Бібліотека Вінницького національного медичного університету ім. М.І.Пирогова

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Brieieva, O.
Causes and consequences of genome instability in cancer / O. Brieieva // Онкологія. - 2021. - Т. 23, № 4. - P231

MeSH-main:
НОВООБРАЗОВАНИЯ -- NEOPLASMS (генетика, диагностика, патофизиология)
ГЕНОМА НЕСТАБИЛЬНОСТЬ -- GENOMIC INSTABILITY
Annotation: Genome instability is currently considered one of the main drivers of tumor heterogeneity, clonal evolution, and cancer progression. At present, a wide range of genetic and epigenetic abnormalities associated with different stages of oncogenesis have been identified. It is believed that many of them may influence disease prognosis and therapy efficiency. In tumor cells, lesions are detected at different levels of genome organization that manifests by changes in both structure and number of single nucleotides and chromosomes. Depending on the kind of genetic changes, there are several types of instability: nucleotide, microsatellite, and chromosomal. Recent studies have significantly deepened our understanding of factors leading to the development of different types of genome instability. Among these factors, abnormalities of DNA replication and repair, exo- and endogenous genotoxic influences, unequal distribution of genetic material during mitosis, and epigenetic modifications are considered the most significant. It is thought that mechanisms underlying genome instability may vary at different stages of oncogenesis. In addition, there is evidence of possible differences in the background of genetic changes and mutator phenotype in cells of patients with hereditary and sporadic forms of cancer. In particular, it is suggested that germline mutations in DNA repair and tumor suppressor genes play a key role in the development of genome instability in hereditary forms of cancer, whereas in sporadic tumors, such instability may be predominantly driven by replicative stress
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Brieieva, O.
Scientific and Practical Conference of Young Scientists “Fundamental Medicine: Integrated Approaches to Cancer Therapy” [Text] / O. Brieieva // Экспериментальная онкология. - 2019. - Т. 41, № 1. - С. 84-86. - Bibliogr. at the end of the art.

Annotation: On February 4–5, 2019, the R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology of the National Academy of Sciences of Ukraine (IEPOR NASU) hosted the Scientific-Practical Conference of Young Scientists “Fundamental Medicine: Integrated Approaches to Cancer Therapy” dedicated to the World Cancer Day. The event took place by the initiative and support of the Council of Young Scientists of IEPOR NASU
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Buchynska, L. G.
Sensitivity to 4-hydroxyestradiol and dna repair efficiency in peripheral blood lymphocytes of endometrial cancer patients [Text] / L. G. Buchynska, O. V. Brieieva // Экспериментальная онкология. - 2018. - Т. 40, № 1. - С. 68-72. - Bibliogr. at the end of the art.

