Breast cancer causes

Breast cancer remains one of the most prevalent forms of cancer affecting women worldwide. While significant progress has been made in understanding and treating this disease, there is still much to learn about its causes. Breast cancer is a multifaceted condition influenced by a range of factors, including genetics, lifestyle choices, environmental exposures, and hormonal imbalances. In this post, we will delve into the complex causes of breast cancer, shedding light on the various factors that contribute to its development.

1. Genetic Predisposition: Certain genetic mutations, such as BRCA1 and BRCA2 gene mutations, can significantly increase the risk of developing breast cancer. However, it's essential to note that only a small percentage of breast cancer cases are directly attributed to inherited genetic factors. Most cases are believed to result from a combination of genetic predisposition and environmental influences.

2. 
   

3. Hormonal Factors: Hormonal imbalances play a pivotal role in breast cancer development. Women with early onset of menstruation, late menopause, or a prolonged history of hormone replacement therapy (HRT) are at a higher risk. Estrogen, a hormone produced by the ovaries, has been linked to the growth of certain types of breast cancer. Additionally, the use of oral contraceptives and exposure to high levels of estrogen over an extended period may slightly increase the risk.

4. 
   

5. Lifestyle Choices: Unhealthy lifestyle choices can contribute to breast cancer risk. Lack of physical activity, a sedentary lifestyle, and being overweight or obese have been associated with an increased likelihood of developing breast cancer. Additionally, excessive alcohol consumption has been linked to higher breast cancer risk, making moderation essential.

6. 
   

7. Environmental Factors: Exposure to certain environmental factors may also play a role in breast cancer development. These include ionizing radiation, such as from medical imaging tests like mammograms, and environmental pollutants like pesticides, industrial chemicals, and air pollution. While the impact of these factors is still being researched, it is crucial to minimize exposure to potential carcinogens where possible.

8. 
   

9. Family History: A family history of breast cancer can elevate an individual's risk, especially if a first-degree relative (parent, sibling, or child) has been diagnosed. Although most cases of breast cancer occur in individuals without a family history, it is important for those with a history to be aware of their increased risk and consider early screening and genetic counseling.

Keep quit smoking!

Cigarette smoking is a chronic and relapsing addictive trait harmful to public health. According to statistics from the World Health Organization (WHO 2013), smoking kills approximately six million people worldwide each year, with more than five million of those deaths resulting from direct cigarette smoking and more than 600,000 from secondary or passive smoke exposure. The number of smokingrelated deaths is expected to increase to more than eight million annually by 2030 if the current pattern of smoking continues unabated (Eriksen et al. 2013). 

The main deadly effect of smoking is a variety of severe diseases, such as cancers and psychiatric disorders. More than 25% of all cancer deaths can be attributed to smoking, especially those from lung cancer, for which about 80% are caused by tobacco smoking (CDC 2010). Moreover, multiple lines of evidence show that a large amount of the morbidity and premature deaths in schizophrenia patients can be attributed to smoking-related diseases (Brady et al. 1993; Crump et al. 2013). Extremely high healthcare expenditures are associated with smoking-related illnesses worldwide. It is estimated that globally, more than US$500 billion in economic damage is caused annually by tobacco smoking. In the United States, the total of public and private healthcare costs related to tobacco smoking were estimated to be about US$170 billion each year (Ekpu and Brown 2015), and in the United Kingdom, the direct expenditures of the British National Health Service (NHS) attributable to smoking have been estimated at between £2.7 billion and £5.2 billion, about 5% of the total annual NHS budget (Allender et al. 2009; Callum et al. 2011; Ekpu and Brown 2015). 

Furthermore, in some developing countries, the economic damage from smoking has substantially increased in the past decade. For example, in China, about USD 6.2 billion was spent for direct smoking-attributed healthcare costs and USD 22.7 billion for indirect economic costs in 2008, the direct and indirect costs were rose by 154% and 376%, respectively, compared with the costs in 2000 (Yang et al. 2011). Prevention of smoking initiation and promotion of smoking cessation, coupled with regulations and legislation, remain to be effective ways to control tobacco use (Koplan and Eriksen 2015; Yang et al. 2015; Zhu et al. 2012). Although abundant benefits accrue from smoking cessation, the cessation rate is still low in many countries. 

A variety of factors have been proposed as causes of the difficulties of obtaining and maintaining smoking cessation, including psychological, genetic, pharmacologic, and social factors (Li and Burmeister 2009). One of the most important factors is nicotine dependence (ND), which is the main contributor to the persistence of smoking (Gunby 1988). Growing evidence (Baker et al. 2007; Branstetter et al. 2015; Branstetter and Muscat 2013; Mercincavage et al. 2013) has shown that time to the first cigarette of the day, one of the best indicators of ND (Fagerstrom 2003), is associated with the likelihood of smoking relapse and with withdrawal symptoms, nicotine intake, tobacco-related carcinogen exposure, and cancer risk. Furthermore, many twin and family studies have shown consistently that the risk of ND is heritable, with an average heritability of 0.59 in male and 0.46 in female smokers (see Chap. 3 for details).

 In light of the severe impact of smoking on the individual and society, many studies have examined the epidemic pattern of smoking and its associated diseases. To help control the trend to more smoking, a battery of effective systemic and scientific measures should be implemented with the hope of assisting in the implementation of current cessation methods and accommodating the specific conditions of particular countries in order to reduce the demand for tobacco. In the following sections, we briefly review the prevalence of smoking in the world and summarize the harmful influence of smoking on people’s health. 

