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

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Activation of the last protein kinases of insulin signaling cascade in peripheral blood mononuclear cells of diabetic patients with different types of cancer [] = Активация конечных протеинкиназ инсулинового сигнального каскада в мононуклеарных клетках периферической крови пациентов с диабетом и различными типами рака / T. S. Vatseba [та ін.] // Ендокринологія. - 2019. - Т. 24, № 4. - P302-310. - Bibliogr. at the end of the art.

MeSH-main:
ЛЕЙКОЦИТЫ МОНОНУКЛЕАРНЫЕ -- LEUKOCYTES, MONONUCLEAR (иммунология, метаболизм, секреция)
НОВООБРАЗОВАНИЯ -- NEOPLASMS (иммунология, кровь, метаболизм)
НОВООБРАЗОВАНИЙ ФАКТОРОВ НЕКРОЗА РЕЦЕПТОРЫ, АССОЦИИРОВАННЫЕ С СИГНАЛЬНЫМИ ПЕПТИДАМИ И БЕЛКАМИ -- TUMOR NECROSIS FACTOR RECEPTOR-ASSOCIATED PEPTIDES AND PROTEINS (биосинтез, иммунология, кровь, метаболизм, секреция)
ПРОТЕИНКИНАЗЫ -- PROTEIN KINASES (биосинтез, иммунология, кровь, метаболизм)
БИОФИЗИЧЕСКИЕ ПРОЦЕССЫ -- BIOPHYSICAL PROCESSES (иммунология)
ДИАБЕТ САХАРНЫЙ, ТИП 2 -- DIABETES MELLITUS, TYPE 2 (кровь, метаболизм, патофизиология)
Annotation: Akt/mTOR/p70S6K1 signaling pathway plays an important role in the pathogenesis of cancer and diabetes. Macrophages and lymphocytes are involved in the pathogenesis of diabetes, diabetic atherosclerosis, formation of insulin resistance as well as immune response to cancer and tumor maintenance. The aim of the study was to determine the activation of Akt/mTOR/p70S6K1 in peripheral blood mononuclear cell (PBMC) of patients with type 2 diabetes (T2D) and cancer. Results. The level of insulin in the blood of diabetic patients with breast and endometrial cancer was significantly higher compared to control, whereas it did not differ from control in the blood of diabetic patients with colorectal and pancreatic cancer. The highest level of insulin was observed in the blood of patients with T2D solely. Almost the same pattern was observed concerning IGF‑1 blood concentration. Akt S473 phosphorylation by mTORC2 was higher than control values in PBMC of breast and endometrial cancer diabetic patients. The level of Akt phosphorylation in PBMC of diabetic patients with colorectal and pancreatic cancer was lower then in control cells that corresponds to insulin and IGF‑1 concentrations in the blood. There was no activation of Akt by mTORC2 in PBMC of diabetic patients. There is no activation of mTORC1 in PBMC of patients with cancer and diabetes but there is its significant activation in the cells of patients with T2D only. Probably the Akt activation by mTORC2 is not associated with activation of mTORC1 in the cells of patients with T2D. The decrease in mTORC1 activity occurred in the cells of diabetic patients with all studied types of cancer. It can be assumed, that diabetes-related PI3K/Akt signaling in PBMC is likely to interfere with cancer-related signaling mechanisms. There were the differences in oncological patientswith T2D between breast/endometrial cancers, and pancreatic/bowel cancers considering IGF/insulin content in the blood and Akt activation in the PMBC, that could be explained by the specific hormonal background of the first types of cancers. Conclusion. The hypothesis of reciprocal Akt phosphorylation by the PDK1 and mTORC2 complexes on Thr308 and Ser473, respectively, is discussed
Сигнальний шлях Akt/mTOR/p70S6K1 відіграє важливу роль у патогенезі раку та діабету. Макрофаги та лімфоцити беруть участь у патогенезі діабету, діабетичного атеросклерозу, формуванні резистентності до інсуліну, а також імунної відповіді на рак та підтримці пухлини. Метою дослідження було вивчення активації Akt/mTOR/p70S6K1 у мононуклеарних клітинах периферичної крові (РВМС) пацієнтів із цукровим діабетом 2-го типу (T2D) і раком. Результати. Рівень інсуліну в крові діабетичних пацієнтів із раком молочної залози та ендометрія був значно вищим порівняно з контролем, але не відрізнявся від контролю в крові діабетичних пацієнтів із коло- ректальним раком і раком підшлункової залози. Найвищий рівень інсуліну спостерігався в крові пацієнтів із T2D. Майже таку ж картину спостерігали відносно концентрації IGF‑1 у крові. Фосфорилювання S473 в Akt кіназою mTORC2 було вищим від контрольних значень у РВМС пацієнтів із діабетом і раком молочної залози та ендометрія. Рівень фосфорилювання Akt у PBMC у пацієнтів із діабетом і колоректальним раком та раком підшлункової залози був нижчим від такого в контрольних клітинах, що відповідає концентраціям інсуліну та IGF‑1 у крові. Активації Akt mTORC2 у PBMC пацієнтів із діабетом не спостерігалося. У PBMC пацієнтів із раком і діабетом не відбувалося активації mTORC1, але спостерігали значну його активацію в клітинах пацієнтів із T2D. Імовірно, активацію Akt mTORC2 не пов’язано з активацією mTORC1 у клітинах пацієнтів із T2D. Зниження активності mTORC1 відбувалося в клітинах хворих на діабет з усіма досліджуваними типами раку. Можна припустити, що пов’язаний із діабетом сигналінг PI3K/Akt у PBMC, імовірно, інтерферує з механізмами передачі сигналів, пов’язаних із раком. Відзначено відмінності в онкологічних пацієнтів із T2D і раком молочної залози/ендометрія та раком підшлункової залози/кишечника з огляду на вміст IGF/інсуліну в крові й активацію Akt у PMBC, що можна пояснити специфічним гормональним тлом перших двох типів раку. Висновок. Обговорюється гіпотеза щодо реципрокного фосфорилювання Akt комплексами PDK1 і mTORC2 по T308 і S473 відповідно
Additional Access Points:
Vatseba, T. S.
Sokolova, L. K.
Pushkarev, V. V.
Kovzun, O. I.
Guda, B. B.
Pushkarev, V. M.
Tronko, M. D.