MeSH-main:
НОВООБРАЗОВАНИЯ ГОРМОНОЗАВИСИМЫЕ -- NEOPLASMS, HORMONE-DEPENDENT (диагностика, патофизиология, этиология)
КАРЦИНОМА ЭНДОМЕТРИОИДНАЯ -- CARCINOMA, ENDOMETRIOID (патофизиология, этиология)
ЛИМФОЦИТЫ -- LYMPHOCYTES (цитология)
ДНК ПОВРЕЖДЕНИЕ -- DNA DAMAGE
РИСКА СТЕПЕНИ ОЦЕНКА -- RISK ADJUSTMENT (статистика, тенденции)
СТАТИСТИЧЕСКАЯ ОБРАБОТКА ДАННЫХ -- DATA INTERPRETATION, STATISTICAL
Annotation: The development of hormone-dependent cancers, including endometrial carcinomas, in great part may be mediated by the genotoxic effects of estrogen metabolites, among which 4-hydroxyestradiol (4OHE2) is characterized by the most prominent DNA-damaging properties. It is assumed that the individual sensitivity to the 4OHE2 may determine the predisposition to endometrial cancer (EС). Aim: To analyze the sensitivity of peripheral blood lymphocytes (PBLs) of EC patients to the 4OHE2 and to evaluate the repair efficiency of 4OHE2-induced DNA damage. Materials and Methods: The study was performed on the PBLs of 53 EC patients and 20 healthy women. The level of DNA damage was measured using the comet assay and was expressed as % tail DNA. The DNA repair efficiency (%) was evaluated by determining the ratio between the amount of repaired DNA damage and the level of 4OHE2-induced damage that appeared after incubation of PBLs with 4OHE2. Results: In PBLs of EC patients, a higher level of 4OHE2-induced DNA damage (32.0 ± 2.2% tail DNA) and lower DNA repair efficiency (34.0 ± 4.5%) was observed compared to PBLs of healthy women (22.3 ± 2.3% tail DNA and 48.8 ± 4.5%, respectively). PBLs of EC patients with deep tumor invasion of myometrium were characterized by more prominent decrease of DNA repair than those with less invasive tumor ( ½ of myometrium) (20.9 ± 7.8 and 43.7 ± 6.7%, respectively). Furthermore, lower DNA repair efficiency was detected in the PBLs of EC patients with a family history of cancer compared to this parameter in patients with sporadic tumors (20.9±7.8 and 47.1 ± 5.5%, respectively). Conclusion: The PBLs of EC patients are characterized by increased sensitivity to the genotoxic effect of 4OHE2 and reduced repair efficiency regarding 4OHE2-induced DNA damage. A lower level of DNA repair is observed in EC patients with deep tumor myometrial invasion and a family history of cancer
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Brieieva, O. V.

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DNA damage in tumor cells and peripheral blood lymphocytes of endometrial cancer patients assessed by the comet assay [Text] / L. G. Buchynska [та ін.] // Экспериментальная онкология. - 2017. - Т. 39, № 4. - С. 299-303. - Bibliogr. at the end of the art.

MeSH-main:
ЭНДОМЕТРИЯ НОВООБРАЗОВАНИЯ -- ENDOMETRIAL NEOPLASMS (этиология)
ГЕНЫ СУПРЕССОРЫ ОПУХОЛЕВОГО РОСТА -- GENES, TUMOR SUPPRESSOR (физиология)
ДНК ПОВРЕЖДЕНИЕ -- DNA DAMAGE (физиология)
ЛИМФОЦИТЫ, ИНФИЛЬТРИРУЮЩИЕ ОПУХОЛЕВЫЕ КЛЕТКИ -- LYMPHOCYTES, TUMOR-INFILTRATING (ультраструктура)
ПЕНЕТРАНТНОСТЬ -- PENETRANCE
СТАТИСТИЧЕСКАЯ ОБРАБОТКА ДАННЫХ -- DATA INTERPRETATION, STATISTICAL
Annotation: To date, genome instability is considered to be a common feature not only of tumor cells, but also of non-malignant cells of cancer patients, including peripheral blood lymphocytes (PBLs). The issue of the association between genome instability in tumor cells and PBLs, as well as of its relationship with tumor progression remains poorly understood. Aim: To evaluate the level DNA damage in tumor cells and PBLs of endometrial cancer (EC) patients with regard to clinical and morphological characteristics of the patients. Materials and Methods: DNA damage was assessed in 106 PBLs samples and 42 samples of tumor cell suspension from EC patients by comet assay. PBLs from 30 healthy women were used as control. The level of DNA damage was expressed as the percentage of DNA in the comet tails (% tail DNA). Results: It was revealed that the amount of DNA damage in PBLs of EC patients was 2.2 times higher in comparison with that of healthy donors (8.3 ± 0.7 and 3.7 ± 0.4% tail DNA, respectively) (p 0.05). In this study, no association between the levels of DNA damage in endometrial tumor cells and PBLs was observed (r 0.05). The amounts of DNA damage both in tumor cells and PBLs were not related to the degree of tumor differentiation as well as the depth of myometrial invasion, but depended on the body mass index (BMI) of EC patients: high level of lesions was observed in patients with elevated BMI values. Furthermore, the level of DNA damage in tumor cells was associated to familial aggregation of cancer and was significantly higher in endometrial cells from patients with family history of cancer vs that from EC patients with sporadic tumors (32.3 ± 2.9 and 22.8 ± 1.8% tail DNA, respectively) (p 0.05). It was also found that for women who had high level of DNA damage in PBLs, the risk of EC was greater (odds ratio value of 3.5) compared to those with low level of such lesions. Conclusion: Genome instability that appears as an increased level of DNA damage in tumor cells and PBLs of EC patients is associated with BMI and family history of cancer and can reflect a predisposition to cancer
Additional Access Points:
Buchynska, L. G.
Brieieva, O. V.
Lurchenko, N. P.
Protsenko, V. V.
Nespryadko, S. V.