 The Global Prevalence of Smoking There are about one billion cigarette smokers worldwide (Mackay et  al. 2013), amounting to approximately 30% of men and 7% of women (Gowing et al. 2015). Smoking rates differ widely between populations across the world (Fig.  1.1). A series of factors impact the prevalence of smoking and trends in prevalence, such as individuals’ educational level, national economic development, and tobacco control policies. In developed countries, such as the United States and the United Kingdom,  the prevalence of smoking increased sharply in the earlier twentieth century, partly as a result of the low prices of cigarettes. The prevalence of smoking has been estimated to have been 37% among men and 25% among women. However, because of better public awareness of smoking as a hazard and the implementation of stringent legislation against smoking in the Western European countries and the United States, smoking prevalence has been greatly reduced. From 1990 to 2009, tobacco consumption in Western Europe declined by about 26% (Brathwaite et al. 2015). In the United States, the proportion of smokers declined from 20.9% in 2005 to 15.1% in 2015 (Jamal 2016). In contrast, the prevalence of smoking has increased remarkably in low- and middle-income countries (Benowitz 2008). 

During the years 1990 to 2009, tobacco consumption increased by 57% in Africa and some Middle Eastern countries (Brathwaite et al. 2015). Throughout the world, more than 80% of smokers now reside in poor countries, especially in Eastern and Southeastern Asia and Africa (Stewart 2014). For example, in China, cigarette consumption in 2016 is approximately twofold higher than it was in 1998 (Gilmore et al. 2015). As the largest user of tobacco worldwide, the smoking rate in China remains high. The nation consumes more than 30% of the world’s cigarettes, and two-thirds of men smoke (Chen et al. 2015; Li et al. 2011; Yang 2014). In China, many smokers do not fully understand the damaging consequences of smoking, and social conventions have linked smoking with a positive image (Yang et al. 2015; Zhang et al. 2011), which plays an important role in preventing smoking cessation. The prevalence of smoking in men and women differs greatly in different regions of the world (Gowing et al. 2015). 

Globally, smoking prevalence in men is more than four times that in women (West 2017). In developing countries, the prevalence of smoking in men is much higher than that in women. For example, there was an estimated prevalence ratio of 22 to 1 for men to women in China (Li et al. 2011). In Eastern, Southeastern, and Western Asia, the prevalence is estimated to be approximately 40% in men, whereas only approximately 4% of women smoke (West 2017). One reason for this phenomenon is that female smoking is considered socially unacceptable (Giovino et al. 2012; Jung-Choi et al. 2012). The difference is much less in most developed countries (West 2017). For example, the prevalence of tobacco smoking among women in the United States is estimated to be 13.6%, which is close to the prevalence of 16.7% among men (Jamal 2016). Moreover, the total number of male smokers in the leading three tobacco-using countries, e.g., China, India, and Indonesia, accounted for 51.4% of the world’s male smokers in 2015, whereas the United States, China, and India were the leading three countries in the total number of female smokers, yet they accounted for only 27.3% of the world’s female smokers (Ali and Hay 2017), suggesting that the epidemic of smoking is less geographically concentrated for women than for men.

The Stages of Change

 You can't make a change until you are ready to change. 
Sometimes, the ''getting ready" takes a long time. 
Let's look at this process of changing. 
A year after you started smoking, you probably didn't think you needed to quit. 
Young smokers often say:
 "Cancer and emphysema are a long way off." 
"Most of my friends smoke."
 "Smoking makes me feel older and more mature."
 "My parents smoke and they don't care if I do."
 "My parents don't smoke and they don't want me to."
"Smoking is a cheap buzz." 
"Who cares?" 
Were some of these your reasons for smoking when you were young? 
As the years passed and you matured, quitting became more important. 
You became more responsible. You didn't have the endurance you once had. Many of your friends quit smoking. Your doctor advised you to quit. And gradually, you began to consider quitting smoking. Consider, yes; quit, no. 
You were thinking about it, wondering about it, maybe even asking for information about itbut you weren't ready to quit just yet.
 That first stage, where smokers refuse to quit or don't see any need to quit, is called the "Precontemplation Stage." 
The second stage, where they think about quitting but aren't quite ready, is called the "Contemplation Stage."
 About 40 percent of all smokers are in each of these two stages at any time. 
The other 20 percent have decided to quit; they are in the "Preparation Stage." 
Which stage are you in today? If you are in the Precontemplation Stage but know you need to quit "some day," Quit and Stay Quit or the first Clean and Free workbook ("Get Ready") can help you make progress. 
Few people in Precontemplation will read this far, so you probably aren't in that stage. People in Contemplation are ambivalent; they want to quit, and they don't want to quit. They know they'd be better off if they quit, but they don't feel ready. 
They anticipate failing and expect to suffer, so they hesitate. They want to be convinced (sort of), but they also wish people would leave them alone.
Are you in the Contemplation Stage? 
If you are barely past Precontemplation, Quit and Stay Quit or the second Clean and Free workbook ("Get Set") will help you make faster progress. 
If you are further along than that, the information in the next section, "Getting Ready to Get Ready," will help you move ahead. People in the Preparation Stage have resolved their ambivalence about quitting. 
They are ready to quit; they want suggestions and solutions to their problems. They're ready to go. Are you in the Preparation Stage? 
If you are, you can find helpful information in Quit and Stay Quit, in the third Clean and Free workbook ("Go"), or in the Countdown to Quit Cards. 
Getting Ready to Get Ready People have probably been telling you that you need to quit smoking for some time. 
In your life, how many different people have advised you or told you to quit smoking?
 Most smokers say "hundreds," and name their relatives and family members, their friends, their co-workers, their doctor, and the surgeon general. 
Who are some of the people that come to your mind? 
Over the years, each of these people (and many others) have given you their reasons for quitting smoking. These reasons may or may not have also been your reasons. 
You might quit for someone else's reasons for a little while, but the chances are good that you would start smoking again if they were not your reasons too. 
Why did those people want you to quit smoking? 
Were any of these reasons your reasons to quit smoking too? 
The problem is that since you have heard these reasons over and over again, you have begun to think that they are your reasons.
 Some of them make perfect sense; we call these reasons logical reasonssuch as "To avoid getting lung cancer" or "To save money." 
These are excellent reasons to quit smoking, but you have known for years that smoking causes lung cancer and that it costs you money. These logical reasons were not enough to get you to quit smoking, because they were not personal reasons. 
You will only be able to quit smoking and recover from your dependence on nicotine and tobacco when you are doing it for your own, very personal reasons. Take a few moments to answer these questions: 
1. How would you be better off if you quit smoking?
 2. If you quit smoking, you might live an extra ten years; what would you want to do with those years? 3. What sort of impression do you want to make on the people you love? 
4.What kind of person are you? 5. What kind of person do you want to become?
5.  What would you be able to accomplish as a nonsmoker that you cannot accomplish as a smoker? 
6. Would you like yourself better if you could quit smoking? 
7. Besides quitting smoking, what other changes do you want to make in your life? 
8. Are you willing to ask yourself these questions?
Follow us for more information!

