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The transition of detached fragments of mitochondrial DNA into the nucleus and their integration into chromosomal DNA is a special kind of genetic variability that highlights the relation between the two genomes and their interaction in a eukaryotic cell. The human genome contains several hundreds of insertions of mtDNA fragments (NUMTS). This paper presents an overview of the current state of research in this area. To date, evidence has been obtained that the occurrence of new mtDNA insertions in the nuclear genome is a seldom but not exceptionally rare event. The integration of new mtDNA fragments into the nuclear genome occurs during double-strand DNA break repair through the non-homologous end joining mechanism. Along with evolutionarily stable “genetic fossils” that were integrated into the nuclear genome millions of years ago and are shared by many species, there are NUMTS that could be species-specific, polymorphic in a species, or “private”. Partial copies of mitochondrial DNA in the human nuclear genome can interfere with mtDNA during experimental studies of the mitochondrial genome, such as genotyping, heteroplasmy assessment, mtDNA methylation analysis, and mtDNA copy number estimation. In some cases, the insertion of multiple copies of the complete mitochondrial genome sequence may mimic paternal inheritance of mtDNA. The functional significance of NUMTS is poorly understood. For instance, they may be a source of variability for expression and splicing modulation. The role of NUMTS as a cause of hereditary diseases is negligible, since only a few cases of diseases caused by NUMTS have been described so far. In addition, NUMTS can serve as markers for evolutionary genetic studies. Of particular interest is the meaning of NUMTS in eukaryotic genome evolution. The constant flow of functionally inactive DNA sequences from mitochondria into the nucleus and its significance could be studied in view of the modern concepts of evolutionary theory suggesting non-adaptive complexity and the key role of stochastic processes in the formation of genomic structure.

Interventional examinations are associated with high levels of patient exposure per examination, which makes it particularly important to monitor individual patient doses and to assess radiation risks. The aim of this study was the assessment of effective doses for fluoroscopy-guided balloon dilatation of benign esophageal strictures, whichwasperformedonpediatricpatientsaged 1 to 2 yearsatthe Departmentof Radiosurgical Methodsof Diagnosis and Treatment of St. Petersburg State Pediatric Medical University. Patient exposure patterns were basedonourowndatacollection. Thecalculationofeffectiveandorgandosesofpatientsnormalizedbythevalue of the dose area product measured during the study was carried out using PCXMC 2.0 software. The conversion coefficients from the dose area product to the effective dose were calculated using tissue weighting coefficients from the ICRP Publications 60 and 103 their values were 10.7 and 11.7 µSv/cGy cm2, respectively. The results of verification of the method indicated that the use of inappropriate conversion coefficients leads to an almost double underestimation of children’s effective doses. Differences in the values of conversion coefficients are significant and are explained by differences in voltage, source to image distance, and irradiation field size. A simplified model of patient exposure was proposed, which is described by a single irradiation field. The assessment of effective doses using multi-field and single-field irradiation model shows comparable results, which allows using the differentiated approach to the assessment of radiation doses of patients.

Analysis of levels of exposure of public of the Russian Federation by sources of ionizing exposure is one of main parts of the activities conducted by the Federal Service for Surveillance on Consumer Rights Protection and Human Wellbeing. Data on the doses of public of the Russian Federation from medical exposure on facility, regional and federal levels is collected using the form of federal governmental statistical surveillance № 3-DOZ “Data on patient doses from medical X-ray examinations”, that is active since 2000. For the last 20 years there were no significant updates of the form № 3-DOZ. According to the decision of the Board of the Rospotrebnadzor from 11.09.2020, a complex program on update and modernization of form № 3-DOZ was initiated, that has resulted in the approvement of new form № 3-DOZ by the order of Rosstat № 880. The form has been significantly changed to reflect the modern condition of X-ray diagnostics in the Russian Federation. The aim of the current study was to analyze main components of medical exposure dose data collection system that required update and modernization. The study was performed based on the results of assessment of the forms № 3-DOZ from different medical facilities and regions in 2015-2020. The results of the study allowed developing main approaches to the update of the form № 3-DOZ that were implemented in a new edition of the form.

