 Neonatal Screening for Fragile X
5.3 Mammography Screening
5.4 PSA Screening for Prostate Cancer


Chapter 6: Serving Society or Serving the Patient?

6.1 Summary of the Analysis So far
6.2 The Public Health – Health Care Tension Area
6.3 The Relevance of a Social Science Perspective
6.4 An Institutional Approach to health-related Ethics: A Sketch
6.5 Applying the Institutional Approach: Three Cases
6.5.1 Institutions, Functions and Ethics: Reproductive Care vs. Communicable Disease
6.5.2 Direct to Consumer Genetic Testing: The Limits of Context Relativity
6.5.3 Screening and Justice: The Case Against Allocating Health Care Resources to Screening


6.6 Revisiting the Wilson and Jungner Criteria for Screening
6.7 Closing

Refrences
Index

Prediction of cancer risk is a minor component of current health risk appraisals. Perception of individual cancer risk is poor. A Cancer Risk Index was developed to predict individual cancer risk for cancers accounting for 80% of the cancer burden in the United States. We used group consensus among researchers at the Harvard Medical School and Harvard School of Public Health to identify risk factors as definite, probable and possible causes of cancer. Risk points were allocated according to the strength of the causal association and summed. Population average risk of cancer and cumulative 10-year risk was obtained from SEER data. Individual ranking relative to the population average was determined. The risk index was evaluated for validity using colon cancer incidence in prospective cohort data. The Harvard Cancer Risk Index provides a broad classification of cancer risk. Validation against cohort data shows good agreement for colon cancer. The Harvard Cancer Risk Index offers a sim...

Higher serum levels of the main circulating form of vitamin D, 25-hydroxyvitamin D (25(OH)D), are associated with substantially lower incidence rates of colon, breast, ovarian, renal, pancreatic, aggressive prostate and other cancers. Epidemiological findings combined with newly discovered mechanisms suggest a new model of cancer etiology that accounts for these actions of 25(OH)D and calcium. Its seven phases are disjunction, initiation, natural selection, overgrowth, metastasis, involution, and transition (abbreviated DINOMIT). Vitamin D metabolites prevent disjunction of cells and are beneficial in other phases. It is projected that raising the minimum year-around serum 25(OH)D level to 40 to 60 ng/mL (100-150 nmol/L) would prevent approximately 58,000 new cases of breast cancer and 49,000 new cases of colorectal cancer each year, and three fourths of deaths from these diseases in the United States and Canada, based on observational studies combined with a randomized trial. Such ...

Consumption of fruits and berries has been associated with decreased risk of developing cancer. The most abundant flavonoid constituents of fruits and berries are anthocyans (i.e. anthocyanins, glycosides, and their aglycons, anthocyanidins) that cause intense colouration. In this review, we describe epidemiological evidence hinting at the cancer preventive activity of anthocyan-containing foods in humans, results of chemoprevention studies in rodent models with anthocyans or anthocyan-containing fruit/vegetable extracts, and pharmacological properties of anthocyans. Anthocyanidins have been shown to inhibit malignant cell survival and confound many oncogenic signalling events in the 10(-6)-10(-4) M concentration range. Studies of the pharmacokinetics of anthocyanins after their consumption as single agents, anthocyanin mixtures or berry extracts suggest that anthocyanins reach levels of 10(-8)-10(-7) M in human blood. It is unclear whether such concentrations are sufficient to explain anticarcinogenic effects, and whether anthocyanins exert chemopreventive efficacy themselves, or if they need to undergo hydrolysis to their aglyconic counterparts. The currently available literature provides tantalising hints of the potential usefulness of anthocyans or anthocyan mixtures as cancer chemopreventive interventions. Nevertheless further studies are necessary to help adjudge the propitiousness of their clinical development.

While breast-feeding initiation and duration among US Latina women appear to decrease with acculturation, health care providers in the Greater Cincinnati area have noted lower rates of breast-feeding among even first-generation Latina immigrants. This study's purpose was to identify determinants of breast-feeding for Latina mothers in Cincinnati through qualitative interviews and Spanish Breastfeeding Self-Efficacy Scale ratings. Our findings suggest that, along with similar levels of breast-feeding self-confidence, foreign-born Latina women in the Greater Cincinnati area share similar breast-feeding determinants with the general population. However, characteristics of these determinants and their impact vary because of unique pressures experienced by this community.