Lung cancer and air pollution

Air pollution episodes that occurred in the middle of the twentieth century were responsible for deaths that ranged from a few excess deaths to several thousand, depending to a large extent on the size of the population exposed. In the most well-known of these episodes, the London Fog of 1952, an estimated 3,500 excess deaths occurred over a period of a few days, with possibly several thousand more in the ensuing weeks. 

While the pollution mix in London during this fog was complex, it is likely that particulate air pollution was largely responsible for the excess deaths. These episodes demonstrate that exposure to urban air pollution can, in extreme cases, cause death. Epidemiological Studies Several studies have confirmed associations between increased PM concentrations and increased cardiopulmonary mortality. They found that for each 10 mg/m3 increase in PM10, mortality increased by a fraction of a percent (2, 3, 4, 5, 6, 7, 8, 9). In spite of the small effect of PM increases, the public health impact could be large if seen across broad populations. Thus, increasing ambient PM concentrations represent a fairly significant risk in terms of mortality. Similar studies have established other health dangers that are associated with increased PM, including increased for lung cancer and heart disease. The American Cancer Society Air Pollution Study was initiated by C. Arden Pope and colleagues based upon a cohort of 1.2 million individuals enrolled in the fall of 1982.1 A subgroup of 552,138 adults lived in 151 United States metropolitan areas that could be matched to air pollution data collected under the auspices of the Environmental Protection Agency (EPA).

 The relationships of sulfate and particulate matter air pollution to all-cause, lung cancer, and cardiopulmonary mortality were examined in this subgroup using multivariate analysis controlling for smoking, education, and other risk factors up to 1989. Deaths due to air pollution were 15%–17% more prevalent in the most polluted communities as compared to the least polluted ones. In a follow-up of this cohort until 1998, when 22.5% of the cohort died, PM2.5 data were collected and estimated with mortality risk ratios estimated by a Cox proportional hazard regression model. Significant mortality associations were found for each 10 mg/m3 increase in PM2.5 for ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest, and in nonsmokers, pneumonia and influenza.2 Each 10 mg/m3 elevation in fine particulate air pollution was associated with approximately a 4%, 6%, and 8% increased risk of all-cause, cardiopulmonary, and lung cancer mortality, respectively3 (see Figure 2.3). Since PM has fallen over the past two decades, Pope and colleagues compiled data on life expectancy, socioeconomic status, and demographic characteristics for fifty-one U.S. metropolitan areas with matching data on fine particulate air pollution for the late 1970s and early 1980s and the late 1990s and early 2000s.4 They found that a decrease of 10 mg/m3 in PM2.5 was associated with an estimated increase in mean (SE) life expectancy of 0.610.20 year (p ¼ 0.004). Reductions in air pollution accounted for as much as 15% of the overall increase in life expectancy in the study areas.

At the same time the American Cancer Society cohort was being assembled, investigators at the Harvard School of Public Health established a longitudinal study on the health effects of air pollution in six cities. The Harvard Six Cities Study was a sixteen-year prospective cohort study of 8,111 adults living in the northeastern and midwestern United States beginning in the 1970s. The study reported that PM2.5 was positively associated with overall mortality, cardiopulmonary causes, and lung cancer. 

Lung cancer is the most common cause of cancer death in the United States, with more than 200,000 new cases and 160,000 annual deaths. It is estimated that lung cancer causes about 1.2 million deaths annually worldwide. Approximately 90% of lung cancer cases are due to cigarette smoking in populations with prolonged cigarette use. The strongest determinant of lung cancer in smokers is duration of smoking; risk also increases with the number of cigarettes smoked. Smoking causes lung cancer in both men and women. 

Cessation of smoking at any age avoids the further increase in risk of lung cancer caused by continued smoking. However, the risk of ex-smokers for lung cancer remains elevated for years after cessation, compared to the risk of never smokers. The impact of smoking on lung cancer in the twentieth century in the United States can be seen in Figure 5.5. Cigarette smoking was rare in the early part of the twentieth century, as was lung cancer. Smoking increased due to mass production of cigarettes, increased advertising, and pervasive use of cigarettes by military personnel during World War I. During the twentieth century, smoking rose first among males and then with a twenty- to thirty-year delay among females. Cigarette smoking peaked in the 1950s and 1960s and began to decline after the wave of studies documenting its risks appeared and the publication of the first Surgeon General’s report in 1964. Mortality due to lung cancer in men can be seen to follow the curve for smoking prevalence by about thirty years, beginning to decrease in the mid-1990s. Lung cancer became the most common cause of cancer death in U.S. women, surpassing breast cancer in 1988.

