Obesity, adipocytokines, and insulin resistance in breast cancer

Rose, David P.; Komninou, Despina; Stephenson, Gina Day

doi:10.1111/j.1467-789x.2004.00142.x

Cited by 423 publications

(354 citation statements)

References 142 publications

(189 reference statements)

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“…We offer two hypotheses for the breast cancer deficit. First, women with HIV/AIDS had alterations of reproductive and perhaps other hormones tied to breast cancer (Rose et al, 2004). Second, HIV infected the breast, impairing proliferation of malignantly transformed cells.…”

Section: Discussionmentioning

confidence: 99%

Risk of breast, ovary, and uterine corpus cancers among 85 268 women with AIDS

et al. 2006

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By linking HIV/AIDS and cancer surveillance data in 12 US regions, breast and reproductive cancer risks with AIDS were compared to those in the general population. Trends in standardized incidence ratios (SIRs) were assessed by CD4 count, AIDS-relative time, and calendar time. Standardized incidence ratios were indirectly adjusted for cancer risk factors using data from AIDS cohort participants and the general population. With AIDS, 313 women developed breast cancer (SIR 0.69, 95% confidence interval (CI) 0.62 -0.77), 42 developed ovary cancer (SIR 1.05, 95% CI, 0.75 -1.42), and 31 developed uterine corpus cancer (SIR 0.57, 95% CI, 0.39 -0.81). Uterine cancer risk was reduced significantly after age 50 (SIR 0.33). Breast cancer risk was reduced significantly both before (SIR 0.71) and after (SIR 0.66) age 50, and was lower for local or regional (SIR 0.54) than distant (SIR 0.89) disease. Breast cancer risk varied little by CD4 count (P trend ¼ 0.47) or AIDS-relative time (P trend ¼ 0.14) or after adjustment for established cancer risk factors. However, it increased significantly between 1980 and 2002 (P trend ¼ 0.003), approaching the risk of the general population. We conclude that the cancer deficit reflected direct or indirect effects of HIV/AIDS and that anti-HIV therapy reduced these effects. Increasing numbers of women have been infected with human immunodeficiency virus (HIV) and now are living with the acquired immunodeficiency syndrome (AIDS). The effects of AIDS on women, particularly in the era of highly active antiretroviral therapy (HAART), are not well defined. In the era before HAART, the risks of developing Kaposi sarcoma, anal cancer, and perhaps lymphoma were lower for women than for men with AIDS (Beral and Newton, 1998;Goedert, 2000). Other than cervical cancer, no differences by gender have been reported for the few other malignancies found in excess among people with AIDS (PWA) (Goedert et al, 1998;Frisch et al, 2001).Breast cancer may occur less often in women with AIDS than in the general population (Goedert et al, 1998;Frisch et al, 2001). Ovary and uterine corpus cancers have not been associated with AIDS or other immune deficiencies, but weak associations or susceptible subgroups may have been overlooked because these malignancies are relatively rare. No previous study has evaluated the effects of improving anti-HIV therapies or whether differences in cancer incidence might merely reflect differences in known risk factors for cancer.Using population-based data, we have investigated whether the risk of breast, ovary, or uterine corpus cancers differ for women with AIDS, whether breast cancer risk differs with increasing severity or duration of immune deficiency, or with increasing availability and efficacy of anti-HIV therapies; also whether menopause or selected risk factors modify or explain any associations. MATERIALS AND METHODS Detection and definition of cancersFrom 2003 through 2005, we linked HIV/AIDS and cancer registration data (including name, race, sex, dates of birth and de...

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Section: Discussionmentioning

confidence: 99%

Risk of breast, ovary, and uterine corpus cancers among 85 268 women with AIDS

et al. 2006

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“…In addition, the −1420G allele, but not the variant −1420A allele, has a binding site of insulin activator factor, although the functions of this binding site remain unclear [31]. Because insulin resistance, diabetes, and obesity related to insulin resistance or hyperinsulinemia have been shown to be associated with increased risk of breast cancer [32,33], we postulated that the −1420A variant allele may cause loss of possible protective effects of insulin activator factor due to the loss of its binding site. Furthermore, the −1187T allele, but not the variant −1187C allele, has a binding site of progesterone receptor.…”

Section: Discussionmentioning

confidence: 99%

Genetic variants in the H2AFX promoter region are associated with risk of sporadic breast cancer in non-Hispanic white women aged ≤55 years

