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This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.
Head and neck cancer (HNC) is a collective name for heterogeneous tumors located in the head and neck regions for which smoking, alcohol and human papillomavirus (HPV) are documented risk factors. The survival of HNC patients has only improved marginally during the last decade. The most important prognostic factors are tumor size, local spread and distant metastases, tumor node metastasis (TNM) staging. Prognostic biomarkers are needed as a complement to TNM staging. The aim for this thesis was to investigate rapid and low cost blood based biomarkers which could indicate the risk of HNC, recurrence of the disease or the survival of HNC patients. Furthermore, the aim was to examine how cigarette smoking influences the levels of biomarkers. In paper I, a possible role of plasma cytokines or proteins associated with immune response or inflammation, as biomarkers for the survival of HNC patients was investigated. Higher levels of C-reactive protein (CRP) and tumor necrosis factor alpha (TNF-α) were detected in plasma of the patients compared with the levels in the controls. The elevated levels of these two biomarkers detected in patients were associated with decreased survival. In paper II, the influence of 45 single nucleotide polymorphisms (SNPs) located in 41 genes associated with cell cycle progression, cell death, DNA repair or immune response on cancer risk, tumor recurrence and survival in HNC patients were investigated. SNPs in immune response genes were associated with risk for HNC, an elevated risk for recurrence and a decreased survival in HNC patients. In paper III, the influence of cigarette smoking on levels of inflammatory cells, proteins or cytokines/chemokines, microRNAs (miRNAs) and SNPs was analysed in healthy smokers and non-smokers. Higher levels of total white blood cells (WBCs), neutrophils, monocytes, lymphocytes, neutrophil to lymphocyte ratio (NLR), CRP, monocyte chemoattractant protein- 1 (MCP-1) and interferon gamma (IFN-γ) were detected in smokers compared to non-smokers and indicate an inflammatory response. Also, a lower level of oncomiRNA miR-21was detected in smokers. This alteration, in combination with the elevated levels of IFN-γ in smokers could be a protective response to cigarette smoke. The higher levels of IFN-γ in smokers compared to non-smokers were however only detected in individuals with SNP rs2069705 genotype AG/GG. This indicates a genetic association of the levels of IFN-γ. In paper IV, the separate effects of cigarette smoking and HNC on inflammatory or immune biomarkers and the impact of high risk human papillomavirus, age and gender were investigated. Comparisons of circulating levels of WBCs and its subpopulations, plasma proteins or cytokines/chemokines between smoking and non-smoking patients, smoking and non-smoking controls and between the patient and control groups were analysed. Smoking had highest impact on elevated levels of WBCs, IFN-γ and MCP-1, and HNC had highest impact on elevated levels of neutrophils, monocytes, NLR, CRP, macrophage inflammatory protein 1 beta and TNF-α. In conclusion, host immune response associated parameters could be suitable as biomarkers for the risk of HNC, risk of recurrence or in predicting survival of HNC patients. This thesis show that HNC are associated with systemic inflammatory response and upregulated CRP and TNF-α is related to shorter survival in HNC patients. Additionally, SNPs in immune response genes such as rs1800629 in the TNF-α gene indicates a risk for HNC or an elevated risk for recurrence and a decreased survival in HNC patients. These rapid and low cost blood based biomarkers could be used in combination or as a supplement to established biomarkers in the clinic for a more personalized treatment modality. Huvud- och halscancer (HH-cancer) innefattar tumörer belägna i huvud och halsområdet. Tobaksrökning ökar risken dramatiskt för olika sjukdomar. Knappt hälften av rökande patienter dör i de av rökning orsakade sjukdomarna. Cancer är orsaken till en tredjedel av de rökrelaterade dödsfallen av vilka HH-cancer är en. En andel av patienterna med HH-cancer dör på grund av att tumören varit för stor redan vid diagnos eller att tumören har spridit sig till övriga delar av kroppen. Men för många patienter är det mycket oklart vad som bestämmer