Статті в журналах: "Cancerogenesi"

1

Roth, Milan. "Skeletal cancerogenesis." Rivista di Neuroradiologia 10, no. 3 (June 1997): 337–40. http://dx.doi.org/10.1177/197140099701000306.

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2

Ryazansky, S. S., and V. A. Gvozdev. "Small RNAs and cancerogenesis." Biochemistry (Moscow) 73, no. 5 (May 2008): 514–27. http://dx.doi.org/10.1134/s0006297908050040.

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3

Pajovic, Snezana, Zorica Saicic, Snezana Pejic, Jelena Kasapovic, Vesna Stojiljkovic, and Dusan Kanazir. "Antioxidative biomarkers and cancerogenesis." Jugoslovenska medicinska biohemija 25, no. 4 (2006): 397–402. http://dx.doi.org/10.2298/jmb0604397p.

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4

Lo Fiego, D. P., A. M. Belmonte, and F. Mezzetti. "Carne suina e salute: un binomio possibile?" Archivos de Zootecnia 67, Supplement (January 15, 2018): 141–45. http://dx.doi.org/10.21071/az.v67isupplement.3591.

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La carne e i prodotti carnei sono fonte importante di nutrienti essenziali per l’organismo, ma recenti studi epidemiologici hanno associato il consumo di carne rossa e di carne trasformata ad un incremento del rischio di comparsa di malattie cardiocircolatorie e del cancro al colon. Ciò a causa della presenza di acidi grassi saturi, di sale aggiunto, di prodotti dell’ossidazione, di nitroso derivati che si formano durante le fasi di trasformazione, e della capacità ossidativa del ferro-EME. Recentemente l’International Agency for Research on Cancer (IARC) ha definito le carni rosse come probabilmente cancerogene e i salumi come cancerogeni. Ciò ha creato un notevole allarmismo nei consumatori, una significativa riduzione dei consumi di questi prodotti e un grosso impatto negativo sul mercato. L’Europa, con circa 150 milioni di suini e una produzione annuale di circa 22 milioni di tonnellate di carcasse, è il secondo produttore mondiale di carne suina, e l’area Mediterranea è conosciuta in tutto il mondo per la produzione di salumi di alto pregio. Appare pertanto di notevole importanza studiare nuove strategie produttive e di trasformazione atte a migliorare le caratteristiche salutistiche della carne suina. Nella relazione verranno prese in esame alcune di queste strategie.

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5

Buendia, MA. "Hepatitis B viruses and cancerogenesis." Biomedicine & Pharmacotherapy 52, no. 1 (January 1998): 34–43. http://dx.doi.org/10.1016/s0753-3322(97)86239-7.

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6

Krustev, L., O. Poliakova-Krusteva, and M. Krusteva-Chichova. "Liver cancerogenesis and fasciola hepatica." Journal of Hepatology 11 (January 1990): S96. http://dx.doi.org/10.1016/0168-8278(90)91716-a.

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7

Grce, M., L. Magdić, and K. Pavelic. "Human cytomegalovirus in cervical cancerogenesis." Journal of Cancer Research and Clinical Oncology 121, S1 (January 1995): S19. http://dx.doi.org/10.1007/bf02559829.

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8

Glushkov, Andrew N. "Immune-hormonal imbalance in chemical cancerogenesis." Russian Journal of Immunology 25, no. 1 (August 3, 2022): 23–36. http://dx.doi.org/10.46235/1028-7221-1091-ihi.

