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Breast Cancer And Stress Pdf

breast cancer and stress pdf

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Psychophysiological stress response of newly-diagnosed breast cancer patients with and without risk of metabolic syndrome. Little is known about how metabolic comorbidity affects stress response during breast cancer BRCa after a recent diagnosis. To evaluate the physiological and psychological differences between the BRCa-RSxM groups and those with BRCa alone, and the influence of psychological variables and comorbidity in terms of stress response.

Challenges, Coping Strategies, and Social Support among Breast Cancer Patients in Ghana

Stress is an inevitable part of life. Recent studies have shown that chronic stress can induce tumorigenesis and promote cancer development. This review describes the latest progress of research on the molecular mechanisms by which chronic stress promotes cancer development.

Primarily, chronic stress activates the classic neuroendocrine system [the hypothalamic-pituitary-adrenal HPA axis] and the sympathetic nervous system SNS and leads to a decline and dysfunction of the prefrontal cortex and the hippocampus under stress. Stress hormones produced during the activation of both the HPA axis and the SNS can promote tumorigenesis and cancer development through a variety of mechanisms. Chronic stress can also cause corresponding changes in the body's immune function and inflammatory response, which is significant because a long-term inflammatory response and the decline of the body's immune surveillance capabilities are implicated in tumorigenesis.

Stress management is essential for both healthy people and cancer patients. Whether drugs that limit the signaling pathways downstream of the HPA axis or the SNS can suppress chronic stress-induced cancers or prolong patient survival deserves further study. Humans have always experienced periods of excessive stress on account of global issues, such as poverty, war, and epidemics 1. Stress can be divided into acute stress and chronic stress.

Acute stress usually exists in emergencies, such as fighting or escaping. Changes in the structure and function of certain molecules and tissues in the brain activate the emotional cognitive system, and we make decisions for stress-coping mechanisms 2. At the same time, the body temporarily produces catecholamines and corticosteroids to improve mobility and responsiveness. Therefore, acute stress is often beneficial to the body.

However, chronic stress is heavily implicated in causing ill health, and today it is considered to encompass occupational stress as well as unusual adversities. Its potential negative effects include not only insomnia, gastrointestinal disorders 3 , 4 , anxiety, and depression 5 , 6 , but also an increased risk of cardiovascular disease, mental illness, and cancer 7.

Surveys have shown that approximately one million new cancer cases occur every year among young people aged 20—39 years 7 , and they have been partly attributed to stress. The relationship between chronic stress and cancers has aroused increasingly widespread interest and concern in the medical community. Many scholars have performed research on the relationships between stress and cancers such as prostate 8 — 10 , breast 8 — 12 , gastric 13 , 14 , lung 15 , 16 , and skin cancer 17 , 18 , and have found evidence indicating that chronic stress can induce tumorigenesis and promote cancer development Table 1.

Table 1. The mechanisms of chronic stress promoting cancer and corresponding targets and drugs. The neuroendocrine pathways are the most widely and comprehensively studied possible mediators of these associations.

The neuroendocrine pathways constituting the hypothalamus-pituitary-adrenal HPA axis and the sympathetic nervous system SNS were the first systems shown to be closely related to stress [ 1 , 19 ; Figure 1 ]. Under chronic stress, the brain's nerve impulses can continuously activate the hypothalamus to produce the corticotropin-releasing factor CRF. CRF is transported through the blood to the pituitary gland, thereby stimulating cells to release the adrenocorticotropic hormone ACTH , which travels through the blood to the adrenal cortex and promotes the synthesis of corticosteroids.

Chronic stress also activates the SNS, thereby stimulating the release of important neurotransmitters such as norepinephrine NA and adrenaline Ad. NA and Ad are also hormones secreted by the adrenal medulla and known as catecholamines because they contain catechol and amine groups.

The corticosteroids and catecholamines produced by the HPA and the SNS can cause a decline in the functions of the prefrontal cortex 20 and the hippocampus 21 , and may enhance the activation of the SNS and the HPA by regulating the expression of glucocorticoid receptors 5 , 22 , Figure 1.

The neuroendocrine mechanisms of chronic stress. Chronic stress produces stress hormones during the activation of the neuroendocrine system hypothalamus-pituitary-adrenal axis and the sympathetic nervous system, which can promote tumor development and regulate the tumor microenvironment.

Stress hormones promote the occurrence and development of cancers through various mechanisms such as by inducing DNA damage, increasing p53 degradation, and regulating the tumor microenvironment Figure 1. Chronic stress can also activate the inflammatory response and the interaction between inflammatory cells and cancer cells to form the inflammatory tumor microenvironment, thereby promoting all stages of tumorigenesis It can also enhance neuroinflammation, which further impairs the brain's cognitive processing of stress.