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Activation of the PI3K/Akt cascade in peripheral blood mononuclear cells. Association with insulin and insulin-like growth factor levels in the blood of patients with cancer and diabetes / V. Pushkarev [et al.] // Пробл. ендокринної патології. - 2019. - N спец.вип. - P209-211

MeSH-main:
НОВООБРАЗОВАНИЯ -- NEOPLASMS (кровь, патофизиология)
ДИАБЕТ САХАРНЫЙ -- DIABETES MELLITUS (кровь, патофизиология)
Additional Access Points:
Pushkarev, V.
Vatseba, T.
Sokolova, L.
Kovzun, O.
Tronko, M.

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Aggregated proteins in malignant and benign neoplasms [Text] / D. I. Zabolotnyi [та ін.] // Экспериментальная онкология. - 2019. - Т. 41, № 1. - С. 61-68. - Bibliogr. at the end of the art.

MeSH-main:
ТКАНЕВЫЕ ЭКСТРАКТЫ -- TISSUE EXTRACTS (анализ, диагностическое применение)
БЕЛКОВ АГРЕГАТЫ -- PROTEIN AGGREGATES (физиология)
НОВООБРАЗОВАНИЯ -- NEOPLASMS (классификация, патофизиология, этиология)
ФОТОГРАФИЧЕСКИЕ СНИМКИ -- PHOTOGRAPHS
ОБМЕН ВЕЩЕСТВ -- METABOLISM (физиология)
Key words(unnormalized):
белковые агрегаты (β-SPA)
Annotation: To evaluate the presence of the aggregated proteins in malignant and benign neoplasms for clarifying the role of impaired protein metabolism in the formation of the altered tissues. Object and Methods: The histological specimens prepared from the operative materials of 196 patients with different forms of malignant and benign neoplasms were stained with Congo red and Thioflavin T and studied under the light and polarization microscope. Results: The various forms of β-stacked protein aggregates (β-SPA) inclusions were detected in amyloids, keloid tissue, benign polyps, and several malignant tumors. Conclusion: The formation of non-functional protein aggregates proves the complex character of the impairment of protein metabolism resulting in local or systemic accumulation of secondary protein toxins results in β-SPA formation as the self-sustaining complex of parametabolic processes. The β-SPA formation is of considerable interest since their properties lead to the impairment of the normal physiological processes in adjacent tissues ensuring the chronic course of the pathology
Additional Access Points:
Zabolotnyi, D. I.
Belousova, A. A.
Zabolotna, D. D.
SavchenkoT., D.
Voroshylova, N. M.
Timchenko, M. D.
Tsvirinko, I. R.
Verevka, S. V.