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Overexpression of the mitochondrial ribosomal protein S 18-2 in the invasive breast carcinomas / L. G. Buchynska [et al.] // Experimental Oncology. - 2018. - Том 40, N 4. - P303-308

MeSH-main:
МОЛОЧНОЙ ЖЕЛЕЗЫ НОВООБРАЗОВАНИЯ -- BREAST NEOPLASMS (диагностика, метаболизм, патофизиология)
ВНУТРИКЛЕТОЧНЫЕ СИГНАЛЬНЫЕ ПЕПТИДЫ И БЕЛКИ -- INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS (метаболизм)
Annotation: Recent studies allow to consider the mitochondrial ribosomal protein S18-2 (MRPS18-2, S18-2) as a potential oncoprotein, which suggests the need for further characterization of its expression in tumors of different genesis including breast cancer (BC). The aim of the study was to analyze the expression of the S18-2 protein in BC of luminal A and basal subtypes. Materials and Methods: Operational material of BC patients stage І–ІІ (luminal A subtype, n = 30, and basal subtype, n = 10) was studied with the use of morphological, immunohistochemical, statistical and bioinformatic methods. Results: Using the immunohistochemical analysis, we found that the S18-2 protein showed the nuclear signal in 66.7% of luminal A subtype BC samples and 80.0% of basal subtype BC samples. The variability of the S18-2 expression in both the luminal A and basal subtypes of BC was revealed. Noteworthy, the number of cells expressing S18-2 in high-proliferating tumors of luminal A and basal subtype is significantly higher than in tumors with a low proliferative potential (p 0.05). In 10 samples of luminal A subtype, the nuclear S18-2 signal was higher than median value. Moreover, the S18-2 protein was overexpressed in 4 out of such 10 samples. Metastases in the lymph nodes were found in 3 out of 4 patients with the stage II BC, low differentiation grade of the tumor and high proliferative activity. The bioinformatic analysis confirms our preliminary findings that the trend for increasing expression of the S18-2 protein in tumors correlates with the aggressiveness of malignant BC. Conclusion: The S18-2 protein may be a marker of cancer aggressiveness in BC patients
Additional Access Points:
Buchynska, L. G.
Iurchenko, N. P.
Kashuba, E. V.
Brieieva, O. V.
Glushchenko, N. M.
Mints, M.
Lukianova, N. Yu.
Chekhun, V. F.

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Brieieva, O.
Genotoxic sensitivity to 4-hydroxyestradiol in peripheral blood lymphocytes of endometrial cancer patients / O. Brieieva, I. Nesina, L. Buchynska // Experimental Oncology. - 2017. - Том 39, N 1. - P93

MeSH-main:
ЭНДОМЕТРИЯ НОВООБРАЗОВАНИЯ -- ENDOMETRIAL NEOPLASMS
ГИДРОКСИЭСТРОНЫ -- HYDROXYESTRONES
ЛИМФОЦИТЫ -- LYMPHOCYTES
Annotation: The endometrial cancer (EC) pathogenesis to a large extent may be determined by genotoxic effects of estrogen metabolites, among which the 4-hydroxyestradiol (4OHE2) is characterized by the most prominent DNA-damaging properties. Genomic instability and sensitivity to genotoxic estrogen metabolites in cells of EC patients depend on the DNA repair efficiency. The aim of the study was to analyze the level of DNA damage in peripheral blood lymphocytes (PBL) of EC patients after treatment with the 4OHE2 and to evaluate the repair efficiency of induced DNA damag
Additional Access Points:
Nesina, I.
Buchynska, L.