The range of total carcinogen exposure in smokers is approximately 1.4–2.2 mg/cigarette, which can be compared to the current sales-weighted average nicotine delivery of about 0.8 mg/cigarette. Some of the strongest carcinogens, such as polycyclic aromatic hydrocarbons (PAH), N-nitrosamines, and aromatic amines, occur in the lowest amounts, while some of the weaker carcinogens (such as acetaldehyde and isoprene) occur in the highest amounts. PAH are incomplete combustion products that were first identified as carcinogenic constituents of coal tar.49 They occur as mixtures in tars, soots, broiled foods, automobile engine exhaust and other materials generated by incomplete combustion. N-nitrosamines are a large class of carcinogens with demonstrated activity in at least thirty animal species. Considerable evidence favors PAH and N-nitrosamines as major etiological factors in lung cancer. PAH are strong, locally acting carcinogens, and tobacco smoke fractions enriched in these compounds are carcinogenic. PAH-DNA adducts have been detected in the human lung, and mutations in the TP53 tumor suppressor gene isolated from lung tumors are similar to those produced in vitro by PAH diol epoxide metabolites and in cell culture by Benzo(a)pyrene.  Persistent DNA adducts can cause miscoding during replication when DNA polymerase enzymes process them incorrectly.52 There is considerable specificity in the relationship between specific DNA adducts caused by cigarette smoke carcinogens and the types of mutations which they cause. G to T and G to A mutations are frequently observed.53 Mutations have been frequently observed in the K-ras oncogene in smokers with lung cancer and in the TP53 tumor suppressor gene in a variety of cigarette smoke-induced cancers. The cancer-causing role of mutations in these genes has been firmly established in animal studies. The K-ras and TP53 mutations observed in lung cancer in smokers appear to reflect DNA damage by metabolically activated PAH, although acrolein can also cause p53 adducts in lung cancer hot spots, and there is far more acrolein in cigarette smoke than PAH. In addition, numerous cytogenetic changes have been observed in lung cancer, and chromosome damage throughout the aerodigestive tract is strongly linked with cigarette smoke exposure. Gene mutations can cause loss of normal cellular growth control functions via a complex process of signal transduction pathways, ultimately resulting in cellular proliferation and cancer. The most commonly mutated gene found in human cancers is the TP53 tumor suppresser gene.51 Among the tobacco related cancers, the most extensive database exists for lung cancer, in which mutations in the TP53 gene have been detected in approximately 70% of tumors. In smokers, the mutations are focused in the central part of the gene, which is the DNA binding region that is essential for its function. Smokers have mutations in hot spots of this region that are a characteristic signature, for example, codons 157, 176, 248, 249, 273. Exposure of lung fibroblasts or epithelial cells in vitro to activated PAH results in DNA adducts on the same codons.

Smoking Cessation

 Mark Twain stated, ‘‘Giving up smoking is easy. I’ve done it a hundred times.’’ In 2008 it was noted that social networks amplify smoking cessation, with one’s spouse, sibling, friend, or coworker, in descending order, influencing a smoker’s possibility of smoking cessation, and that smokers over time are increasingly marginalized socially.  The Lung Health Study was a randomized clinical trial of smoking cessation and inhaled bronchodilator (ipratropium) therapy in smokers 35 to 60 years of age who were in good health but had evidence of mild to moderate airway obstruction.  They enrolled 5,887 smokers at ten clinical centers, with an intervention group of twelve smoking cessation sessions and nicotine gum; the intervention group had smaller declines in FEV1 than the control group. At five years, 21.7% of special intervention participants had stopped smoking since study entry, compared with 5.4% of usual care participants. At 14.5 years’ follow-up, there was a lower mortality in the intervention group, with the hazard ratio for usual care 1.18 (95% CI 1.02–1.37), and differences in death rates were greatest for lung cancer and cardiovascular disease. Tobacco cessation programs have difficulty exceeding sustained quit rates above 15%, which is the typical success rate of those attempting to stop ‘‘cold turkey.’’ Treatment of tobacco dependence with nicotine gum and patches may double this rate.   Nicotine is the addictive substance in tobacco, and cigarette manufacturers are very sophisticated at mixing tobacco blends to achieve maximal nicotine delivery via the cigarette. Nicotine has a rather short half-life of about 20 minutes, requiring another cigarette to be smoked to keep blood levels of nicotine at sufficient levels to prevent withdrawal symptoms. Smoking provides an immediate delivery of nicotine to the blood and to the brain, where nicotinic acetylcholine receptors are critical for the development of dependence. The highest levels of these receptors, the a4b2, are in the reward center of the brain. A treatment strategy is to have a competitor for this receptor that doesn’t or only partially activates it; varenicline, a plant alkaloid cytisine, is such a drug.  This drug had a higher sustained quit rate in comparative clinical trials with bupropion or nicotine-replacement therapy.