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Alternative direction of inhibition of malignant properties in tumor cells in vitro and in vivo by gene therapy with INF-beta gene in recombinant baculovirus vector / O. Lykhova [et al.] // Experimental Oncology. - 2017. - Том 39, N 1. - P90

MeSH-main:
НОВООБРАЗОВАНИЯ -- NEOPLASMS (терапия)
ГЕННАЯ ТЕРАПИЯ -- GENETIC THERAPY
BACULOVIRIDAE -- BACULOVIRIDAE (генетика)
Annotation: The aim of the study was to investigate the influence of recombinant baculovirus containing the interferon-β gene (rBV/IFN) on phenotypic characteristics of tumor cells in vitro: morphology, growth, cytogenetic characteristics and expression of proteins associated with proliferative activity, cell cycle regulation, epithelial-mesenchymal transition (EMT), invasiveness, and the migration potential
Additional Access Points:
Lykhova, O.
Strokovska, L.
Kovaleva, O.
Bezdieniezhnych, N.
Semesiuk, N.
Adamenko, I.
Vorontsova, A.
Kudryavets, Yu.

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Analgesic choice in patients presenting to emergency department with cancer pain: a prospective study / Seref Emre Atis [et al.] // Медицина невідкладних станів. - 2021. - Т. 17, № 5. - С. 79-84. - Бібліогр. в кінці ст.

MeSH-main:
НОВООБРАЗОВАНИЯ -- NEOPLASMS (осложнения, патофизиология)
ОСТРАЯ БОЛЬ -- ACUTE PAIN (лекарственная терапия)
ПАРАЦЕТАМОЛ -- ACETAMINOPHEN (терапевтическое применение)
АНАЛГЕЗИРУЮЩИЕ СРЕДСТВА ОПИОИДНЫЕ -- ANALGESICS, OPIOID (терапевтическое применение)
Annotation: Acute onset pain is one of the common reasons for cancer patients to present to the emergency department. In our study, we compared painkillers used in cancer patients admitted to the emergency department with pain complaints and their effectiveness and the superiorities of these painkillers in pain relief and their superiorities over each other. Materials and methods. The pain scores of the patients were asked at the time of admission by showing a visual analogue scale. Before treatment, pain scores were recorded. The patients were divided into four different groups according to the type of given treatment: non-steroidal anti-inflammatory drugs; opioid painkillers; paracetamol; paracetamol and opioid therapy. After the treatment, we asked which painkiller written in the treatment form was administered to the patient and recorded the pain score. Results. It was observed that the median pain score before and after treatment of the patients in all painkiller groups differed statically. When the median scores before and after treatment were compared according to drug types, no difference was found between the decrease in pain scores (p = 0.956 and p = 0.705, respectively). It was concluded that the pre-treatment and post-treatment median pain scores of patients who are using non-steroid anti-inflammatory drugs and opioids at home did not differ statistically (p = 0.063). Conclusions. The use of non-steroidal anti-inflammatory drugs, paracetamol or opioids was not found to be superior to each other in patients with acute severe cancer pain
Гострий біль є однією з найпоширеніших причин, через які пацієнти з раком можуть потрапляти до відділення невідкладної допомоги. У нашому дослідженні ми порівняли ефективність знеболювальних препаратів, що застосовуються в онкохворих, які надійшли до відділення невідкладної допомоги зі скаргами на біль, а також переваги цих засобів одного над одним. Матеріали та методи. Біль у пацієнтів оцінювали під час надходження за допомогою візуальної аналогової шкали. Перед лікуванням реєстрували оцінку болю в балах. Хворих розподілили на чотири різні групи за типом проведеного лікування: нестероїдні протизапальні препарати; опіоїдні знеболювальні; парацетамол; парацетамол з опіоїдною терапією. Після лікування ми запитували, яке знеболювальне отримував пацієнт, і реєстрували оцінку болю. Результати. Було відзначено, що середній показник болю до і після лікування хворих у всіх групах знеболювальних препаратів статистично відрізнявся. Коли середні показники до і після лікування порівнювали за типами препаратів, не було виявлено різниці в зменшенні показників болю (p = 0,956 і p = 0,705, відповідно). Зроблено висновок, що середній показник болю до і після лікування пацієнтів, які вдома використовують нестероїдні протизапальні препарати й опіоїди, статистично не відрізнявся (p = 0,063). Висновки. При використанні нестероїдних протизапальних препаратів, парацетамолу або опіоїдів не встановлено переваги жодного засобу над іншими в онко-хворих із сильними гострими болями
Additional Access Points:
Atis, Seref Emre
Cekmen, Bora
Kalkan, A.
Bozan, Oner
Senturk, Mucahit
Karaaslan, Edip Burak