This is a vicious circle. Chronic stress can also selectively suppress the type 1 helper T cells Th1 , suppress the cytotoxic T cells CTL -mediated cellular immunity and interferon production, and weaken immune surveillance and other processes, thereby increasing the risk of cancer invasion and metastasis and reducing the effectiveness of anti-tumor therapy 25 , In summary, chronic stress can promote tumorigenesis and oncogenesis through the production of stress hormones, the activation of inflammation, and the suppression of immunity.

Therefore, the present review has focused on these three stress-mediated activities. Stress hormones are classified into classical corticosteroids and catecholamines, as well as the non-classical CRF and thyroid hormones. Corticosteroids include glucocorticoids and corticosterones.

Elevated glucocorticoid levels increase the activity of the negative regulator murine double minute 2 MDM2 through induction of the serum-and-glucocorticoid-regulated kinase SGK1 and mediate the inhibition of p53 P53 can initiate DNA repair, cell cycle arrest, aging, and apoptosis, which are related to the body's ability to inhibit tumor formation and respond to various types of cancer treatment Therefore, the loss or impairment of the p53 function mediated by corticosteroids can considerably promote tumorigenesis.

Increased hormone levels could lead to the activation of glucocorticoid receptors that were involved in the activation of multiple processes in metastasis and the up-regulation of kinase orphan receptor 1 ROR1 at distant metastatic sites. Inhibition of ROR1 expression can reduce metastasis and prolong the survival rates of breast cancer patients.

Catecholamines can regulate the tumor microenvironment Src is a non-receptor cytosolic tyrosine kinase that is involved in the VEGF and interleukin IL-6 production in adipocytes and cancer cells, respectively Figure 2.

Signaling pathways activated by catecholamines. Hara's team 38 clarified the specific mechanism of stress-mediated DNA damage. The synergy of these two pathways leads to the accumulation of DNA damage. Angiogenesis is an important part of tumor development and metastasis. VEGF plays a central role in the pathogenesis of various cancers as the best-known angiogenesis stimulator MMPs can degrade multiple protein components in the extracellular matrix, destroy the histological barrier of tumor cell invasion, and play a key role in tumor invasion and metastasis.

Cui et al. Jang et al. They further found that VDCC could trigger calcium mobilization, thereby inducing the activation of the insulin-like growth factor receptor IGF-1R and promoting cancer metastasis through the exocytosis of IGF2. Zhang et al. Hassan et al. Therefore, vitamin C may be a potential factor to combat stress-related breast cancer.

CRF is widely present in the central nervous system, that has been detected in breast cancer tissues and cell lines, and affects breast cancer cell proliferation and invasion in an autocrine or paracrine manner The antagonist of CRF, antalarmin, inhibits neovascularization in 4T1 breast cancer cell lines in vivo Thyroid hormone is secreted by the thyroid gland, which is closely related to the body's metabolism, growth, and development, and is regulated by the hypothalamus-pituitary-thyroid axis.

When people are emotional, their emotions stimulate the hypothalamus to release thyrotropin-releasing hormones and regulate the secretion of thyroid-stimulating hormones. This further affects the thyroid gland, and causes its gland cells to secrete a large amount of thyroid hormone. Frick et al. The use of thyroxine replacement therapy can reverse the above process.

Therefore, thyroid hormone may be a critical neuroendocrine regulator of tumor evolution, most likely through the regulation of T cell-mediated immunity. Chronic stress and stress hormones can up-regulate the expression of stress-related pro-inflammatory genes in the circulating white blood cells, thereby increasing the release of pro-inflammatory cells and the production of pro-inflammatory cytokines, and can activate the aging-inflammatory response without the trigger of an exogenous inflammation, leading to the promotion of tumorigenesis and metastasis Niraula et al.

Inhibiting corticosterone overproduction through surgery adrenalectomy and drug therapy metyrapone can reduce these inflammatory responses to stress. Moreover, research by Antoni's group shows that stress management in patients with early-stage breast cancer can reverse the up-regulation of the stress-related proinflammatory genes in white blood cells in the circulation Immune cells in the tumor microenvironment are called pro-tumorigenic immune cells and include the tumor-associated macrophages TAMs , the dendritic cells DCs , the myeloid-derived suppressor cells MDSCs , and the tumor-infiltrating lymphocytes TILs.