Clonal hematopoiesis is a common age-dependent state accompanied by the expansion of mutant hematopoietic stem cells as a result of somatic mutations and is associated with a high risk of hematopoietic neoplasms and cardiovascular diseases. Clonal hematopoiesis in human ontogenesis occurs asymptomatically, and the fraction of mutant clones can exceed more than 2% of the total pool of circulating nucleated blood cells by age 70. Due to the variability of the accumulation rate of mutant clones, signs of clonal hematopoiesis can be observed at a younger age. Clonal hematopoiesis may act as a benign, precancerous condition and a strong factor for acute cardiovascular events such as myocardial infarction and stroke. Current evidence indicates that somatic mutations in driver genes of clonal hematopoiesis significantly increase the risk of acute conditions such as acute myeloid leukemia and acute myocardial infarction. The high mortality and morbidity of cardiovascular and cancer diseases, and their strong association with clonal hematopoiesis, make it of indeterminate potential worthy of close attention.

The structure of diseases in humans is heterogeneous, which is manifested by various combinations of diseases, including comorbidities associated with a common pathogenetic mechanism, as well as diseases that rarely manifest together. Recently, there has been a growing interest in studying the patterns of development of not individual diseases, but entire families associated with common pathogenetic mechanisms and common genes involved in their development. Studies of this problem make it possible to isolate an essential genetic component that controls the formation of disease conglomerates in a complex way through functionally interacting modules of individual genes in gene networks. An analytical review of studies on the problems of various aspects of the combination of diseases is the purpose of this study. The review uses the metaphor of a hermeneutic circle to understand the structure of regular relationships between diseases, and provides a conceptual framework related to the study of multiple diseases in an individual. The existing terminology is considered in relation to them, including multimorbidity, polypathies, comorbidity, conglomerates, families, “second diseases”, syntropy and others. Here we summarize the key results that are extremely useful, primarily for describing the genetic architecture of diseases of a multifactorial nature. Summaries of the research problem of the disease connection phenomenon allow us to approach the systematization and natural classification of diseases. From practical healthcare perspective, the description of the disease connection phenomenon is crucial for expanding the clinician’s interpretive horizon and moving beyond narrow, disease-specific therapeutic decisions.

Risk communication is one of the stages of health risk analysis and is an interactive process of exchange of information and opinions about risks, including medical risks, between risk assessment specialists, decision makers, the media, stakeholder groups and the public. In organizing interaction with stakeholders in the risk communication process, sociological research helps to explore the attitudes of the actors. One of risk communication situations in the field of radiation protection is information provision to patients and their legal representatives about radiation health risks due to the medical radiology examinations. The aim of this study was to assess the radiation risk perception among parents and legal representatives of children undergoing radiological examinations. Parents and legal representatives of children undergoing hospital treatment from November 2021 to March 2022 were interviewed in a large pediatric infectious diseases hospital. A questionnaire designed at St. Petersburg Research Institute of Radiation Hygiene was used for the interviews. In total, 125 people were interviewed. The study showed that there were no significant differences in the perception of radiation risks among parents and legal representatives of children undergoing inpatient treatment with different socio-demographic characteristics. The level of knowledge was not identified as a factor shaping a tolerant attitude toward medical radiation risks. Parents and legal representatives of children undergoing hospital treatment show high rates of trust in the attending physicians and medicine in general. The study results show that those who have been informed about the risks generally have lower risk perception for radiological medical examinations than those who have not been informed about the risks.

The number and contribution of high dose imaging modalities, computed tomography in particular, is rapidly increasing both in the 'Russian Federation and other developed countries. Maximal increase in the number of computed tomography examinations in Russia was observed in 2020 due to the full-scale application of this imaging modality for the diagnostics of the novel coronavirus infection COVID-19. The use of computed tomography for the examination of the chest for the pregnant women is associated with several issues. An internationally accepted approach for the provision of the radiation safety of the pregnant patients is the assessment of the absorbed dose in the fetus after each X-ray examination. However, there are no existingn approved methods for the assessment of the absorbed dose in the fetus in the Russian Federation. The aim of the current study was to assess the doses in the fetus for the pregnant women undergoing computed tomography of the chest due to the COVID-19 and to estimate the probability of the development of the deterministic effects for the fetus. The study was based on the collection of the parameter of Russian and international computed tomography protocols. Parameters of the international computed tomography protocols were collected viameta-analysis of the existing publications; Russian protocols — via data collection in computed tomography departments in St-Petersburg hospitals. Absorbed dose in the uterus of the female patient and effective dose for the fetus were calculated using NCICT 3.0 software for 8, 10, 15, 20, 25, 30, 35 and 38 weeks of pregnancy. The results of the calculations indicate the lack of significant differences between absorbed doses in the uterus and effective doses for the fetus for all stages of pregnancy. Maximal doses for the selected computed tomog­ raphy protocols were in the range of 0.5 mGy (mSv) for 8-25 weeks, 0.6 mGy (mSv) for 30 week, 1.4 mGy (mSv) for 35 week and 2.7 mGy (mSv) for 38 week. The threshold for the development of the deterministic effects equal to 100 mGy cannot be exceeded even for repeated (10-15) computed tomography chest scans. Hence, the use of computed tomography as the primary method of COVID-19 diagnostics and staging will not be associated with the development of deterministic effects in the fetus.