SO2 Health Effects 

In several studies, SO2 exposure has been linked with increased mortality due to all causes and to lung cancer specifically. For example, the study of the American Cancer Society cohort that reported the link between mortality and criteria air pollutants, the relative risk (RR) of all-cause mortality from sulfate exposure was 1.25 (95% CI [confidence interval] 1.13–1.37) and was higher at the county level with an RR of 1.5.2 The National Mortality and Morbidity Air Pollution Study (NMMAPS) also analyzed SO2 and found no significant associations with total mortality.3 An international study of pulp and paper workers with 40,704 SO2-exposed workers found a reduced overall standardized mortality ratio of 0.89 (95% CI 0.87–0.96) but a marginally increased rate of 1.08 for lung cancer (95% CI 0.98–1.18).4 After adjustment for occupational co-exposures, the lung cancer risk was increased compared with unexposed workers (rate ratio ¼ 1.49; 95% CI 1.14–1.96). There was a suggestion of a positive relationship between weighted cumulative SO2 exposure and lung cancer mortality. These confirm that SO2 exposure increases mortality. SO2 is a respiratory irritant with exposures at 10 ppm, causing cough, dyspnea, irritation of the eyes and throat, and reflex bronchial constriction. In July 1990, Hong Kong introduced a requirement that all power plants and road vehicles had to use fuel oil with a sulfur content no greater than 0.5% by weight.5 In the ensuing twelve months, there was a reduction in seasonal deaths followed by a peak in the cool season death rate between thirteen and twenty-four months, returning to the expected pattern during years 3–5. There were declines in the average annual trend in deaths from all causes (2.1%, p ¼ 0.001), respiratory 3.9%, and cardiovascular 2.0%. The average gain in life expectancy per year of exposure to the lower pollutant concentration was twenty days for females and forty-one days for males. In the two years after the intervention, there was a reduction in chronic bronchitic symptoms and bronchial hyperresponsiveness in children. SO2 declined 45% over five years and respirable particulates declined for two years. In twelve Canadian cities, daily SO2 concentrations were significantly associated with daily mortality, with an average concentration of only 5 mg/ m3 . 6 In a district of Chongqing, China, daily mortality was analyzed from January through December 1995 for associations with daily ambient sulfur dioxide and fine particles.7 Particulate matter less than 2.5 mm in diameter (PM2.5) was monitored for seven months, while SO2 was monitored for the entire year. The investigators found positive associations between daily ambient SO2 concentrations and mortality from respiratory and cardiovascular disease. For example, the effect of a 100 mg/m3 (0.04 ppm) increase in daily SO2 concentrations was a relative risk of 1.20 (95% CI 1.11–1.30) for cardiovascular mortality, with up to a three-day lag. The SO2 association remained robust when controlled for PM2.5. No associations were observed between daily ambient PM2.5 concentration and any cause of mortality. A weakness of this study was the absence of measurements of carbon monoxide, ozone, or nitrogen dioxide. Chongqing is surrounded by mountains, is one of China’s largest cities at 30 million people, and uses high-sulfur coal for energy, with sulfur ranging from 4% to 12%.

COVID and cancer

 

COVID-19 vaccination in cancer patients: 

What are the vaccines being developed and nearing approval?

The World Health Organization (WHO) currently counts more than two hundred research projects for the development of a vaccine conferring protective immunity against the SARS-CoV-2 virus, among which more than fifty are in clinical development. New technologies, previous experience with vaccine projects against related viruses and the presence of a pandemic health hazard accelerated the usual development cycle from years to months. Presentation of SARS-CoV-2 antigens to the host, in the context of vaccine development, relied on technologies based on messenger RNA (mRNA), inactivated/attenuated or genetically modified viruses, synthetic long viral peptides and plasmid DNA vaccines. Four vaccines have been authorised until April 2021 for use in the European Union (Comirnaty Pfizer/BioNTech, COVID-19 Vaccine Moderna, Vaxzevria AstraZeneca, COVID-19 Vaccine Janssen) while three more are under rolling review by the European Medicines Agency (EMA; CVnCoV, NVX-CoV2373, Sputnik V). More vaccines are under clinical development and are being assessed for efficacy and safety.

Overall mRNA-based vaccines have shown >90% protection from COVID-19 disease with good tolerance, whereas non-replicating adenoviral vector-based vaccines have shown protection rates of 62%-90% conferred by different dosing regimens. Storage requirements and number of doses differ between vaccines and operational practicalities related to transport, administration, recording and follow-up of vaccinated people, and pharmacovigilance are pivotal for the successful roll-out of vaccination programmes and their optimal impact on public health. Despite some preclinical data of reduced neutralising potential of generated antibodies against new, mutated forms of the virus, available clinical evidence suggests that approved vaccines confer protective immunity against new mutational variants of SARS-CoV-2. Moreover, a rational strategy for minimising the risk of emergence of additional virus variants is based on effective mass vaccination programmes for establishment of vaccine-induced immunity in order to prevent new infections and, thus, mutations. Additional questions exist that necessitate generation of data, including long-term safety, duration of immunity, protective immunity against mild as opposed to severe cases of infection as well as immunity in the elderly, vaccine impact on contagious potential of vaccinated people and repeat vaccination intervals.  A combination of severe thrombosis and thrombocytopaenia, of possible immune pathogenesis similar to that seen in heparin-induced thrombocytopaenia, has been observed very rarely following vaccination, mostly with adenoviral vector-based vaccines (Vaxzevria, COVID-19 Vaccine Janssen), occurring during the first few weeks after inoculation. Healthcare professionals and patients should be alert to the signs and symptoms of thromboembolism and/or thrombocytopaenia, and if present, seek specialist medical treatment promptly. In view of the rarity of the side-effect and the risk from COVID-19, the risk/benefit profile of the vaccines is considered favourable by the EMA. The use of all approved COVID-19 vaccines should be in accordance with official national recommendations.

Specifically, for patients with cancer or a history of cancer, strategies of continued generation of data within trials as well in real world settings will provide more insights on vaccine activity, optimal dose and frequency, safety, potential for interaction with malignant disease, antineoplastic therapies or other comorbidities. Consequently, prospective observational studies focusing on patients with active cancer receiving chemotherapy, targeted therapy or immunotherapy, as well as in patients in the chronic phase of disease or in the survivorship phase are warranted and may lead to interventional clinical trials, if needed.

A large array of other vaccine candidates against SARS-CoV-2 are currently under investigation applying various techniques such as mRNA-, protein subunit-, viral vector- or inactivated virus vaccines.