Penile cancers are rare primary malignancies located on the glans, foreskin, or shaft of the penis, excluding the urethra. The vast majority of penile cancers are epithelial tumors representing histological subtypes of squamous cell carcinoma (SCC). Most penile SCCs are believed to develop through preinvasive lesions known as penile intraepithelial neoplasia and penile carcinoma in situ.

Penile cancers account for 0.1%–0.3% of all incident cancers (excluding non-melanoma skin cancers) in the United States and other developed countries and up to 1% of all cancers in some countries in sub-Saharan Africa. Annual incidence rates per 100,000 men (world standardized) are typically between 0.3 and 1.0 in developed countries, being 0.5 in the United States. During 2002–2011, SEER data showed rather stable penile cancer rates with no statistically significant changes in incidence or mortality.

Being rare in men younger than 40 years, penile cancers are typically diagnosed among men above age 60. The 5-year relative survival rate after penile cancer was 67% for all stages combined in US patients recorded in SEER registries during 2004–2010, with foreskin cancers having a more favorable prognosis than cancers at other penile sites.

The two most important risk factors for penile cancer are pathological phimosis and infection with high-risk types of human papillomaviruses (HPV), which are both preventable conditions. Non-surgical strategies to reduce the frequency of pathological phimosis need consideration, particularly because rates of newborn circumcision are declining in the United States and elsewhere. Increased awareness among doctors and parents about the importance of non-interference with the physiological foreskin separation process in young boys, and the promotion of safe-sex practices, possibly combined with preadolescent gender-neutral HPV vaccination programs, will likely reduce the frequencies of pathological phimosis and sexually acquired HPV infections and, eventually, reduce the burden of penile cancer at the population level.

Background: It has been reported that noni has multiple health benefits for over 2000 years. In this study, the cancer preventive effects of Tahitian noni® juice (TNJ) at the initiation stage on DMBA-induced mammary tumorigenesis in female SD rats was investigated.

Objective: We took advantage of the DMBA-induced mammary carcinogenic model to study the preventive effects of TNJ at the initiation stage of mammary carcinogenesis in female SD rats by using clinical observation, pathological examination, and 32P-postlabeling assay.

Methods: One hundred and sixty female SD rats were divided into eight groups with 20 rats in each group. Three doses of TNJ or placebo was given to the animals at the age of 35 days until the end of the experiment. When the animals were 55 days old, 25 mg/kg DMBA was fed to the animals in the DMBA group, placebo, and TNJ groups. The 20 rats were kept at age-matched controls. Palpable tumors were examined twice a week after DMBA administration in each group by an experienced professional. The size of tumor was measured by a graduated caliper. A piece of tumor, vascularization area, and mammary glands in the thoracic and abdomen areas of each rat were dissected respectively and fixed in 10% neutral buffered formalin for light microscope examination. The DMBA-DNA adduct formation in mammary tissues was detected by 32P-postlabeling assay.

Results: The tumor latency in TNJ groups was delayed about 60-90 days when compared with positive controls. The number of palpable tumors per group was significantly reduced by 73%, 72% and 80% in 3%, 5%, and 10% TNJ groups respectively when compared with positive controls at the end of 330 days after DMBA administration. The number of palpable tumors in the placebo groups was slightly reduced in the early stage, but much less than that in the TNJ groups. The multiplicity and malignancy of lesions were significantly reduced and the survival rate of animals in the TNJ groups was significantly increased compared with positive controls at different time points. Histological examination showed that the malignancy of lesions in TNJ groups did not show a significant change when compared with that in positive and placebo groups.

Conclusion: In conclusion, this is the first study which indicates that TNJ possesses a cancer preventive effect at the initiation stage of chemical carcinogenesis induced by DMBA in female SD rates.