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Molecular phenotype of high-grade endometrioid carcinoma of the endometrium [Text] / L. G. Buchynska [та ін.] // Экспериментальная онкология. - 2020. - Т. 42, № 4. - С. 300-305. - Бібліогр.: в кінці ст.

MeSH-main:
КАРЦИНОМА ЭНДОМЕТРИОИДНАЯ -- CARCINOMA, ENDOMETRIOID (микробиология, патофизиология, этиология)
МОЛЕКУЛЯРНАЯ БИОЛОГИЯ -- MOLECULAR BIOLOGY (методы, тенденции)
НОВООБРАЗОВАНИЙ МАРКЕРЫ БИОЛОГИЧЕСКИЕ -- TUMOR MARKERS, BIOLOGICAL (анализ, физиология)
ГЕНЫ MYC -- GENES, MYC (физиология)
НОВООБРАЗОВАНИЙ СУПРЕССОРНЫЕ БЕЛКИ -- TUMOR SUPPRESSOR PROTEINS (анализ, диагностическое применение)
ДИАГНОСТИКИ МОЛЕКУЛЯРНОЙ МЕТОДЫ -- MOLECULAR DIAGNOSTIC TECHNIQUES (использование, статистика, тенденции)
СТАТИСТИЧЕСКАЯ ОБРАБОТКА ДАННЫХ -- DATA INTERPRETATION, STATISTICAL
Key words(unnormalized):
р53highFOXP3lowc-Mychigh
Annotation: Prognosis of the course of tumor progression is one of urgent problems of clinical oncology. A relevant specificity of endometrial cancer is its clinical polymorphism within the same histological type of the disease. The search for molecular-biological features associated with the aggressive phenotype of endometrioid carcinomas is indisputably urgent. Aim: To study molecular-biological features of endometrioid carcinoma of the endometrium (ECE) and to identify the molecular subtype of tumors with high potential of malignancy. Materials and Methods: Surgical specimens of 127 patients with EC, stages I–II, aged 36–72 (the average age — 59.3 ± 3.2) were studied using morphological and immunohistochemical methods. The multivariant analysis with the Kullback’s informative measure and PanelomiX were used to estimate the significance of the expression of specific biomarkers. Results: The expression of a complex of multifunctional markers was evaluated in ECE cells of different malignancy stage: p53, FOXP3, p21WAF1/CIP1, р16INK4a, E2F1, cyclins Е and D1, Her2/neu, с-Myc, Е-cadherin, β-catenin, vimentin, CD44, CD24. A triad of biomarkers with threshold expression levels was determined (р53 > 45%; FOXP3 < 14%; с-Myc > 10%). The high expression of oncogene c-Myc and oncosuppressor p53 along with the low level of FOXP3 in tumor cells of ECE was associated with high proliferative potential, low differentiation grade, and deep invasion of a tumor into the myometrium. Conclusions: The molecular phenotype of ECE, most informative in terms of specificity and sensitivity (95%) — р53highFOXP3lowc-Mychigh, was first characterized, which would help identify a high-grade subtype of this cancer form
Additional Access Points:
Buchynska, L. G.
Glushchenko, N. M.
Nesina, I. P.
Brieieva, O. V.
Iurchenko, N. P.

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Oxidative and mutagenic effects of low intensity GSM 18OO MHz microwave radiation / I. Yakymenko [et al.] // Experimental Oncology. - 2018. - Том 40, N 4. - P282-287