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Antiproliferative and apoptotic effects of anti-human HB-EGF neutralizing polyclonal antibodies in vitro / A. A. Siromolot [et al.] // Experimental Oncology. - 2020. - Том 42, N 1. - P25-30

MeSH-main:
АНТИТЕЛА НЕЙТРАЛИЗУЮЩИЕ -- ANTIBODIES, NEUTRALIZING (физиология)
НОВООБРАЗОВАНИЯ -- NEOPLASMS (патофизиология, терапия)
Annotation: Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a member of the epidermal growth factor family and has a variety of physiological and pathophysiological functions. Also, HB-EGF plays a pivotal role in progression of different tumors. So, HB-EGF seems to be a target molecule for the treatment of some cancer types. Aim: To obtain HB-EGF neutralizing polyclonal antibodies and test their anti-proliferative properties in vitro. Materials and Methods: Lab rabbits and mice were used for immunization with recombinant HB-EGF. The effect of generated polyclonal antibodies on viability and apoptosis of human epidermoid carcinoma derived A431 cell line was assessed using MTT and Annexin V-propidium iodide assays. Results: Rabbit polyclonal anti-HB-EGF serum could block binding of soluble HB-EGF to epidermal growth factor receptor/human epidermal growth factor receptor. Also, anti-HB-EGF antibodies could bind to surface of A431 cells which express abnormally high levels of membrane bound proHB-EGF and its receptor. It has been shown that immune serum with polyclonal antibodies against HB-EGF was able to block the mitogenic activation of the cells with HB-EGF and cause apoptotic cell death. Conclusion: Inhibition of HB-EGF activity with neutralizing polyclonal antibodies can effectively inhibit mitogenic activation and cause apoptosis of cancer cells with significant epidermal growth factor receptor overexpression
Additional Access Points:
Siromolot, A. A.
Krynina, O. I.
Kolybo, D. V.
Komisarenko, S. V.

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Moazeni-Roodi, A.
Association bewtween XPO5 rs 1 1077 polymorphism and cancer susceptibility: a meta-analysis of 7284 cases and 85 1 1 controls / A. Moazeni-Roodi, M. Taheri, M. Hashemi // Experimental Oncology. - 2019. - Том 41, N 4. - P346-352

MeSH-main:
ПОЛИМОРФИЗМ ГЕНЕТИЧЕСКИЙ -- POLYMORPHISM, GENETIC
ПРОДРОМАЛЬНЫЕ СИМПТОМЫ -- PRODROMAL SYMPTOMS
НОВООБРАЗОВАНИЯ -- NEOPLASMS (генетика, этиология)
ФАКТОРЫ РИСКА -- RISK FACTORS
СТАТИСТИЧЕСКАЯ ОБРАБОТКА ДАННЫХ -- DATA INTERPRETATION, STATISTICAL
ТАБЛИЦЫ -- TABLES
Key words(unnormalized):
полиморфизм rs11077 XPO5
Annotation: Several studies evaluated the association between rs11077 polymorphism located in the 3’UTR of the XPO5 gene and cancer susceptibility. We conducted a meta-analysis to assess the impact of XPO5 rs11077 polymorphism on cancer risk. Materials and Methods: The online databases were searched for relevant case-control studies published up to July 2018. 15 articles of 16 studies, with totally 7284 cancer cases and 8511 healthy controls, were eligible for inclusion in the meta-analysis. The data were extracted from the eligible studies and were processed using Stata 14.1 and Revman 5.3 software. Pooled estimates of odds ratio with 95% confidence intervals were used to evaluate the strength of association between XPO5 rs11077 and cancer risk. Results: Overall, our finding showed no significant association between XPO5 rs11077 variant and overall cancer risk, either performed subgroup analysis by cancer types and ethnic groups in all genetic model. Conclusion: The findings did not support an association between rs11077 variant and cancer risk. Due to small sample sizes particularly in stratified analysis, further large-scale well designed studies between this polymorphism and cancer risk are warranted
Additional Access Points:
Taheri, M.
Hashemi, M.