Computed tomography is associated with high patient doses. CT is actively used for pediatric, however, currently there is no reliable data on the pediatric patient doses in the Russian Federation. The current study presents the data on the anthropometric characteristics of 5, 10 and 15-year-old pediatric patients, as well as the results of a comparative assessment of the effective doses of these patients during CT-examinations of chest, considering their anthropometric data. The effective doses were calculated using three methods: based on the actual guidelines (MU 2.6.1.3584-19) using the age specific conversion coefficients; using the conversion coefficients considered patient body mass and effective diameter; using a specialized software NCICT 3.0. The difference between effective doses according to actual guidelines and considering patient body mass and effective diameter was about 7.1 % (max-65 %). High deviations were observed in patients with abnormally large or abnormally low body mass. Effective doses calculated using NCICT 3.0 were higher compared to doses calculated according to actual guidelines on average by 18 % (max — 53 %). Such differences are explained by the fact that in MU 2.6.1.3584-19 conversion coefficients are presented for the most common CT-scan parameters of protocols, and in NCICT 3.0 the calculation considers individual scan parameters for each patient. The difference between effective doses according to NCICT 3.0 and considering patient body mass and effective diameter was about 32 % (max-70 %). This difference can be explained by the differences in the anthropometric data of some patients, and by the use of different types of phantoms: a stylized phantom (Golikov et al) and a voxel phantom in NCICT 3.0.

Objective was to determine the presence and the main manifestations of professional burnout syndrome among intensive care doctors and nurses from the department of anesthesiology and intensive care. Material and methods. Resuscitators and secondary medical staff were asked to pass a questionnaire, which included a survey by V.V. Boyko «Emotional burnout», a test by C. Spielberger in the modification Y.A. Hanin, the technique of Munsterberg. Results and discussion. Professional burnout syndrome is typical for 55 % of resuscitators and 35 % of mid-level medical staff of the department of anaesthesiology and intensive care of the pediatric University clinic. As for the respondents of the first group, the presence of the «resistance» phase is characteristic, while the second group has the «resistance» and «exhaustion» phases. According to the Spielberger scale, both groups have a middle degree of situational and personal anxiety. The Munsterberg method found that selectiveness and concentration of attention before and after the daily shift is more decreased in resuscitators. Conclusion. High rates of susceptibility of specialists of the department of anaesthesiology and intensive care to the formation of professional burnout syndrome, which affects their psychological health, were established. It is necessary to develop appropriate measures to prevent this occurrence.

The study of the phenomenon of a combination of several diseases at the same time in an individual, actualized in the second half of the 19th century, is being actively analyzed 150 years later using genetic approaches. We present an overview of the results of such studies in relation to allergic diseases, in particular, a special variant, the so-called «atopic march», the sequential development of eczema, allergic rhinitis and asthma («atopic march» syntropy). The data of genetic and epidemiological studies were summarized, the analysis of genome-wide associative studies was carried out, and the role of mutations in the filaggrin gene (FLG) in the development of the «atopic march» syntropy was considered.