behandlingsresultatet. Tumörerna är till synes lika och behandlingen standardiserad. Målet med denna doktorsavhandling var att undersöka billiga och lättillgängliga biologiska markörer som kan indikera risk för att drabbas av HH-cancer eller om dessa markörer kan förutspå behandlingsresultat och överlevnad hos de drabbade patienterna. Dessutom undersöktes hur cigarettrökning påverkade nivåerna av markörerna. I studie I, undersöktes om molekyler i blodet (biomarkörer), förknippade med immunförsvaret, kunde förutsäga överlevnaden hos HH-cancerpatienter. I jämförelse med friska individer sågs högre nivåer av molekylerna TNF-α och CRP hos patienterna och dessa förhöjningar var relaterade till förkortad överlevnad hos patienterna. I studie II, var målet att undersöka om variationer i gener, förknippade med immunförsvaret, celldelning, celldöd eller enzymer som reparerar skadat DNA, kunde påverka risk och prognos för HH-cancer. Resultatet visade framför allt att små ärftliga variationer i gener som reglerar immunförsvaret kunde påverkade risk för HH-cancer, risk för återfall i sjukdomen samt överlevnaden hos patienterna. I studie III, jämfördes inflammatoriska och immunförknippade biomarkörer som kunde påverkas av cigarettrökning mellan friska rökare och friska icke-rökare. Rökarna hade en högre inflammatorisk aktivitet med högre nivåer av totalt antal vita blodkroppar och tre av dess olika undergrupper (neutrofiler, monocyter och lymfocyter) samt av biomarköerna CRP, MCP-1 och IFN-γ. De funna lägre nivåerna av den cancerförknippade biomarkören miR-21 och högre nivåer av den förmodat skyddande biomarkören IFN-γ hos rökarna, kan vara ett uttryck för kroppens försvar mot den cancerframkallade cigarettröken. Ärftliga faktorer tycks kunna påverka de högre nivåerna av IFN-γ hos rökarna, eftersom ökningen endast fanns i en grupp individer med viss typ av genetisk uppsättning. Eftersom både rökning och HH-cancer ger upphov till inflammation, undersöktes i studie IV hur dessa var för sig påverkade nivåerna av inflammatoriska biomarkörer. Detta för en bättre förståelse hur immunförsvaret reagerar på rökning och HH-cancer. Jämförelser av inflammatoriska markörer från rökande och icke-rökande patienter, och rökande och ickerökande friska individer genomfördes. Rökning hade störst påverkan på de högre nivåerna av totalt antal vita blodkroppar och signalmolekylerna MCP-1 och IFN-γ. HH-cancer hade störst påverkan på högre nivåerna av neutrofiler, monocyter, kvoten mellan neutrofiler och lymfocyter, CRP, MIP-1b och TNF-α. Uppkomsten av HH-cancer, behandlingsresultat och överlevnad bland patienterna kan antas inte bara bero på tumörens egenskaper, utan även på värdfaktorer hos patienten. Dessa kan vara ärftliga, eller bero på reglering av gener eller tumörens omgivning av t.ex. immunceller och inflammatoriska molekyler och hur dessa samverkar med miljöfaktorer som tobaksrökning. I denna avhandling presenteras biomarkörer som kan bidra med information om risk och prognos för HH-cancer samt hur tobaksrökning påverkar dessa markörer.
Without early detection, oral cancer is deadly. Protect your patients by applying the latest clinical interventions. Rates of new oral cancer cases continue to increase and mortality rates remain alarmingly high. Oral cancer may be preceded by clinically identifiable precancerous changes in the oral mucosa, which offer a therapeutic window of opportunity to intervene and halt disease progression to carcinoma development. Written and edited by prominent researchers in the field, Oral Precancer: Reviews current scientific research on precancer conditions of the oral cavity providing evidence-based analysis of the nature and behavior of potentially malignant and deforming oral diseases Explains the principles of prevention, diagnosis and management of potentially malignant disorders of the oral cavity Details a practical and reliable interventional treatment strategy to facilitate early diagnosis and effective treatment of both precancer and early invasive carcinoma Contains a chapter devoted to illustrative case histories, high-quality, color, clinical photos, reference sections in each chapter listing relevant review articles, and more From start to finish, Oral Precancer offers undergraduate students, clinicians, and professors an invaluable resource to minimise the morbidity and mortality of this most significant and life threatening of oral conditions.