MeSH-main:
МИКРОВОЛНЫ -- MICROWAVES (вредные воздействия)
ЗДОРОВЬЯ ИЗМЕНЕНИЯ ПРИ ВОЗДЕЙСТВИИ ИЗЛУЧЕНИЙ -- RADIOLOGIC HEALTH (тенденции)
Annotation: Despite a significant number of epidemiological studies on potential carcinogenicity of microwave radiation (MWR) from wireless devices and a bulk of experimental studies on oxidative and mutagenic effects of low intensity MWR, the discussion on potential carcinogenicity of low intensity MWR is going on. This study aims to assess oxidative and mutagenic effects of low intensity MWR from a typical commercial model of a modern smartphone. Materials and Methods: The model of developing quail embryos has been used for the assessment of oxidative and mutagenic effects of Global System for Mobile communication (GSM) 1800 MHz MWR from a commercial model of smartphone. The embryos were exposed in ovo to 0.32 µW/cm2, discontinuously — 48 s — On, 12 s — Off, during 5 days before and 14 days through the incubation period. Results: The exposure of quail embryos before and during the incubation period to low intensity GSM 1800 MHz has resulted in expressive statistically significant oxidative effects in embryonic cells, including a 2-fold increase in superoxide generation rate and 85% increase in nitrogen oxide generation rate, damages of DNA integrity and oxidative damages of DNA (up to twice increased levels of 8-oxo-dG in cells of 1-day old chicks from the exposed embryos). Finally, the exposure resulted in a significant, almost twice, increase of embryo mortality. Conclusion: The exposure of model biological system to low intensity GSM 1800 MHz MWR resulted in significant oxidative and mutagenic effects in exposed cells, and thus should be recognized as a significant risk factor for living cells
Additional Access Points:
Yakymenko, I.
Burlaka, A.
Tsybulin, O.
Brieieva, O.
Buchynska, L.
Tsehmistrenko, S.
Chekhun, V.

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Cipher: ЕУ12/2020/42/4
Journal

Экспериментальная онкология [Text]
2020year Т. 42 № 4 . - 51.52, р.