Co-occurrence of cardiovascular diseases is significantly common among patients with bronchial asthma. Genetic factors can have a significant effect on the development of hypertension in patients with asthma. Objective of the study was to investigate the associations of polymorphic variants relating to quantitative changes in the expression profile (eQTL) of the CAT, TLR4, and IL10 genes with the development of bronchial asthma co-morbid with arterial hypertension.Material and methods. Genotyping of 48 eQTL SNPs of the CAT, TLR4, and IL10 genes was performed using MALDI-TOF mass spectrometry in patients with «isolated» asthma (n = 145) and arterial hypertension (n = 144) and their combination (n = 146), as well as in the control group of healthy individuals (n = 152). Using logistic regression, an analysis of the associations of haplotypes with the studied diseases was carried out.Results. An association of bronchial asthma in combination with arterial hypertension with haplotypes formed by eQTL SNPs of the CAT and TLR4 genes was established. The spectrum of haplotypes associated with comorbidity of asthma and hypertension differs from the haplotypes associated with “isolated” asthma.Conclusion. The molecular base of asthma and hypertension comorbidity can be associated with variants that control the expression of TLR4 and CAT genes.

The goal of the study was to analyze copy number variation (CNV) in the GBP3 gene between white blood cells and atherosclerotic plaques of patients with carotid atherosclerosis. The material was both blood samples and atherosclerotic plaques obtained from the same patients with carotid atherosclerosis (n = 94). Assessment of CNV was performed using digital droplet PCR. As a result, it was shown that among 94 patients with carotid atherosclerosis, the CNV frequency was 44 % in the GBP3 gene in leukocytes. Deletion was detected in 5 (5.3 %) patients, and loss in 36 (38.3 %) patients. The gain was identified in one patient. Somatic mosaicism was found in 12 (13 %) of patients, comparing DNA samples of atherosclerotic plaque tissue and white blood cells from the same patients. Mosaic copy number losses predominantly were detected in white blood cells, in contrast mosaic copy number gains were identified in atherosclerotic plaques. Somatic mosaicism of the GBP3 gene is widespread in atherosclerosis. Different ratio of mosaic clones carrying certain type of CNV in GBP3 gene is presented.

Study of the causes and mechanisms leading to sudden death is one of the most important goals in cardiology. Multiple studies suggest substantial role of mitochondrial dysfunction in the sudden death pathogenesis. Lack of ATP, excess of reactive oxygen species, and disruption of ionic balance in mitochondria are all able to provoke life-threatening arrhythmia. Mitochondrial DNA, which encodes several subunits of mitochondrial respiratory chain, is characterized by considerably high variability in human populations. It has been shown that cell respiration can depend on common mtDNA polymorphisms. In addition, there are data on associations of mtDNA polymorphisms with predisposition to cardiovascular diseases, including those associated with high risk of sudden death. The differences in cell bioenergetics between mtDNA genotypes do not influence myocardial function in normal state but may appear to be critical under acute ischemic conditions. So, mitochondrial genome should be considered as one of main components in the pathogenetics of sudden cardiac death.

Aim. Identification of the genes, different in the level of DNA methylation among the cells of intact or atherosclerotic arteries in patients with coronary and carotid atherosclerosis.Material and methods. Into the study group, atherosclerosis patients were included, who had undergone coronary bypass surgery or carotid endarterctomy, and relatively healthy individuals. The assessment of methylation level of various 27578 CpG-sites/14475 genes was done with the microchip Infinium Human Methylation27 BeadChip (Illumina) in the specimens of atherosclerotically changed coronary (n=6), carotid (n=6), intact internal thoracal arteries (n=8) and large saphenous veins (n=8). Level of methylation in the locus 2q31.1 (HOXD4/HOXD3/MIR10B) was measured with bisulphite pyrosequencing of DNA in the vessels specimens and leucocytes of the same patients (n=130), as in the leucocytes of relatively healthy men (n=110).Results. In the cells of atherosclerotically changed arteries, comparing to intact vessels, the change of methylation level by 20% and more is found for 46 CpG-sites/42 genes (pFDR

The review is focused on current views on the structural variation of genome of somatic cells as components related to atherosclerosis. The original data presented on the variation spectrum of DNA areas copies in peripheral blood leucocytes and arterial cells in human atherosclerosis. The future directions sketched for the research on somatic cells genome variation with the aim for pathogenetics of multifactorial diseases.

