Disorders in Cytokine Gene Expression in Endometrial Hyperplasia and Effect of Hormone Therapy

Сухих, Г. Т.; Zhdanov, Alexander V.; Davydova, M. P.; Slukina, T. V.; Chernukha, Chernukha G.E.; Samoilova, T. E.; Smetnik, V P

doi:10.1007/s10517-005-0257-7

Cited by 9 publications

(7 citation statements)

References 9 publications

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“…Several authors have described the presence of TNF-α in different benign hyperplasias [18][19][20]. In the present study, we detected TNF-α and TNF-R1 in more than 84% of cases with benign ovarian lesions, whereas TNF-R2 was detected in a low number of cases (24%).…”

Section: Discussionsupporting

confidence: 59%

Tumor necrosis factor-alpha and its receptors in epithelial ovarian cancer.

Dobrzycka

Terlikowski²,

Garbowicz³

et al. 2010

Folia Histochem Cytobiol.

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Abstract:The aim of the present study was to characterize the expression pattern of tumor necrosis factor (TNF)-α and its receptors (TNF-Rs) in the epithelial ovarian cancer (EOC) and compare these results with the outcome of 126 patients. Presence of TNF-α, TNFR-1 and TNFR-2 were studied by Western blotting and immunohistochemistry. The proportion of samples positive for TNF-α and TNF-R2 was higher in epithelial ovarian cancer patients than in benign ovarian diseases (p<0.001 and p=0.016, respectively). Immunostaining intensity of TNF-R2 were correlated with tumor stage (p<0.001) and with reduced mean survival time (MST) (p=0.002). The results of the present study suggested that tissue expression of TNF-R2 in epithelial ovarian cancer was correlated with the highest risk of cancer progression. Thus, the clinical value of activated TNF system in epithelial ovarian cancer needs to be further investigated.Keywords: tumor necrosis factor-α (TNF-α); tumor necrosis factor receptor 1 (TNF-R1); tumor necrosis factor receptor 2 (TNF-R2); epithelial ovarian cancer (EOC) Correspondence: B. Dobrzycka,

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Section: Discussionsupporting

confidence: 59%

Tumor necrosis factor-alpha and its receptors in epithelial ovarian cancer.

Dobrzycka

Terlikowski²,

Garbowicz³

et al. 2010

Folia Histochem Cytobiol.

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“…In the present study, the increase in uterine TNFα is in harmony with the results of Abdelzaher et al [38] who reported a significant increase in TNFα in estradiol valerate-induced EH in rats. In contrast, the expression of the IL10 gene did not change in patients with EH [39], although in the current study, EH was associated with decreased IL10 expression. The EH+IRB-treated rats showed lower uterine TNFα and enhanced IL10 compared to EH untreated rats.…”

Section: Discussioncontrasting

confidence: 95%

Protective Effects of Irbesartan, an Angiotensin Receptor Blocker with PPARγ Agonistic Activity, against Estradiol Benzoate-Induced Endometrial Hyperplasia and Atypia in Female Rats via Modulation of TNFα/Survivin Pathway

et al. 2021

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Endometrial hyperplasia (EH) is a common gynecological problem and may progress to carcinoma. Early detection and management of EH are mandatory for the prevention of endometrial cancer. Activation of the renin–angiotensin system and angiotensin II signaling are involved in the progression of precancerous and cancerous lesions. However, no studies have evaluated the role of this system in estradiol benzoate (EB)-induced EH and atypia. Irbesartan (IRB), an angiotensin II receptor blocker with peroxisome proliferator-activated receptor gamma (PPARγ) agonistic activity was administered (30 mg/kg/d) in EB-treated (60 µg/100 g bodyweight, intramuscularly, three times per week) or untreated rats for 4 weeks. Uterine weight changes, malondialdehyde, superoxide dismutase (SOD), tumor necrosis factor-alpha (TNFα), survivin, cleaved caspase 3, interleukin-10 (IL10), and PPARγ were measured in addition to undergoing histopathological examination. Results showed that EB-induced EH and atypia significantly increased the uterine body weight, malondialdehyde, TNFα, and survivin, accompanied with significantly decreased SOD, cleaved caspase 3, IL10, and PPARγ, with typical histopathological changes of EH and atypia. Coadministration of IRB significantly prevented EB-induced biochemical and histopathological changes. The protective effects of IRB may be attributed to its anti-inflammatory and antioxidant properties, reduction of survivin, and increased levels of cleaved caspase 3.