Contents:
Commitment to ideals of science. To the 90th birthday anniversary of academician Vadym Pinchuk. - С.250-251
Naleskina, L. A. Modern views on the role of main components of stroma and tumor microinvironment in invasion, migration and metastasis / L. A. Naleskina, L. M. Kunska, V. F. Chekhun. - С.252-262. - Бібліогр.: в кінці ст.
Gaptulbarova, K. A. NF-kB as a potential prognostic marker and a candidate for targeted therapy of cancer / K. A. Gaptulbarova [та ін.]. - С.263-269. - Бібліогр.: в кінці ст.
Other authors: Tsyganov M. M., Pevzner A. M., Ibragimova M. K., Litviakov N. V.
Tykhomyrov, A. A. Plasminogen/plasmin affects expression of glycolysis regulator TIGAR and induces autophagy in lung adenocarcinoma A549 cells / A. A. Tykhomyrov [та ін.]. - С.270-276. - Бібліогр.: в кінці ст.
Other authors: Nedzvetsky V. S., Aĝca C. A., Guzyk M. M., Korsa V. V., Grinenko T. V.
Kumar, A. Microarray based gene expression profiling of advanced gall bladder cancer / A. Kumar [та ін.]. - С.277-284. - Бібліогр.: в кінці ст.
Other authors: Gupta R., Mathur N., Iyer V. K., Thulkar S., Prasad C. P., Das P., Rani L., Maqbool M., Shukla N. K., Pal S., Sundar D., Sharma A.
Auziņa, D. Dickkopf-related protein 1 expression in bone marrow of multiple myeloma patients: correlation with bone disease and plasma cell malignancy type / D. Auziņa [та ін.]. - С.285-288. - Бібліогр.: в кінці ст.
Other authors: Beinaroviča I., Janicka-Kupra B., Lejniece S., Lejnieks A., Groma V.
Buchynska, L. G. Expression of microRNA in tumor cells of endmetrioid carcinoma of endometrium / L. G. Buchynska [та ін.]. - С.289-294. - Бібліогр.: в кінці ст.
Other authors: Borykun T. V., Iurchenko N. P., Nespryadko S. V., Nesina I. P.
Kovalevska, L. Expression pattern of MRPS18 family genes in malignantly transformed b-cells / L. Kovalevska, E. Kashuba. - С.295-299. - Бібліогр.: в кінці ст.
Buchynska, L. G. Molecular phenotype of high-grade endometrioid carcinoma of the endometrium / L. G. Buchynska [та ін.]. - С.300-305. - Бібліогр.: в кінці ст.
Other authors: Glushchenko N. M., Nesina I. P., Brieieva O. V., Iurchenko N. P.
Shamrai, D. Granulosa and theca cell tumor in rat’s ovary after modified Biskind operation / D. Shamrai, E. Koshik, N. Melnyk. - С.306-309. - Бібліогр.: в кінці ст.
Bolgova, L. S. Histogenesis of central lung cancer: cytological investigation / L. S. Bolgova [та ін.]. - С.310-313. - Бібліогр.: в кінці ст.
Other authors: Tuganova T. N., Alekseenko O. I., Litvinets O. M., Suprun G. A., Ponomarenko A. A.
Shcherbynina, M. Histological criteria for “intraepithelial squamous cell carcinoma” of the esophagus: continued dialogue between Ukrainian and Japanese pathologists / M. Shcherbynina, M. Itabashi, N. Soloviova. - С.314-317. - Бібліогр.: в кінці ст.
Yevstakhevych, Yu. L. Autoimmune cytopenia in chronic lymphocytic leukemia: diagnosis and treatment / Yu. L. Yevstakhevych [та ін.]. - С.318-323. - Бібліогр.: в кінці ст.
Other authors: Vyhovska Ya. I., Yevstakhevyc I. Y., Vyhovsk O. Y., Pelenyo N. V., Semerak M. M., Novak V. L., Loginsky V. E.
Korovin, S. Burden of malignant melanoma in Ukraine in 2002–2013: incidence, mortality and survival / S. Korovin [та ін.]. - С.324-329. - Бібліогр.: в кінці ст.
Other authors: Fedorenko Z., Michailovich Yu., Kukushkina M., Sekerija M., Ryzhov A.
Burlaka, A. P. Cytochrome P450 content in primary tumors and liver metastases of patients with metastatic colorectal cancer / A. P. Burlaka [та ін.]. - С.330-332. - Бібліогр.: в кінці ст.
Other authors: Virko S. V., Burlaka A. A., Chernobai V. А., Yatsyna O. I., Ganusevich I. I.
Kitsera, N. Woman with Turner syndrome and her child with acute leukemia (a case report) / N. Kitsera, O. Dorosh, H. Makukh. - С.333-336. - Бібліогр.: в кінці ст.
Buchatskyi, L. P. Hypoxia induces melanotic pseudotumors in the larvae of mosquitoes of Culicidae family / L. P. Buchatskyi. - С.337. - Бібліогр.: в кінці ст.
Mykola Oleksandrovych Druzhyna (1940–2020). - С.338
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Cipher: ЕУ12/2019/41/1
Journal

Экспериментальная онкология [Text]
2019year Т. 41 № 1 . - 45.41, р.