The pro-tumorigenic immune cells maintain a relative balance within a certain range of promoting tumor inflammation and anti-tumor immunity. After chronic stress breaks this balance through a long-term pro-inflammatory response, these cells and cytokines can act on all stages of tumor development, including initiation, promotion, malignant transformation, invasion, and metastasis through mutation, epigenetic modification, and regulation of the tumor microenvironment [ 50 , 51 ; Figure 3 ].

Moreover, activated inflammatory cells produce excess reactive oxygen species ROS to drive inflammation and mutagenesis through different pathways By regulating the expression of many genes that can inhibit tumor cell death, promote tumor cell survival, and induce the production of chemokines, cytokines also attract more tumor-promoting immune cells to maintain a tumor-related inflammation.

Figure 3. Effects of stress hormones on the immune system. The decrease in IL and the increase in IL lead to selective Th1 inhibition, thereby suppressing the CTL-mediated cellular immunity and interferon production.

As the core immune cells, thymus-dependent lymphocytes T cells provide a robust line of defense against infections and cancers. The cellular immunity mediated by them includes specific binding to their target cells for direct cell destruction or elimination and the release of cytokines to enhance and expand the immune effects.

Based on different cytokine functions, the helper T cells are divided into Th1 or Th2 cells, which are differentiated from TH0 cells by their regulation by the cytokines IL and IL Their main function is to enhance the humoral immune response and stimulate the B cells to produce antibodies. Stress tests show that the plasma concentration of stress hormones is inversely proportional to the function of immune cells Increased stress hormone production significantly reduces the activity of the antigen-presenting cells APC , such as monocytes, macrophages, the dendritic cells, and the natural killer cells, that produce human IL Yang et al.

Additionally, Saul et al. PGE2 is a biologically active lipid that can trigger inflammation and cancer. There is no doubt that this is harmful to the body. Excessive levels of stress hormones promote carcinogenesis by inducing DNA damage accumulation, increasing p53 degradation, and other, related pathways. Excessive stress hormones also prevent immune cells from effectively controlling cancer cells by increasing inflammation and suppressing immunity.

Further, they can act on tumor and stromal cells in the tumor microenvironment to promote tumor growth, invasion, and metastasis. In addition to these pathways, emerging trends include investigation of the correlation between chronic stress and the microbiota-gut-brain axis 61 — 63 , and its impact on intestinal diseases The effects of daily stress on the neuroendocrine and immune function of healthy human individuals, which may be modulated by the individual's personality, have been confirmed, for example, by Biondi et al.

Therefore, we need to actively manage stress 66 , A large amount of clinical evidence shows that supportive psychological therapy has a positive effect on anticancer treatment and prognosis of cancer patients 68 , These drugs have been shown in animal experiments to not only significantly improve anxiety-like behavior 47 , 48 , and inhibit chronic tumor-promoting tumor growth, but also to block a stress-induced increase in angiogenesis and lymphatic metastasis At the same time, we suggest that stress hormones should be used with caution, especially glucocorticoids 77 to treat patients with cancer and related complications.

Oxidative stress in breast cancer

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. A vast body of research has been carried out to examine the relationship between psychological stress and the risk of breast cancer.

breast cancer and stress pdf

PDF | Objective Breast cancer is the world's leading cause of cancer mortality in women. Stress is an imminent risk factor with a documented.


Challenges, Coping Strategies, and Social Support among Breast Cancer Patients in Ghana

Association between stress and breast cancer in women: a meta-analysis. The objective of the current meta-analysis was to verify the association between stressful life events and primary breast cancer incidence in women. Eight studies were selected six case-controls and two cohorts. The studies were grouped in three analyses, two of which based on the categories widowhood and divorce and the other based on self-rated intensity and frequency of stressful events.

Accumulating evidence suggests that exposures to elevated levels of either endogenous estrogen or environmental estrogenic chemicals are associated with breast cancer development and progression. These natural or synthetic estrogens are known to produce reactive oxygen species ROS and increased ROS has been implicated in both cellular apoptosis and carcinogenesis. Though there are several studies on direct involvement of ROS in cellular apoptosis using short-term exposure model, there is no experimental evidence to directly implicate chronic exposure to ROS in increased growth and tumorigenicity of breast cancer cells. Therefore, the objective of this study was to evaluate the effects of chronic oxidative stress on growth, survival and tumorigenic potential of MCF-7 breast cancer cells.

Oxidative stress and breast cancer biomarkers: the case of the cytochrome P450 2E1

Stress, coping and health-related quality of life in breast cancer women.