These recommendations should be used as guidance for prioritising the various aspects of cancer care in order to mitigate the negative effects of the COVID-19 pandemic on the management of cancer patients. The situation is evolving, and pragmatic actions may be required to deal with the challenges of treating patients, while ensuring their rights, safety and wellbeing.

Statements:

• Effective and safe vaccines against COVID-19, authorised after thorough, independent and robust scientific review by regulatory authorities, should be administered in the context of operationally sound vaccination programmes [V]. A pharmacovigilance plan is mandatory in the context of the vaccination programme.
• Effective mass vaccination programmes coupled to robust pharmacovigilance are key for preventing infections and emergence of viral mutations, while safeguarding favourable vaccine risk/benefit profiles [V].
• Ongoing scientific assessment by medical and regulatory authorities underpins the safe and effective use of COVID-19 vaccines. Use of the vaccine during vaccination campaigns take into account the pandemic situation and vaccine availability at national level.
• Continued research in the context of clinical trials and registries as well as in-trial and post-trial follow-up is advised in order to generate more data on vaccine efficacy and safety in the general population as well as in special populations, including patients with active cancer or history of cancer [V].

• Patients with cancer as a group have been shown to be at higher risk of severe COVID-19 [1]. Among patients with cancer, it seems that haematological and lung malignancies and the presence of metastatic disease are associated with a persistently increased risk. Patients with solid tumours appear to suffer an increased risk, particularly in the first year after diagnosis which drops to baseline if diagnosis is >5 years ago [2]. For any malignancy, active disease confers a significantly increased risk of severe COVID-19 [IV] [3, 4]. However, the higher incidence and severity of COVID-19 in patients with cancer, as opposed to those without cancer, are observations based on non-comparative retrospective studies. Data on the true incidence and direct comparisons remain elusive. Most studies do not have the full denominator to calculate the true incidence [IV].

  Severity and mortality rates from the COVID-19 and Cancer Consortium (CCC19) registry and other cohorts have ranged from 5% to 61% (meta-analysis showed 26%) which is much higher than in the overall population (~2%-3%), but this is with caveats of unadjusted rates, while the cancer population is an older population with more comorbidities, poorer performance status, and many unmeasured confounding and selection biases [IV].

  SARS-Cov-2 infection may also result in significant and devastating delays in screening, diagnosis, treatment and monitoring/surveillance strategies in patients with cancer which can ultimately cause an increased risk of cancer-related morbidity and mortality, as well as major economic burden and high patient volumes needing care in the healthcare systems. Moreover, the impact on clinical trials accrual appears to be very significant and detrimental, although it is hard to measure.

• Although evidence regarding vaccination in patients with cancer is limited, there is enough evidence to support anti-infective vaccination in general (excluding live-attenuated vaccines and replication-competent vector vaccines) even in patients with cancer undergoing immunosuppressive therapy [5-7]. Reduced protective effects may occur in patients treated with B cell-depleting agents (anti-CD19, anti-CD20, anti-CD10 monoclonal antibodies and CD19 CAR-T cells) in view of suboptimal immune response [8-12]. The level of efficacy may be expected to be generally reduced in certain populations of cancer patients with intense immunosuppression, such as recipients of haematopoietic stem cell transplantation [V] [5-7]. However, based on data extrapolation from other vaccines and the mechanism of action of the COVID-19 vaccines (not live), it is conceivable that the efficacy and safety of vaccination against COVID-19 may be estimated to be similar to that of patients without cancer, although data from clinical trials are lacking [V]. Beyond stem cell transplantation, the efficacy of COVID-19 vaccines can also vary in patients with distinct contexts of malignant disease (tumour type, disease extent, intrinsic or therapy-induced immunosuppression); however, the benefits of vaccination seem to significantly and substantially outweigh the risks [V].

  The timing of vaccination depends on individual therapy scenarios and may ideally occur before systemic therapy starts; however, if the patient has already started systemic therapy, it is reasonable to vaccinate during therapy [V].

• Vaccinating healthcare staff against influenza has been shown to reduce nosocomial transmission of the infection in cancer care [13]. Furthermore, certain immunocompromised cancer patients might not achieve a sufficient immune response to vaccination. This provides a rationale for vaccinating healthcare staff who work in a high-risk setting against COVID-19 as well [Evidence III for influenza]

  Statements:

  • Patients with cancer have an increased risk of severe COVID-19 (i.e. haematological malignancy requiring chemotherapy or active, advanced solid tumour or history of solid tumour <5 years ago) and should be vaccinated against SARS-CoV-2 regardless of any other indications (i.e. age) and positioned at high prioritisation [V]. Patients who have received B cell depletion in the past 6 months may derive reduced protection. The time-point for vaccination after allogeneic stem cell transplantation should follow general recommendations – usually, in the absence of graft-versus-host disease (GvHD), the vaccine can be applied 6 months post stem cell transplantation [V]. Patients in clinical trials, e.g. immunotherapy, should not be deprived of COVID-19 vaccination; therefore, efforts should be made for clinical trial protocols to allow concurrent COvID-19 vaccines.
  • Healthcare workers caring for patients with cancer with increased risk should be prioritised in receiving vaccination to minimise nosocomial transmission.
  • The efficacy and duration of immunity in patients with cancer are still unknown and unexplored. Given the often-immune compromised status and the frailty of these patients, we suggest monitoring in the context of registries and dedicated clinical trials.
  • Close surveillance and monitoring of patients with cancer is required after COVID-19 vaccination to assess potential adverse events and measure clinical outcomes, e.g. infection, severity and mortality from COVID-19, complications from cancer, etc.
  • Physical distancing measures, masks, face shields, sanitizers and other hygiene measures are still required during the pandemic, including for patients with cancer, and should certainly accompany the vaccination strategies.