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“…However, for both receptors, the immunostaining intensities were scant, and this suggests that TNF-α has little effect on benign breast pathologies. Several authors have described the presence of TNF-α in different benign hyperplasias, including prostatic, (23) gallbladder mucosa, (30) gastric (31) and endometrial (32) hyperplasias. However, the effects mediated by TNF-α in these hyperplasias would be slight, as expression of both receptor types was scant.…”

Section: Discussionmentioning

confidence: 99%

Role of tumor necrosis factor‐α and its receptors in human benign breast lesions and tumors (in situ and infiltrative)

et al. 2006

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The aim of the present study was to characterize the expression pattern of tumor necrosis factor (TNF)-α α α α and its receptors in breast samples (benign diseases, in situ carcinomas and infiltrating carcinomas), and to compare these results with those obtained previously for interleukin-6, p53 and p21 using the same samples in order to elucidate the effects of these cytokines on the proliferationapoptosis equilibrium. Immunoexpression of TNF-α α α α and its receptors (TNFRI and TNFRII) were studied by western blotting and immunohistochemistry. The percentage of samples positive for TNF-α α α α and TNFRII was higher in in situ carcinoma than in benign breast diseases, and TNFRII was even higher in infiltrating tumors. The percentage of samples positive for TNFRI was similar in the three groups. For the three proteins and in the three patient groups, immunoreactions were observed in the peripheral cytoplasm. In the positive samples, immunostaining for TNF-α α α α was more intense in infiltrating tumors than in the other two patient groups, whereas immunostaining for both receptors was higher in in situ carcinoma than in benign breast diseases, and even higher in infiltrating tumors. Comparing the TNF-α α α α results with previous results for mtp53, p21 and interleukin-6, we found an association between the expression of these four proteins and increasing malignancy. TNF-α α α α might be an important factor in breast cancer promotion as its proliferation and survival effects seems to be enhanced through the increased expression of TNFRII. Also, the pro-apoptotic pathway of TNFRI could be inhibited by p21 (which appeared increased in breast cancer), altering TNFRI effects in promoting the expression of several factors, such interleukin-6, which contribute to tumor promotion. (Cancer Sci 2006; 97: 1044-1049) T umor necrosis factor (TNF)-α seems to exert a key role in promoting many tumors to breast cancer. TNF-α is a 17-kDa polypeptide that was first described as a serum-derived substance that causes tumor cell death, (1) and is involved in skin carcinogenesis and the spread of a variety of carcinomas and sarcomas. It can induce tumor necrosis by affecting tumor vascularization and initiating apoptotic cell death, but paradoxically, it also can promote cell proliferation.(2,3) The action of TNF-α is mediated by two distinct receptors, named TNFRI (55 kDa) and TNFRII (75 kDa), both of which show a similar affinity for TNF-α in humans.(4-6) TNFRI is the major mediator of most TNF-α activities, (7) including apoptosis. (8,9) However, cell proliferation through Nuclear Factor kappa B(NF-κB) transcription factor activation (10,11) has also been reported in fibroblasts.(12) TNFRII has been described to mediate proliferation in some cells by acting as a thymocyte. (13) Another cytokine related to TNF-α and cell proliferation is interleukin (IL)-6. Recent studies have reported that high expression of IL-6 is associated with proliferation markers in breast cancer.(14) Both TNF-α and IL-6 could also be related to different f...

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Disorders in Cytokine Gene Expression in Endometrial Hyperplasia and Effect of Hormone Therapy

Cited by 9 publications

References 9 publications

Tumor necrosis factor-alpha and its receptors in epithelial ovarian cancer.

Tumor necrosis factor-alpha and its receptors in epithelial ovarian cancer.

Protective Effects of Irbesartan, an Angiotensin Receptor Blocker with PPARγ Agonistic Activity, against Estradiol Benzoate-Induced Endometrial Hyperplasia and Atypia in Female Rats via Modulation of TNFα/Survivin Pathway

Role of tumor necrosis factor‐α and its receptors in human benign breast lesions and tumors (in situ and infiltrative)

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