Challenges, Coping Strategies, and Social Support among Breast Cancer Patients in Ghana

The present study was undertaken to evaluate the place of oxidative stress on breast cancer. Lipid peroxidation as evidenced by malondialdehyde MDA and the status of the antioxidants superoxide dismutase SOD , catalase CAT , and glutathione peroxidase GPx were estimated in tissues of 10 fibroadenoma and 40 breast cancer patients. The results of our study have shown higher oxygen-free-radical production and decreased CAT activity support the oxidative stress hypothesis in breast carcinogenesis. This is a preview of subscription content, access via your institution. Rent this article via DeepDyve.

Correspondence Address: Dr. E-mail: cdemonacos manchester. Demonacos joined the University of Manchester, Manchester Pharmacy School in where he is involved in the investigation of the role of ROS in cellular energy metabolism and breast carcinogenesis. In addition, Dr. Demonacos' laboratory explores the signaling events that facilitate cancer cells to evade immunosurveillance. Adenosine triphosphate ATP assay was used to measure ATP production and lactate assay to quantify the efflux of lactic acid in breast cancer cells treated with the CYP2E1 inhibitor chlormethiazole, the mitochondrial membrane potential and cell viability assays were employed to assess the pathway of cellular energy production and cellular death respectively after treatment of MCF-7 and MDA-MB with the CYP2E1 activator acetaminophen or the CYP2E1 inhibitor chlormethiazole.

Stress is an inevitable part of life. Recent studies have shown that chronic stress can induce tumorigenesis and promote cancer development. This review describes the latest progress of research on the molecular mechanisms by which chronic stress promotes cancer development. Primarily, chronic stress activates the classic neuroendocrine system [the hypothalamic-pituitary-adrenal HPA axis] and the sympathetic nervous system SNS and leads to a decline and dysfunction of the prefrontal cortex and the hippocampus under stress. Stress hormones produced during the activation of both the HPA axis and the SNS can promote tumorigenesis and cancer development through a variety of mechanisms.

Key Points

Metrics details. Women diagnosed with breast cancer frequently attribute their cancer to psychological stress, but scientific evidence is inconclusive. We investigated whether experienced frequency of stress and adverse life events affect subsequent breast cancer risk. Breast cancer incidence was analysed with respect to stress variables collected at enrolment in a prospective cohort study of , women in the United Kingdom, with incident breast cancer cases. Relative risks RR were obtained as hazard ratios using Cox proportional hazards models.

 Если Танкадо перестанет быть фактором? - вслух размышлял Нуматака.  - Тогда мы с вами придем к соглашению. - Буду держать вас в курсе, - произнес голос, и вслед за этим в трубке раздались короткие гудки.

 Я готов рискнуть. - Чепуха. Вы жаждете обладать ею еще сильнее, чем Цифровой крепостью. Я вас знаю. На такой риск вы не пойдете.

Створки стали стремительно сближаться. Стратмор попытался их удержать, но не сумел. За мгновение до того, как они сомкнулись, Сьюзан, потеряв равновесие, упала на пол за дверью.

Chronic Stress Promotes Cancer Development

Секрет выражения без воска был ему слишком дорог. Он уходил корнями в давние времена. В эпоху Возрождения скульпторы, оставляя изъяны при обработке дорогого мрамора, заделывали их с помощью сеrа, то есть воска.

Базу данных защищали трехуровневое реле мощности и многослойная система цифровой поддержки. Она была спрятана под землей на глубине 214 футов для защиты от взрывов и воздействия магнитных полей. Вся деятельность в комнате управления относилась к категории Совершенно секретно. УМБРА, что было высшим уровнем секретности в стране.

Stress and breast cancer: a systematic update on the current knowledge

Створки стали стремительно сближаться. Стратмор попытался их удержать, но не сумел. За мгновение до того, как они сомкнулись, Сьюзан, потеряв равновесие, упала на пол за дверью. Коммандер, пытаясь приоткрыть дверь, прижал лицо вплотную к узенькой щелке.

Хорошенькое зрелище, - подумал Беккер.  - Где, черт возьми, регистратура. За едва заметным изгибом коридора Беккер услышал голоса. Он пошел на звук и уткнулся в стеклянную дверь, за которой, судя по доносящемуся оттуда шуму и гвалту, происходило нечто вроде драки. Преодолев отвращение, Беккер открыл дверь.

Беккер замолчал. Он опять перегнул палку. Его план не сработал. Почему она не хочет ему поверить.

В них использовалось разное топливо - разные элементы. Соши хлопнула в ладоши. - Он прав. Я читала об. В бомбах было разное топливо.

1 Comments

  1. Steven T.

    21.04.2021 at 22:54
    Reply

    Despite the high incidence and mortality rate of breast cancer BC in Ghana, little attention has been given to the issue of how adult women cope with having BC.

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