Source: https://www.esmo.org/

Breast cancer symptoms

Breast cancer is one of the most common cancer in the world, women must to pay atention to the first sign of breast  cancer. 

Screening program hellp women to get acces to a mammography in the early stages.

 Symptoms of breast tumors vary from person to person. Some common, early warning signs of breast cancer include:

• Skin changes, such as swelling, redness, or other visible differences in one or both breasts
• An increase in size or change in shape of the breast(s)
• Changes in the appearance of one or both nipples
• Nipple discharge other than breast milk
• General pain in/on any part of the breast
• Lumps or nodes felt on or inside of the breast

Symptoms more specific to invasive breast cancer are:

• Irritated or itchy breasts
• Change in breast color
• Increase in breast size or shape (over a short period of time)
• Changes in touch (may feel hard, tender or warm)
• Peeling or flaking of the nipple skin
• A breast lump or thickening
• Redness or pitting of the breast skin (like the skin of an orange) 

Symptoms of invasive breast cancer

Breast cancer that’s spread from where it began into the tissues around it is called invasive or infiltrating. You may notice:

• A lump in your breast or armpit. You might not be able to move it separately from your skin or move it at all.
• One breast that looks different from the other
• A rash or skin that’s thick, red, or dimpled like an orange
• Skin sores
• Swelling in your breast
• Small, hard lymph nodes that may be stuck together or stuck to your skin
• Pain in one spot

Symptoms of metastatic breast cancer

Without treatment, breast cancer can spread to other parts of your body, including other organs. This is called metastatic, advanced, or secondary breast cancer. Depending on where it is, you may have:

• Bone pain
• Headache
• Changes in brain function
• Trouble breathing
• Belly swelling
• Yellow skin or eyes (jaundice)
• Double vision
• Nausea
• Loss of appetite and weight loss
• Muscle weakness

Symptoms of triple-negative breast cancer

Breast cancer is called triple-negative if it doesn’t have receptors for the hormones estrogen and progesterone and doesn’t make a lot of a protein called HER2. This kind tends to grow and spread faster than other types, and doctors treat it differently.

Triple-negative tumors make up 10% to 15% of breast cancers. They cause the same symptoms as other common types. Get an overview on triple-negative breast cancer symptoms and treatment.

Symptoms of male breast cancer

About 1% of breast cancers happen in men. Because it’s so rare, you may not pay attention to the symptoms until the cancer has grown. Watch for:

• A lump or thick spot in your breast or armpit
• Changes in the skin of your breast or nipple, such as redness, puckering, scales, or discharge

Learn more about breast cancer in men.

Symptoms of Paget’s disease of the breast

This type often happens along with ductal carcinoma. It affects the skin of your nipple and areola. Symptoms may look like eczema and include:

• Nipple skin that’s crusted, scaly, and red
• Bloody or yellow discharge from the nipple
• A flat or inverted nipple
• Burning or itching

FOTO from VectorStock

Top 10 cancer causing food

Today's food contains many toxic substances, including BPA, but also genetic changes that our body is unable to recognize and eliminate. These changes lead to changes in the body's cells, causing cancer.

Causes of Heart Disease

Causes of Heart Disease

Coronary artery disease, the most common form of cardiovascular disease, is one of the leading causes of death today. But thanks to many studies involving thousands of patients, researchers that have been able to shortlist certain factors that are the Causes of Heart Disease in a person. These are called risk factors. These risk factors contribute to two categories: major and contributing. The major Causes of Heart Disease are:

High Blood Pressure (Hypertension): High blood pressure increases your risk of heart disease, heart attack, and stroke. Though other risk factors can lead to high blood pressure, you can have it without having other risk factors. Blood pressure can vary with activity and with age. A healthy adult who is resting generally has a systolic pressure reading between 120 and 130 and a diastolic pressure reading between 80 and 90.

High Blood Cholesterol: this is another risk factor that causes of Heart Disease is high blood cholesterol. Cholesterol is a fat-like substance carried in your blood. This is found in all of your body cells. Your liver produces all of the cholesterol your body needs to form cell membranes and to make certain hormones. Extra cholesterol enters your body when you eat foods that come from animals

Diabetes: Heart problems are the leading cause of death among people with diabetes, especially in the case of adult-onset. If you know that you have diabetes, you should already be under a doctor's care, because good control of blood sugar levels can reduce your risk. If you think you may have diabetes but not sure, you must consult your doctor for tests.

Obesity and Overweight: Extra weight is thought to lead to increased total cholesterol levels. High blood pressure, increased risk of coronary artery disease. Obesity increases your chances of developing other risk factors for example, heart disease, especially high blood pressure, diabetes and high blood cholesterol.

Smoking: Most people realize that cigarette and tabacco smoking increases your risk of lung cancer, but fewer realize that it is one of the causes of Heart Disease and also other peripheral vascular disease.

Heredity: Heart disease tends to run in families. For example, if your siblings or parents had a heart or circulatory problem before the age of 55. But then you are at greater risk of heart disease than someone who does not have complains for heart disease in their family history.

Age: Older age is a risk factor for heart disease. In fact, about 4 out of every 5 deaths occur due to heart diseases that occur in people older than 65.