Cancer chemoprevention is a new approach in cancer prevention, in which chemical agents are used to prevent cancer in normal and/or high-risk populations. Although chemoprevention has shown promise in some epithelial cancers, currently available preventive agents are limited and the agents are costly, generally with side effects. Natural products, such as grape seed, green tea, and certain herbs have demonstrated anti-cancer effects. To find a natural product that can be used in chemoprevention of cancer, we tested Arizona cactus fruit solution, the aqueous extracts of cactus pear, for its anti-cancer effects in cultured cells and in an animal model. Aqueous extracts of cactus pear were used to treat immortalized ovarian and cervical epithelial cells, as well as ovarian, cervical, and bladder cancer cells. Aqueous extracts of cactus pear were used at six concentrations (0, 0.5, 1, 5, 10 or 25%) to treat cells for 1, 3, or 5 days. Growth inhibition, apoptosis induction, and cell cycl...

Abstract This research introduces Sorush Cancer Treatment Ptotocol (SCTP) based on successful cancer treatment methodology which has done by Dr. Somayeh Zaminpira and Dr. Sorush Niknamian in 54 cancer patients in Violet Cancer Institute (VCI), Combining Specific Ketogenic Diet (SKD)- which has 80% saturated fat, 15% Protein with the lowest glutamine and 5% complex-high fiber carbohydrate- and intravenous ozone therapy which has had marvelous results in the treatment of several cancers in human models. The aim of this protocol is to weaken and starve cancer cells, decreasing acidity, increasing the immune system response, decreasing the possibility of metastasis and decreasing the cachexia without any serious side effects in cancer patients. This protocol introduces mega vitamins and minerals plus several supplements based on some tried and true protocols mainly the Budwig and Bill Henderson Protocol (BHP) with serious revisions. The BHP incorporates principal components of the Budwig Diet which was developed in the early 1950s by German chemist Dr. Johanna Budwig (1908-2003). Budwig’s theory is based upon the work of Otto Warburg (1883-1970). Warburg was an earlier Nobel Prize Laureate (1931) for the discovery of the nature and action of the respiratory enzyme, the first of the so-called yellow enzymes, or flavoproteins. Warburg’s scientific efforts produced a large body of work and publications in highly respected journals such as Science (1928, 1956). According to Budwig, Warburg theorized that cellular respiration, like many chemical reactions, was dependent upon substrate availability, specifically a sulphydryl group and an unknown saturated fatty acid, which he failed to identify. According to Dr. S. Zaminpira and Dr. S. Niknamian, Cancer is an Evolutionary Metabolic disease (EMHC) and the main cause of cancer is the Butterfly Effect inside normal cells as a result of increasing the amounts of Reactive Oxygen Species (ROS).

Apigenin, a naturally occurring plant flavone, abundantly present in common fruits and vegetables, is recognized as a bioactive flavonoid shown to possess anti-inflammatory, antioxidant and anticancer properties. Epidemiologic studies suggest that a diet rich in flavones is related to a decreased risk of certain cancers, particularly cancers of the breast, digestive tract, skin, prostate and certain hematological malignancies. It has been suggested that apigenin may be protective in other diseases that are affected by oxidative process, such as cardiovascular and neurological disorders, although more research needs to be conducted in this regard. Human clinical trials examining the effect of supplementation of apigenin on disease prevention have not been conducted, although there is considerable potential for apigenin to be developed as a cancer chemopreventive agent.