BACKGROUND:Genome-wide association studies have identified novel genetic associations for asthma, but without taking into account the role of active tobacco smoking. This study aimed to identify novel genes that interact with ever active tobacco smoking in adult onset asthma. METHODS:We performed a genome-wide interaction analysis in six studies participating in the GABRIEL consortium following two meta-analyses approaches based on 1) the overall interaction effect and 2) the genetic effect in subjects with and without smoking exposure. We performed a discovery meta-analysis including 4,057 subjects of European descent and replicated our findings in an independent cohort (LifeLines Cohort Study), including 12,475 subjects. RESULTS:First approach: 50 SNPs were selected based on an overall interaction effect at p

Aim. To study the clinical and predictive importance of polymorphism of rs1800629 (G-308A) of TNF gene in patients with STEMI.Material and methods. Research included patients (171 persons with STEMI), hospitalized to the Kemerovo cardiological center and 188 individuals without the diagnosed cardiovascular diseases. In all patients the genotype had the polymorphism of rs1800629 of TNF gene. Investigation was carried out with help the original DNA microarray.Results. Associations of the rs1800629 (G-308A) polymorphic variant in the TNF gene with the concentration of the tumor necrosis factor alpha (TNFa) in the blood serum and cardiovascular complications in patients with myocardial infarction with the elevated ST segment (MIST) have been studied. Allele A rs1800629 frequency in patients with MIST (n=171) was 11,7% which did not differ from the frequency in healthy controls (n=188) – 12,2%. Allele A careerstatus was associated with the higher levels of the TNFa concentration in the blood serum measured at the day 10th-14th after MI: 11,02 pg/ml compared to 9,49 in G homozygotes (p=0,045). While analyzing the clinical status of MIpatients after one year follow up, it was revealed that A allele has the frequency 19% in patients with progressive angina pectoris (AP) compared to 10% in patients without progressive AP, and 16% in patients with cardiovascula rcomplications (CVC) such as repeated MI, stroke, instable AP or death from cardiovascular reasons compared to 9% frequency in patients without CVC, which was not statistically significant. We had shown in earlier s tudy that TNFa high level in patients with MI is related to the risk of CVC. Although, in current study we did not detect an association of the rs1800629 with progression of the AP, chronic heart failure decompensation, CVC or death from cardiovascularreasons in one year after IM. Thus, rs1800629 allele A does influence TNFa concentrations, but there is no data supporting the fact that this variant is an independent risk factor for IM and its complications.Conclusion. The results indicate possible predictive value of rs1800629 polymorphism of TNF gene to predict the cardiovascular events in patients with STEMI during 12 months of follow up.

The purpose of this study was to identify the features of methylation status of genes whose products are involved in the cell proliferation in vascular tissues of patients with atherosclerosis. We tested the vascular samples from carotid arteries, internal mammary arteries and saphenous veins, which differ in their morphological and functional characteristics and the degree of susceptibility to pathology. DNA methylation profiling was performed by using the microarray «Infinium Human-Methylation27 BeadChip» («Illumina», USA), methylation-sensitive polymerase chain reaction and methylation-specific PCR. For the first time we identified 45 CpG-sites of 36 genes with differential DNA methylation between vascular tissues. The most pronounced differences in the DNA methylation level were registered for CpG-dinucleotides of genes ALOX12, CARD11, DAB2IP, PTPRC, RA-SIP1, THRB, TLR4, TNFRSF9 and WNT16. Our data do not support the hypothesis of epigenetic dysregulation of cell-cycle genes (CDKN2A (p16INK4a and p14ARF), CDKN2B (p15INK4b)) in atherosclerosis.

