Psychosocial Factors in Risk of Cervical Intraepithelial Lesions

Wilkerson, Jennifer E.; Bailey, Joanne; Bieniasz, Mary E.; Murray, Sandra I.

doi:10.1089/jwh.2008.0982

Cited by 11 publications

(15 citation statements)

References 24 publications

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“…Unhealthy life style, negatively rated life events, lack of social support, coping style, and distress, often associated with smoking, alcohol abuse, and illegal drugs addition, have been reported as risk factors for cervical cancer [ 45 – 47 ], especially among low-educated women [ 48 , 49 ].…”

Section: Discussionmentioning

confidence: 99%

Smoking and Cervical Cancer

Fonseca-Moutinho

2011

ISRN Obstetrics and Gynecology

115

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Cervical cancer (CC) is the third most common cancer in women worldwide; however, CC is a preventable disease, and much effort should be done to prevent it. Persistence of high-risk HPV infection is the strongest epidemiologic risk factor for CC, however it is not sufficient for development of the disease it cofactors should be present. In 2004; IARC listed cervical cancer among those causally related to smoking. Smoking interferes with incidence and prevalence of HPV infection and is associated with cervical intraepithelial neoplasia and invasive CC. Multiple factors seem to intervene on cervical carcinogenesis related with tobacco, especially by direct local carcinogenic effect and local immunosuppression. Smoking addition is also closely related with other confounding factors, like unfavorable psychosocial events, systemic immunity, contraception, and nutrition, which got difficult epidemiologic evaluation of smoking role on cervical carcinogenesis. Smoking habits should be taken in account in clinical practice and in research concerning CC.

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Section: Discussionmentioning

confidence: 99%

Smoking and Cervical Cancer

Fonseca-Moutinho

2011

ISRN Obstetrics and Gynecology

115

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“…Considering the suppressive effects of chronic stress and increased GC levels on CMI, and given the importance of cell-mediated immune responses in HR-HPV clearance, chronic psychological stress may participate in promoting HR-HPV persistence and thus HPV-associated cervical cancer progression mediated by cortisol. Indeed, several studies have demonstrated associations between psychosocial stress and prevalence and progression of HPV-associated cervical dysplasia and cancer [ 25 – 31 ], although not unequivocally so [ 32 , 33 ]. Among the hitherto published studies, however, most used cross sectional or retrospective designs and focused on the association between stress and cervical dysplasia or cancer; only two studies were of prospective nature [ 31 , 32 ] and only one directly focused on the association between chronic stress (i.e., bereavement) and HR-HPV infection [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Is stress related to the presence and persistence of oncogenic human papillomavirus infection in young women?

et al. 2021

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Background Persistent infection with high-risk human papillomavirus (HR-HPV) is the most important risk factor for the development of cervical cancer, but factors contributing to HR-HPV persistence are incompletely understood. The objective of this study was to test for associations of chronic stress and two aspects of diurnal cortisol secretion (i.e., the cortisol awakening response [CAR] and total cortisol output over the day [AUCgday]) with HR-HPV status at baseline and 12 months later (follow-up). Methods We evaluated 188 women (25 ± 3 years) at baseline. Follow-up investigation was restricted to HR-HPV infected women at baseline. Of the initial 48 HR-HPV positive participants, 42 completed the follow-up (16 HR-HPV positive and 26 HR-HPV negative). At baseline and follow-up, we determined HR-HPV status in cervical smears, assessed chronic stress, and repeatedly measured salivary cortisol over the day. At baseline, we analyzed salivary cortisol only in a subgroup of 90 participants (45 HR-HPV negative and 45 HR-HPV positive). Results At baseline, higher chronic stress (excessive demands at work: p = .022, chronic worrying: p = .032), and a higher CAR (p = .014) were related to baseline HR-HPV positivity. At follow-up, there was a statistical trend for a positive association between the CAR and HR-HPV positivity (p = .062). Neither the CAR nor the AUCgday mediated the associations between chronic stress and HR-HPV status. Conclusions Our findings suggest that both chronic stress and diurnal cortisol are related to the presence of HR-HPV infection and may thus play a role in HPV-associated cervical carcinogenesis.

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“…There are some observed (biochemical) changes in plasma protein levels, as confirmed by studies of their values during illness and stress. There are various study results on animals and humans which support the association between psychological stress, infections and carcinogenesis (Table 1 and Table 2) [25,48,[53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][70]. Animal model studies show that stress increases values of acute phase proteins [71].…”

Section: Discussionmentioning

confidence: 99%

The Influence of Psychological Stress on HPV Infection Manifestations and Carcinogenesis

2021

Cell Physiol Biochem

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Psychological stress is an important factor involved in disease manifestations of human papillomavirus (HPV) infection, and it can participate in HPV-associated carcinogenesis. The impact or effect which stress can have (exert) depends on a person’s genetic pool, experiences and behaviors. Due to inconsistencies in some study results, this issue remains a subject of research. Concerning the course of HPV manifestations, it has been observed that a higher number of life stressors in at least the previous 6 months, the absence of social support and the types of personal coping mechanisms employed, all influence HPV progression. In women with cervical dysplasia, a connection between greater stress experiences and dysregulation of specific immune responses has been observed. Once HPV enters a cell via the α6 integrin there are three possible sequences: latent infection, subclinical infection, and clinically manifest disease. HPV proliferation in differentiated epithelial cells induces morphologically cytopathic changes (koilocytosis, epidermal thickening, hyperplasia, hyperkeratosis). Oncogenic transformation requires the integration of the virus genome into the host genome. In doing so, DNA in the E1 region of E2 breaks down, leading to transcription disorders of E6 and E7. For the formation of irreversible malignancy, the following sequence is necessary: initial expression of E6 and E7 genes followed by suppression of apoptosis and the stabile expression of E6 and E7 proteins that protect transformed cells from apoptosis. A successful immune response is characterized by a strong, local cell-mediated immune response. Several factors are important for the regression of HPV manifestation/infection, among which is psychological stress which can prolong the duration and severity of HPV disease. Stress hormones may reactivate latent tumor viruses, stimulate viral oncogene expression, and inhibit antiviral host responses. In the regression of HPV infection, increased activity of Th1 cells was observed. However, during psychosocial stress, a decrease in the Th1 type of immune response is seen, and there is a shift towards a Th2 response. Understanding perceived stress and biological changes in stress, as well as the evaluation of immune parameters, gives researchers a better picture of how stress influences HPV infections and how to improve disease management and outcomes.

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Psychosocial Factors in Risk of Cervical Intraepithelial Lesions

Cited by 11 publications

References 24 publications

Smoking and Cervical Cancer

Smoking and Cervical Cancer

Is stress related to the presence and persistence of oncogenic human papillomavirus infection in young women?

The Influence of Psychological Stress on HPV Infection Manifestations and Carcinogenesis

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