Cervical Cancer and Microchimerism

Hyun, Dong; Khosrotehrani, Kiarash; Kim, Youngtae; Stroh, Helene; Bianchi, Diana W.; Johnson, Kirby L.

doi:10.1097/00006250-200310000-00020

Cited by 41 publications

(59 citation statements)

References 24 publications

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“…As at least some of the engrafted fetal cells have stem cell potential, these cells might be part of a repair process. For thyroid diseases, this hypothesis seems to be supported by the fact that MCH is also observed in nonautoimmune diseases (15, this study) and for other tissues by the recent observation of MCH in non-autoimmune diseases of the vagina and uterus (32,33). Moreover, Srivatsa et al (16) were able to identify the microchimeric cells in at least one patient as normal thyrocytes (and not immuncompetent cells).…”

Section: Discussionsupporting

confidence: 71%

Fetal microchimerism in Hashimoto’s thyroiditis: a quantitative approach

et al. 2006

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Objective: Fetal microchimerism (MCH) has been implicated in the etiology of autoimmune diseases such as autoimmune thyroiditis. The goal of the study was to reliably estimate the number of fetal engrafted cells and to further investigate factors influencing the development of MCH. Methods: Quantitative real-time PCR amplification using Y-chromosome specific (DYS14) and autosomal (b-globin) loci was performed on thyroid gland specimens. Furthermore, we compared the distribution of ABO and rhesus systems in mothers with and without blood MCH in relation to the blood groups of the children. Results: MCH was detected in eight of 21 Hashimoto patients in a frequency range of 15 to 4900 male cells per 100 000 total cells (median 97 cells), but in none of 17 healthy thyroid glands. In a third group, consisting of 18 nodular goiters, only one sample was positive (182 male cells/100 000 total cells). No woman who had not had a prior pregnancy with a male fetus showed MCH. Mothers both with and without MCH showed the same rate of mother/child incompatibilities for the ABO and rhesus systems. Conclusions: The percentage of microchimeric cells varies to a great extent in Hashimoto's thyroiditis, and this phenomenon can occur in nodular goiter in rare instances, but it appears to be absent from normal thyroid glands. Nevertheless, the biological significance of MCH remains unclear. Moreover, we have concluded that the tested blood group systems (as opposed to their role in graft vs host disease after transplantations) have no effect on fetal MCH.European Journal of Endocrinology 154 237-241

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Section: Discussionsupporting

confidence: 71%

Fetal microchimerism in Hashimoto’s thyroiditis: a quantitative approach

et al. 2006

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“…Cases and controls from the selected studies were assessed for our inclusion/exclusion criteria. Eleven of 35 studies had subjects meeting the inclusion criteria (7,(11)(12)(13)(15)(16)(17)(18)(19)(20)(21). Individual data from 124 of 447 study subjects were extracted from these 11 studies and analyzed (Table 1).…”

Section: Resultsmentioning

confidence: 99%

The influence of fetal loss on the presence of fetal cell microchimerism: A systematic review

Khosrotehrani¹,

Johnson²,

Lau³

et al. 2003

Arthritis & Rheumatism

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Objective. Fetal cells enter the maternal circulation during most pregnancies. Their persistence for years occurs in only some women and has been associated with several autoimmune diseases such as systemic sclerosis. The objective of this study was to determine whether pregnancy history influences the persistence of fetal microchimeric cells.Methods. We reviewed all reports of studies on fetal cell microchimerism, defined as male DNA in maternal tissue, that describe individual pregnancy histories, disease diagnoses, and microchimerism status. The total numbers of pregnancies, births, and sons, the history of fetal loss (spontaneous abortion and elective termination), and the presence of a maternal autoimmune disease were tested as factors potentially associated with persistent microchimerism.Results. One hundred twenty-four subjects from 11 studies met the inclusion criteria. Only fetal loss was significantly associated with the presence of microchimerism (odds ratio 2.4, 95% confidence interval 1.2-6.0).Conclusion. These results suggest that fetomaternal cell trafficking following fetal loss may be important for the engraftment of microchimeric cells in maternal tissue. This may be due to an increased amount of fetomaternal transfusion or to transfer of a cell type that is more likely to engraft. We recommend that investigators in future studies on microchimerism report detailed pregnancy information, since these data are critical for the understanding of factors that influence the development of fetal cell microchimerism.

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“…One can speculate whether microchimerism during pregnancy, that is, the phenomenon that foetal cells may pass into the maternal circulation and tissues, play a role in the highly increased risk of breast cancer seen among the mothers giving birth to an AT child. It has been suggested that microchimerism is associated with various immunological conditions of pregnancy and some chronic autoimmune conditions predominantly found in women (Bianchi, 2000), and in one study it has been associated with cervical cancer (Cha et al, 2003). It is conceivable that being pregnant with a foetus affected with AT may facilitate this biological phenomenon, and that the presence of foetal AT cells in the circulation or tissues of the mother may contribute to the development of maternal breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Breast and other cancers in 1445 blood relatives of 75 Nordic patients with ataxia telangiectasia

et al. 2005

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Epidemiological studies have consistently shown elevated rates of breast cancer among female blood relatives of patients with ataxia telangiectasia (AT), a rare autosomal recessive disease. A large proportion of the members of AT families are carriers of AT-causing gene mutations in ATM (Ataxia Telangiectasia Mutated), and it has been hypothesised that these otherwise healthy carriers are predisposed to breast cancer. This is an extended and enlarged follow-up study of cancer incidence in blood relatives of 75 patients with verified AT in 66 Nordic families. Blood relatives were identified through population registry linkages, and the occurrence of cancer was determined from cancer registry files in each country and compared with national incidence rates. The ATM mutation carrier probabilities of relatives were assigned from the combined information on location in family, consanguinity, if any, and supplementary carrier screening in some families. Among the 1445 blood relatives of AT patients, 225 cancers were observed, with 170.4 expected, yielding a standardised incidence ratio (SIR) of 1.3 (95% confidence interval (CI), 1.1 -1.4). Invasive breast cancer occurred in 34 female relatives (SIR, 1.7; 95% CI, 1.2 -2.4) and was diagnosed in 21 women before the age of 55 years (SIR, 2.9; 95% CI, 1.8 -4.5), including seven mothers of probands (SIR, 8.1; 95% CI,. When the group of mothers was excluded, no clear relationship was observed between the allocated mutation carrier probability of each family member and the extent of breast cancer risk. We concluded that the increased risk for female breast cancer seen in 66 Nordic AT families appeared to be restricted to women under the age of 55 years and was due mainly to a very high risk in the group of mothers. The findings of breast cancer risk in mothers, but not other likely mutation carriers, in this and other studies raises questions about the hypothesis of a simple causal relationship with ATM heterozygosity.

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Cervical Cancer and Microchimerism

Cited by 41 publications

References 24 publications

Fetal microchimerism in Hashimoto’s thyroiditis: a quantitative approach

Fetal microchimerism in Hashimoto’s thyroiditis: a quantitative approach

The influence of fetal loss on the presence of fetal cell microchimerism: A systematic review

Breast and other cancers in 1445 blood relatives of 75 Nordic patients with ataxia telangiectasia

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