Wei

Bondy

Brewster

et al. 2007

Breast Cancer Res Treat

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The histone protein family member X (H2AFX) is important in maintaining chromatin structure and genetic stability. Genetic variants in H2AFX may alter protein functions and thus cancer risk. In this case-control study, we genotyped four common single nucleotide polymorphisms (i.e., −1654A > G [rs643788], −1420G > A [rs8551], and −1187T > C [rs7759] in the H2AFX promoter region and 1057C > T [rs7350] in the 3′ untranslated region (UTR)) in 467 patients with sporadic breast cancer and 488 cancer-free controls. All female subjects were non-Hispanic whites aged ≤55 years. We found that significantly increased risk of breast cancer was associated with variant genotypes in the H2AFX promoter: adjusted odds ratio [OR] = 1.80, 95% confidence interval [CI] = 1.38-2.34 for −1654AG/GG; OR = 1.40, 95% CI = 1.07-1.83 for −1420GA/AA; and OR = 1.65, 95% CI = 1.26-2.16 for −1187TC/CC. Furthermore, the number of variant alleles in the promoter haplotypes was associated with increased risks of breast cancer in a dose-response manner (OR = 6.08, 95% CI = 3.25-11.38; OR = 6.83, 95% CI = 3.83-12.18; and OR = 23.61, 95% CI = 3.95-140.99 for one, two, and three variant alleles, respectively) (P trend < 0.0001). Age at onset of breast cancer significantly decreased as the number of variant alleles increased (P trend = 0.024). However, these effects were not observed in the 3′UTR 1057C > T polymorphism. Therefore, we believe that H2AFX promoter polymorphisms may contribute to the etiology of

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“…This cytokine was initially identified as a polypeptide produced by macrophages in chronic diseases as well as during infectious processes contributing to cachexia (Rose, Komninou, Stephenson, 2004). In WAT, TNF-α is synthesized and secreted by vascular stromal cells and matrix fractions including macrophages, although its mRNA is expressed in adipocytes (Fain, Bahouth, Madan, 2004).…”

Section: Tumor Necrosis Factor Alphamentioning

confidence: 99%

Obesity, inflammation, and insulin resistance

Martins

Oliveira

Cruz

et al. 2014

Braz. J. Pharm. Sci.

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White adipose tissue (WAT) is considered an endocrine organ. When present in excess, WAT can influence metabolism via biologically active molecules. Following unregulated production of such molecules, adipose tissue dysfunction results, contributing to complications associated with obesity. Previous studies have implicated pro-and anti-inflammatory substances in the regulation of inflammatory response and in the development of insulin resistance. In obese individuals, pro-inflammatory molecules produced by adipose tissue contribute to the development of insulin resistance and increased risk of cardiovascular disease. On the other hand, the molecules with anti-inflammatory action, that have been associated with the improvement of insulin sensitivity, have your decreased production. Imbalance of these substances contributes significantly to metabolic disorders found in obese individuals. The current review aims to provide updated information regarding the activity of biomolecules produced by WAT.Uniterms: Obesity. Inflammation. Adipose tissue. Adipokines. Insulin resistance.O tecido adiposo branco (WAT) é considerado um órgão endócrino, que, em excesso, é capaz de controlar o metabolismo, pela ação de moléculas biologicamente ativas. A produção desregulada destas substâncias pela disfunção do tecido adiposo pode contribuir para as complicações presentes na obesidade. As pesquisas atuais têm esclarecido fatores e mecanismos envolvidos na atuação de substâncias pró e anti-inflamatórias na modulação da inflamação e da resistência à insulina. Em indivíduos obesos, as moléculas pró-inflamatórias produzidas pelo tecido adiposo têm sido implicadas como fator contribuinte para o desenvolvimento da resistência à insulina e aumento do risco de doença cardiovascular. Por outro lado, as moléculas com ação anti-inflamatória, que atuam na melhora da sensibilidade à insulina, têm sua produção reduzida. O desequilíbrio entre essas substâncias contribui de forma significativa para as desordens metabólicas presente em indivíduos obesos. Assim, esta revisão visa a trazer informações atualizadas sobre a atuação de moléculas secretadas pelo tecido adiposo. Unitermos:Obesidade. Inflamação. Tecido adiposo. Adipocinas. Resistência à insulina.

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Obesity, adipocytokines, and insulin resistance in breast cancer

Cited by 423 publications

References 142 publications

Risk of breast, ovary, and uterine corpus cancers among 85 268 women with AIDS

Risk of breast, ovary, and uterine corpus cancers among 85 268 women with AIDS

Genetic variants in the H2AFX promoter region are associated with risk of sporadic breast cancer in non-Hispanic white women aged ≤55 years

Obesity, inflammation, and insulin resistance

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