A working group of sixteen experts from seven countries re-evaluated the evidence of the carcinogenicity of betel-quid and areca-nut chewing and some areca-nut related nitrosamines. Betel-quid and areca-nut chewing are widely practised in many parts of Asia and in Asian-migrant communities elsewhere in the world. There are hundreds of millions of users worldwide. They evaluated betel quid with tobacco as carcinogenic to humans (Group 1) on the basis of sufficient evidence of an increased risk of cancer of the oral cavity, pharynx and oesophagus. The working group reviewed epidemiological studies of human cancer, mainly studies from India, Pakistan and Taiwan (China). Studies on betel quid with tobacco and areca nut with tobacco in experimental animals now also provide sufficient evidence of carcinogenicity. The working group also evaluated betel quid without tobacco as carcinogenic to humans (Group 1), on the basis of sufficient evidence of an increased risk of oral cancer. Studies on betel quid without tobacco and areca nut without tobacco in experimental animals now also provide sufficient evidence of carcinogenicity. Areca nut, a common ingredient of betel quid and many different chewing preparations, including those available commercially, has been observed to cause oral submucous fibrosis
This comprehensive multidisciplinary book examines all aspects of cancers of the mouth and oropharynx with the aim of equipping advanced students and practitioners in the early stages of specialist training with an up-to-date guide and reference. A multinational team of authors – all experts in the field of oral oncology – provide illuminating contributions on the full range of relevant topics: epidemiology, risk factors, clinical features, staging and prognostic factors, pathology, diagnostic techniques, disease prevention, surgery, radiotherapy, and chemotherapy. Molecular biology, molecular targeted therapies for advanced cases, and future diagnostic and prognostic applications of new technologies also receive careful attention. In providing a wealth of essential information and guidance in a practical format, the book will be a superb asset for senior graduate students in dentistry and specialist trainees in head and neck oncology. It will also be of high value for the many physicians, surgeons, pathologists, dentists, and specialists involved in the prevention, diagnosis, and management of squamous cell carcinomas of the oral cavity and oropharynx.
Biomarkers are of critical medical importance for oncologists, allowing them to predict and detect disease and to determine the best course of action for cancer patient care. Prognostic markers are used to evaluate a patient’s outcome and cancer recurrence probability after initial interventions such as surgery or drug treatments and, hence, to select follow-up and further treatment strategies. On the other hand, predictive markers are increasingly being used to evaluate the probability of benefit from clinical intervention(s), driving personalized medicine. Evolving technologies and the increasing availability of “multiomics” data are leading to the selection of numerous potential biomarkers, based on DNA, RNA, miRNA, protein, and metabolic alterations within cancer cells or tumor microenvironment, that may be combined with clinical and pathological data to greatly improve the prediction of both cancer progression and therapeutic treatment responses. However, in recent years, few biomarkers have progressed from discovery to become validated tools to be used in clinical practice. This Special Issue comprises eight review articles and five original studies on novel potential prognostic and predictive markers for different cancer types.
This Surgeon General's report returns to the topic of the health effects of involuntary exposure to tobacco smoke. The last comprehensive review of this evidence by the Department of Health and Human Services (DHHS) was in the 1986 Surgeon General's report, The Health Consequences of Involuntary Smoking, published 20 years ago this year. This new report updates the evidence of the harmful effects of involuntary exposure to tobacco smoke. This large body of research findings is captured in an accompanying dynamic database that profiles key epidemiologic findings, and allows the evidence on health effects of exposure to tobacco smoke to be synthesized and updated (following the format of the 2004 report, The Health Consequences of Smoking). The database enables users to explore the data and studies supporting the conclusions in the report. The database is available on the Web site of the Centers for Disease Control and Prevention (CDC) at http://www.cdc.gov/tobacco.
This eighty-ninth volume of the IARC Monographs is the third and last of a series on tobacco-related agents. Volume 83 reported on the carcinogenicity of tobacco smoke and involuntary smoking (second-hand smoke or environmental tobacco smoke) (IARC 2004a). Volume 85 summarized the evidence on the carcinogenic risk of chewing betel quid with and without tobacco (IARC 2004b). That volume explored the variety of products chewed in South Asia and other parts of the word that contain areca nut in combination with other ingredients, often including tobacco. In this eighty-ninth volume, the carcinogenic risks associated with the use of smokeless tobacco, including chewing tobacco and snuff, are considered in a first monograph. The second monograph reviews some tobacco-specific nitrosamines. These agents were evaluated earlier in Volume 37 of the Monographs (IARC 1985) and information gathered since that time has been summarized and evaluated.
The second report from the U.S. Surgeon General devoted to women and smoking. Includes executive summary, chapter conclusions, full text chapters, and references.