Cancer development is a complex process driven by inherited and acquired molecular and cellular alterations. Prevention is the holy grail of cancer elimination, but making this a reality will take a fundamental rethinking and deep understanding of premalignant biology. In this Perspective, we propose a national concerted effort to create a Precancer Atlas (PCA), integrating multi-omics and immunity – basic tenets of the neoplastic process. The biology of neoplasia caused by germline mutations has led to paradigm-changing precision prevention efforts, including: tumor testing for mismatch repair (MMR) deficiency in Lynch syndrome establishing a new paradigm, combinatorial chemoprevention efficacy in familial adenomatous polyposis (FAP), signal of benefit from imaging-based early detection research in high-germline risk for pancreatic neoplasia, elucidating early ontogeny in BRCA1-mutation carriers leading to an international breast cancer prevention trial, and insights into the intricate germline-somatic-immunity interaction landscape. Emerging genetic and pharmacologic (metformin) disruption of mitochondrial (mt) respiration increased autophagy to prevent cancer in a Li-Fraumeni mouse model (biology reproduced in clinical pilot) and revealed profound influences of subtle changes in mt DNA background variation on obesity, aging, and cancer risk. The elaborate communication between the immune system and neoplasia includes an increasingly complex cellular microenvironment and dynamic interactions between host genetics, environmental factors, and microbes in shaping the immune response. Cancer vaccines are in early murine and clinical precancer studies, building on the recent successes of immuno-therapy and HPV vaccine immune prevention. Molecular monitoring in Barrett's esophagus to avoid overdiagnosis/treatment highlights an important PCA theme. Next generation sequencing (NGS) discovered age-related clonal hematopoiesis of indeterminate potential (CHIP). Ultra-deep NGS reports over the past year have redefined the premalignant landscape remarkably identifying tiny clones in the blood of up to 95% of women in their 50s, suggesting that potentially premalignant clones are ubiquitous. Similar data from eyelid skin and peritoneal and uterine lavage fluid provide unprecedented opportunities to dissect the earliest phases of stem/progenitor clonal (and microenvironment) evolution/diversity with new single-cell and liquid biopsy technologies. Cancer mutational signatures reflect exogenous or endogenous processes imprinted over time in precursors. Accelerating the prevention of cancer will require a large-scale, longitudinal effort, leveraging diverse disciplines (from genetics, biochemistry, and immunology to mathematics, computational biology, and engineering), initiatives, technologies, and models in developing an integrated multi-omics and immunity PCA – an immense national resource to interrogate, target, and intercept events that drive oncogenesis.

Summary The major causes of cancer are: 1) smoking, which accounts for 31% of U.S. cancer deaths and 87% of lung cancer deaths; 2) dietary imbalances which account for about another third, e.g., lack of sufficient amounts of dietary fruits and vegetables. 3) chronic infections, mostly in devel- oping countries; and 4) hormonal factors, which are influenced primarily by lifestyle.

NRP/B, a family member of the BTB/Kelch repeat proteins, is implicated in neuronal and cancer development, as well as the regulation of oxidative stress responses in breast and brain cancer. Our previous studies indicate that the NRP/B-BTB/POZ domain is involved in the dimerization of NRP/B and in a complex formation with the tumor suppressor, retinoblastoma protein. Although much evidence supports the potential role of NRP/B as a tumor suppressor, the molecular mechanisms of NRP/B action on E2F transcription factors have not been elucidated. Three-dimensional modeling of NRP/B was used to generate point mutations in the BTB/Kelch domains. Tet-on inducible NRP/B expression was established. The NRP/B deficient breast cancer cell line, MDA-MB-231, was generated using lentiviral shNRP/B to evaluate the effect of NRP/B on cell proliferation, invasion and migration. Immunoprecipitation was performed to verify the interaction of NRP/B with E2F and histone deacetylase (HDAC-1), and the exp...

In humans, genetic variation and dietary factors may alter the biological effects of exposure to 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), one of the major heterocyclic amines generated from cooking meats at high temperatures that has carcinogenic potential through the formation of DNA adducts. Previously, we reported grilled red meat consumption associated with PhIP-DNA adduct levels in human prostate. In this study, we expanded our investigation to estimate the associations between beverage consumption and PhIP-DNA adduct levels in prostate for 391 prostate cancer cases. Of the 15 beverages analyzed, red wine consumption had the strongest association with PhIP-DNA adduct levels showing an inverse correlation in both tumor (P = 0.006) and nontumor (P = 0.002) prostate cells. Red wine consumption was significantly lower in African American compared with white cases, but PhIP-DNA adduct levels in prostate did not vary by race. In African Americans compared with whites, however, associations between red wine consumption and PhIP-DNA adduct levels were not as strong as associations with specific (e.g., SULT1A1 and UGT1A10 genotypes) and nonspecific (e.g., African ancestry) genetic variation. In a multivariable model, the covariate for red wine consumption explained a comparable percentage (13%-16%) of the variation in PhIP-DNA adduct levels in prostate across the two racial groups, but the aforementioned genetic factors explained 33% of the PhIP-DNA adduct variation in African American cases, whereas only 19% of the PhIP-DNA adduct variation in whites. We conclude that red wine consumption may counteract biological effects of PhIP exposure in human prostate, but genetic factors may play an even larger role, particularly in African Americans.