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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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CD150/SLAMF1 as a new potential target for anti-tumor therapy / S. P. Sidorenko [et al.] // Experimental Oncology. - 2017. - Том 39, N 1. - P90-91

MeSH-main:
НОВООБРАЗОВАНИЯ -- NEOPLASMS (лекарственная терапия, терапия)
ПРОТИВООПУХОЛЕВЫЕ СРЕДСТВА -- ANTINEOPLASTIC AGENTS
Annotation: CD150/SLAMF1 is a prototype member of SLAM family within the immunoglobulin superfamily of surface receptors that are widely expressed on cells within hematopoietic system. Six of nine SLAMF receptors have a paired unique immunoreceptor tyrosine-based switch motif (ITSM) that serves as a docking site for SH2-containing proteins. In T and B lymphocytes, natural killer cells, macrophages and dendritic cells CD150 is a co-receptor molecule that mediates different signal transduction pathways depending on the availability of downstream signaling elements, especially, the adaptor protein SH2D1A/SAP. Due to highly glycosylated and sialylated extracellular Ig domains, CD150 is involved in homotypic interactions and could be considered as a pattern-recognizing receptor. It is a major entry receptor for several Morbilliviruses, including measles virus, and also a bacterial sensor that control the killing of Gram-negative bacteria. Functionally it serves as a bridge between innate and adaptive immunity
Additional Access Points:
Sidorenko, S.P.
Romanets-Korbut, O.
Gordiienko, I.
Kovalevska, L.
Shlapatska, L.

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10.

Gordienko, I.
Cell signalling in cancer biology and management / I. Gordienko // Онкологія. - 2021. - Т. 23, № 4. - P232

MeSH-main:
КЛЕТОЧНАЯ МЕХАНОТРАНСДУКЦИЯ -- MECHANOTRANSDUCTION, CELLULAR
БИОХИМИЧЕСКИЕ ПРОЦЕССЫ -- BIOCHEMICAL PROCESSES
НОВООБРАЗОВАНИЯ -- NEOPLASMS (лекарственная терапия, терапия)
Annotation: A signal transduction pathway is a series of steps by which a signal on a cell’s surface is converted into a specific cellular response. Signal transduction, which occurs in each cell of the body, is largely required for the correct functioning of the whole organism. Regulation of cell cycle and proliferation, migration, differentiation, viability versus cell death, metabolism is not all processes that are coordinated by signal transduction pathways. That is why it is not surprising that deregulation in cell signaling may have a considerable impact on the homeostasis of the cell. This lecture will be discussed three main signaling pathways: JAK/STAT, Ras/MEK/Erk, and PI3K/Akt/mTOR by the reason, they are very frequently activated in all types of cancer and are common effectors of different upstream lesions. It will be discussed how to use knowledge about signal transduction pathways in normal and cancer cells for the development of target therapy. On the example of one signal molecule, cell surface receptor SLAMF1 or CD150 will be showed complexity, diversity, and multifunctionality of cell signaling and its potential in improving diagnosis, prognosis, and therapy prediction of cancer. The differential expression among various types of hematological malignancies allows considering CD150 as a diagnostical and potential prognostic marker. Moreover, CD150 may be a target for antibody-based or measles virus oncolytic therapy. Due to CD150 signaling properties, it is involved in the regulation of malignant cell fate decision and tumor microenvironment in Hodgkin’s lymphoma and chronic lymphocytic leukemia
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