In addition to this, there are also certain contributing factor that enhances the causes of Heart Disease. They are: Stress, Sex hormones, Birth control pills and Alcohol. Stress is considered an important contributing risk factor for heart disease. The effects of behavior habits, emotional stress, and socioeconomic status on the risk of heart disease and heart attack have not been proven

Endocarditis

Endocarditis

Endocarditis is the inflammation inside the layer of the heart, known as the endocardium. The heart valves are the most common portions of the heart that is involved. The classification of endocarditis is done by infection or non-infection. The cause depends entirely on the microorganism that has caused the problem. The valves in the heart do not get any blood supply of their own due to which the defense mechanisms in the blood (such as white blood cells) cannot enter the heart. It so happens that if an organism (like bacteria) gets inside the valves of the heart, the body is unable to get rid of them. There are many kinds of heart diseases from which there are millions who suffer from. The types of heart diseases are such that they can create severe complications if it is neglected or diagnosed wrongly.

The flow of blood is normal through the valves inside the heart. Bacteria enter the heart when one has ailments like rheumatic fever and other such bacterial diseases. Infective endocarditis is divided into two forms known as acute and subacute. In the subacute version of endocarditis, patients tend to live longer than the acute ones. The classification of the disease can show the progression rate and intensity of endocarditis. Subacute bacterial endocarditis (SBE) is caused by streptococci of low virulence and illness. The illness can be mild and moderate along with slow progress over weeks or months. Acute bacterial endocarditis (ABE) is a fulminant illness that can be caused by the staphylococcus aureus that is of more intense disease causing factor. In infective endocarditis, there are two types known as culture positive and culture negative.

Culture-negative endocarditis is caused due to micro-organisms requiring longer time to be identified in the laboratory. Organisms of these kinds are termed as'fastidious' because they have certain requirements. Pathogens causing culture-negative endocarditis are Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria. There is marked difference between native-valve endocarditis and prosthetic-valve endocarditis. The identification of the two types is very important. Endocaditis can happen when an individual is injecting narcotics intravenously that enters the staphylococcus aureus in the heart. Those without intravenous experience, have endocarditis on the left side of the heart.

In endocarditis, the valves are damaged severely. The damage can be caused by congenital defects, auto-immune mechanisms, surgeries or by mere old age. The damaged valve has clots formed on it that in clinical term is known as non-bacterial thrombotic endocarditis (NBTE). When there is clot inside the valve of the heart, the bacteria present attaches itself with the clot thereby giving rise to infections inside it. Bacteremia that is the flowing of the bacteria with the blood stream from cut; can be caused by dental process like extraction of teeth or other procedures. Those suffering from heart diseases are first administered with medications in order to prevent any kind of bacterial infections that can lead to endocarditis. The bacteria that cause endocarditis can also enter the body by diseases like colorectal cancer, urinary tract infections and IV drug. Those using the IV drugs have the right side of their heart valves affected.

Inflammatory bowel disease symptoms

Inflammatory bowel disease symptoms are variable, affecting tissues outside digestive system and having an important mark on person’s self esteem; many times patients suffering from this disease are very depressive and unable to perform their activities. When we mention inflammatory bowel disease symptoms we have in mind Chron disease and ulcerative colitis.

Inflammatory bowel disease symptoms list

Inflammatory bowel disease symptoms are represented by digestive symptoms and non-digestive symptoms:

•  diarrhea is the most frequent and annoying symptom among the inflammatory bowel disease symptoms; some patients may have numerous watery stools,
• constipation: this is an often symptom in rectitis, (patients with ulcerative colitis complain of constipation, because this disease affects the rectum at the onset),
• abdominal pain- it is one of the frequent inflammatory bowel disease symptoms, it can be diffuse, or located in the iliac fossa (Chron disease affects, more frequently, the terminal ileum, which is the most distant part of the small intestine, located in the right iliac fossa, while ulcerative colitis affects rectum in most of the cases),
• stool with blood-it is a common finding among inflammatory bowel disease symptoms,
• weigh loss because of the diarrhea, which stops the intestine to absorb nutrients,
• fever, it is the response of the body to the inflammation of the intestine,
• abnormal communication among different parts of the intestine, or among intestine and urinary bladder or vagina (in medical practice this condition is called fistula),
• intestine stenosis (it is one of the inflammatory bowel disease symptoms known as Chron disease)-meaning a narrowing of the intestine lumen,
• blood cells abnormalities: anemia (low number of red blood cells and hemoglobin), a large number of platelets (a condition that predisposes to blood clots),
• deficits of vitamins and other nutrients, due to diarrhea, which favors malabsorption,
• intestine perforation,
• digestive cancer.

Non-digestive inflammatory bowel disease symptoms are represented by different medical conditions: liver disease (cholangiocarcinoma, primitive sclerosing cholangitis), arthritis, myositis (these patients need treatment with cortisone, which can determine, as an adverse effect, myositis), renal failure (due to dehydration), oral ulcerations, stomatitis etc.
How do we diagnose it? Once there is a clinical suspicion, a colonoscopy and intestine biopsy are needed in order to confirm the inflammatory bowel disease and also to distinguish between the two forms of inflammatory bowel disease (for each disease, there is a different histological pattern, the macroscopic aspect and the lesions location are criteria used to confirm which one of the inflammatory bowel disease is responsible for symptoms).
What is the treatment for this disease? Depending on whether there are complications, inflammatory bowel disease can be treated with cortisone (there are schemes of treatment starting with increasing doses of cortisone, which will be diminished gradually once the disease is under control), anti-inflammatory agents (like sulfasalazine), immunosuppressive medication (if the first two types of drugs are not effective) or surgery if there are complications like fistula, stenosis or intestine perforation or if disease can’t be controlled with medication.
What is the evolution of the inflammatory bowel disease? Inflammatory bowel disease symptoms have a fluctuanting evolution; there are periods with symptoms, followed by “free” periods. There are medical scales which can estimate the severity of the disease, using indices like red blood cell sedimentation rate, heart rate, body temperature, numbers of stools per day.

If any of the inflammatory bowel disease symptoms occur do not treat yourself and call a doctor.