Contents:
Solyanik, G. I. Quinazoline compounds for antitumor treatment / G. I. Solyanik. - С.3-6. - Bibliogr. at the end of the art.
Mahmoudian, J. Expression profiling of plac1 in murine cancer cell lines / J. Mahmoudian [та ін.]. - С.7-13. - Bibliogr. at the end of the art.
Other authors: Ghods R., Nazari M., Jeddi-Tehrani M., Ghahremani M. H., Ostad S. N., Zarnani A. H.
Kolesnik, D. L. Time-dependent cytotoxicity of dichloroacetate and metformin against Lewis lung carcinoma / D. L. Kolesnik [та ін.]. - С.14-19. - Bibliogr. at the end of the art.
Other authors: Pyaskovskaya O. N., Yakshibaeva Yu. R., Solyanik G. I.
Lozovska, Yu. V. The influence of lactoferrin on elemental homeostasis and activity of metal-containing enzymes in rats with Walker-256 carcinosarcoma / Yu. V. Lozovska [та ін.]. - С.20-25. - Bibliogr. at the end of the art.
Other authors: Andrusishina I. M., Lukianova N. Yu., Burlaka A. P., Naleskina L. A., Todor I. N., Chekhun V. F.
Burlaka, A. A. DNA oxidation in patients with metastastic colorectal cancer: clinical significance of 8-hydroxy-deoxyguanosine as an independent prognostic factor / A. A. Burlaka [та ін.]. - С.26-31. - Bibliogr. at the end of the art.
Other authors: Vovk A. V., Burlaka A. P., Kolesnik O. O.
Stakheyeva, M. Integral characteristic of the immune system state predicts breast cancer outcome / M. Stakheyeva [та ін.]. - С.32-38. - Bibliogr. at the end of the art.
Other authors: Eidenzon D., Slonimskaya E., Patysheva M., Bogdashin I., Kolegova E., Grigoriev E., Choinzonov E., Cherdyntseva N.
Bilous, N. Analysis of LPL gene expression in patients with chronic lymphocytic leukemia / N. Bilous [та ін.]. - С.39-45. - Bibliogr. at the end of the art.
Other authors: Abramenko I., Chumak A., Dyagil I., Martina Z.
Alghamdi, S. Evaluation of dose calculation algorithms using different density materials for in-field and out-of-field conditions / S. Alghamdi, A. Tajaldeen. - С.46-52. - Bibliogr. at the end of the art.
Poluben, L. Copy number alterations and copy-neutral loss of heterozygosity in Ukrainian patients with primary myelofibrosis / L. Poluben [та ін.]. - С.53-56. - Bibliogr. at the end of the art.
Other authors: Bryke Ch. R., Hsu Y., Shumeiko O., Neumerzhitska L., Klimuk B., Rybchenko L., Klymenko S., Balk S. P., Fraenkel P. G.
Bakai, O. A. Radiation research to determine local tumor invasion in patients with cervical cancer / O. A. Bakai [та ін.]. - С.57-60. - Bibliogr. at the end of the art.
Other authors: Golovko T. S., Ganich A. V., Gavriluk O. N., Ashykhmin A. V.
Zabolotnyi, D. I. Aggregated proteins in malignant and benign neoplasms / D. I. Zabolotnyi [та ін.]. - С.61-68. - Bibliogr. at the end of the art.
Other authors: Belousova A. A., Zabolotna D. D., SavchenkoT. D., Voroshylova N. M., Timchenko M. D., Tsvirinko I. R., Verevka S. V.
Shirin, V. Assessment of trace elements in serum of acute lymphoblastic and myeloid leukemia patients / V. Shirin [та ін.]. - С.69-71. - Bibliogr. at the end of the art.
Other authors: Sayfidin J., Mina E. -R., Shohren K., Reza S.
Tkachenko, R. Parathyroid carcinoma: a case report / R. Tkachenko [та ін.]. - С.72-75. - Bibliogr. at the end of the art.
Other authors: Zakhartseva L., Golovko A., Golovko A., Kuryk O., Lazarenko G.
Semko, S. A case of synchronous bilateral calyx urothelial carcinoma: combined treatment approach / S. Semko [та ін.]. - С.76-79. - Bibliogr. at the end of the art.
Other authors: Pikul M., Voylenko O., Stakhovskyi O., Kononenko O., Vitruk Yu., Stakhovsky E.
De, Giorgi V. Cutaneous leiomyosarcoma: a clinical, dermoscopic, pathologic case study / Giorgi V. De [та ін.]. - С.80-81. - Bibliogr. at the end of the art.
Other authors: Scarfì F., Silvestri F., Maida P., Gori A., Trane L., Massi D.
Langabeer, S. E. Suboptimal molecular response to tyrosine kinase inhibition associated with acquisition of a T240A ABL1 kinase domain mutation in a patient with chronic myeloid leukemia / S. E. Langabeer [та ін.]. - С.82-83. - Bibliogr. at the end of the art.
Other authors: Haslam K., Crampe M., MacDonagh B., McHugh J.
Brieieva, O. Scientific and Practical Conference of Young Scientists “Fundamental Medicine: Integrated Approaches to Cancer Therapy” / O. Brieieva. - С.84-86. - Bibliogr. at the end of the art.
Tumor and Host: Novel Aspects of Old Problem. - С.87
Ludmyla Zakharivna Polishchuk (1937–2019). - С.88
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