Цель. Изучение полиморфных маркеров генов нейрональной и эндотелиальной синтаз оксида азота (NOS1 и NOS3), а также иммунологических показателей (клеточный иммунитет, гуморальный иммунитет, структурно-метаболический статус и функциональная активность нейтрофильных гранулоцитов) у больных СД1 на популяционном и семейном уровне. Материалы и методы. Для исследования было выбрано два дизайна. Первый дизайн: случай (163 ребенка больных СД1) ? контроль (243 индивида русской национальности, проживающих в Томске и не имеющих по данным клинического, инструментального обследования СД1 и признаков сердечно-сосудистых нарушений). Второй дизайн: случай (80 детей и подростков больных СД1) ? контроль (родственники первой степени родства ? 220 человек). Были изучены один полиморфный маркер гена NOS1 ? C/T (в 18 экзоне) и четыре полиморфных маркера гена NOS3 (VNTR в интроне 4, -691C/T в области промотора и две нуклеотидные замены ? 774С/T, 894G/T в 6-м и 7-м экзонах соответственно). Результаты. Анализ методом ?случай-контроль? (больные сахарным диабетом ? здоровые лица) показал наличие статистически значимой ассоциации полиморфного маркера С/Т гена NOS1, при этом OR составил 1,491. Дети с генотипом ВВ полиморфного маркера VNTR гена NOS3 имели достоверно меньшее отношение CD4/CD8, чем дети с генотипами АА и АВ, что обусловлено снижением количества CD4 у детей с генотипом ВВ. Соотношение CD4/CD8 у больных СД1 с генотипами АА и АВ не отличалось от показателей здоровых детей (2,26?0,19) Томска. Выводы. Больные сахарным диабетом 1 типа русского населения Томской области достоверно чаще являются носителями аллеля С полиморфного маркера С/Т гена нейрональной синтазы NO, аллеля В полиморфного маркера VNTR, аллеля С полиморфного маркера С691Т, аллеля С полиморфного маркера С774Т и аллеля G полиморфного маркера G894Т гена эндотелиальной синтазы NO. Получены следующие ассоциации иммунологических показателей с полиморфными маркерами: CD4/CD8 ? VNTR, поглотительная способность нейтрофилов ? C774T, поглотительная способность нейтрофилов ? G894T гена эндотелиальной синтазы NO.

Цель. Поиск ассоциаций инсерционно-делеционного полиморфизма гена АСЕ с СД 1 типа, его клиническими особенностями и количественными показателями иммунитета и липидного обмена. Материалы и методы. Обследованы 113 детей с СД 1 типа в возрасте 13,1 ?0,3 лет, (мальчиков 53,1 %, девочек 46,9 %). Дети находились под наблюдением в клинике НИИ медицинской генетики Томского научного центра РАМН и эндокринологическом отделении детской больницы № 1 Томска. Исследовали иммунный статус 1-го уровня с определением уровня IL-1, IL-2, 1L-4, IL-6, FNO-rx. Исследовали содержание общего холестерина (ХС), холестерина липопротеидов высокой плотности (ХС ЛПВП) и триглицеридов (ТГ). У всех пациентов определяли показатели перекисного окисления липидов (ПОЛ) по содержанию малонового диальдегида; о состоянии антиоксидантной защиты судили по уровню каталазы. Выводы. В Сибирской популяции сахарный диабет 1 типа у большинства детей манифестируется в возрасте 7-11 лет, чаще встречается среди мальчиков, у которых имеет стабильное течение; чаще достигается ремиссия на первом году заболевания, ниже потребность в инсулине, реже развивается диабетическая нефропатия. Результаты теста на неравновесие по сцеплению на семейном материале показали наличие взаимосвязи аллеля D с диабетической нефропатией. Установлены ассоциации показателей липидного обмена, 1L-6 и потребности в экзогенном инсулине с генотипами I/D полиморфизма гена АСЕ.

Aim. Analysis of associations between idiopathic disturbances of cardiac conduction (DCC) and polymorphism of mitochondrial genome. Material and methods. A family examination was performed in 431 probands with various DCC and 1347 relatives of the first, second and third degree of kinship (the study group). All the examinees were divided into four subgroups. These included 158 probands with atrioventricular block (A VB) of various degree and their 518 relatives (subgroup 1); 50 probands with a complete right bundle-branch block (BBB) and their 161 relatives (subgroup 2); 108 probands with a complete left BBB and left anterior branch of the His bundle and their 152 relatives (subgroup 3); 115 probands with sick sinus syndrome (SSS) and their 327 relatives (subgroup 4). The control group consisted of 104 probands without clinical ECG manifestations of cardiac diseases and their 321 relatives. All the examinees have undergone ECG, atropin test, echocardioscopy, electrophysiological examination of the heart and mitochondrial DNA (mDNA). Results. Comparison of the incidence of mDNA D-loop restriction sites in the group of patients with idiopathic DCC and controls has found higher frequency of the Hae III 16517 site in the group of the patients (p = 0.0480). By location of the blocks (atrioventricular and intraventricular), the site occurred more frequently in patients with AVB (86.36%). The variant "+" by the site of Hae III 16517 mDNA was found to associate with disturbances of cardiac conduction, more closely in AVB. Conclusion. Variability of mDNA may be an etiological factor of idiopathic DCC pathogenesis.