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The present article deals with experimental and clinical aspects of immuno-hormonal interactions in chemical carcinogenesis i.e., formation of DNA-adducts with chemical carcinogens as a trigger of tumor initiation; synthesis of specific antibodies as markers of human exposure to environmental carcinogens; immunomodulation of chemical carcinogenesis by the specific antibodies in experimental studies; interactions of antibodies against environmental carcinogens with endogenous steroid hormones in human carcinogenesis; immunological interference and inversion of immuno-hormonal interactions by the action of antibodies against environmental carcinogens; immune stimulation of tumor progression in cancer patients. It is shown that antibodies specific to estradiol and progesterone participate in regulation of serum estradiol and progesterone levels in healthy women. Excessive production of antibodies against benzo[a]pyrene is associated with impaired physiological balance between the levels of antibodies to estradiol and progesterone, thus causing disturbed physiological balance between serum estradiol and progesterone. Immuno-hormonal imbalance promotes tumor initiation, its growth and progression. The new approaches to the personalized cancer immunoprediction and immune prevention are discussed. Coordinated synthesis of antibodies against benzo[a]pyrene and estradiol seems to reflect production of DNA-adducts with genotoxic metabolic effects of these compounds manifesting as synergistic carcinogenic effects upon the target cells. Hence, simultaneously increased levels of serum antibodies against benzo[a]pyrene and estradiol in healthy people may be considered an immunological marker of high oncological risk and an reason to use of new immunoprotective tools against polycyclic aromatic hydrocarbons and phytoestrogens. However, ability of these antibodies to raise the blood serum levels of environmental carcinogens and endogenous estradiol, as shown in vitro and in vivo, excludes the opportunity for active cancer immune prevention. Usage of anticarcinogen vaccines aimed for induction of protective secretory antibodies is likely to further increase high levels of procarcinogenic serum antibodies against benzo[a]pyrene and estradiol, followed by additional enhancement of immuno-hormonal imbalance and promotion of carcinogenesis. Development of probiotics transduced with genes encoding human antibodies against environmental carcinogens may present an alternative approach to cancer immune prevention. The antibodies produced by such probiotics would bind appropriate carcinogens and prevent their invasion into the organism, thus inhibiting emergence of DNA-adducts and suppressing synthesis of specific autoantibodies that may promote carcinogenesis. The aim is to substantiate the concept of immuno-hormonal imbalance for the carcinogen-induced hormone-dependent tumors.

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9

Uhoda, Isabelle, Pascale Quatresooz, Claudine Piérard-Franchimont, and Gérald E. Piérard. "Nudging Epidermal Field Cancerogenesis by Imiquimod." Dermatology 206, no. 4 (2003): 357–60. http://dx.doi.org/10.1159/000069957.

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10

Siewinski, Maciej, Jan Gutowicz, Andrzej Zarzycki, and Wojciech Mikulewicz. "Role of Cysteine Endopeptidases in Cancerogenesis." Cancer Biotherapy and Radiopharmaceuticals 11, no. 3 (June 1996): 169–76. http://dx.doi.org/10.1089/cbr.1996.11.169.

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11

Bjelakovic, Gordana, Ivana Stojanovic, Tatjana Jevtovic Stoimenov, Dusica Pavlovic, Gordana Kocic, Goran B. Bjelakovic, Dusan Sokolovic, and Jelena Basic. "Polyamines, folic acid supplementation and cancerogenesis." Pteridines 28, no. 3-4 (December 20, 2017): 115–31. http://dx.doi.org/10.1515/pterid-2017-0012.

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AbstractClinical practice and experimental studies have shown the necessity of sufficient quantities of folic acid intake for normal embryogenesis and fetal development in the prevention of neural tube defects (NTDs) and neurological malformations. So, women of childbearing age must be sure to have an adequate folate intake periconceptionally, prior to and during pregnancy. Folic acid fortification of all enriched cereal grain product flour has been implemented in many countries. Thus, hundreds of thousands of people have been exposed to an increased intake of folic acid. Folate plays an essential role in the biosynthesis of methionine. Methionine is the principal aminopropyl donor required for polyamine biosynthesis, which is up-regulated in actively growing cells, including cancer cells. Folates are important in RNA and DNA synthesis, DNA stability and integrity. Clinical and epidemiological evidence links folate deficiency to DNA damage and cancer. On the other hand, long-term folate oversupplementation leads to adverse toxic effects, resulting in the appearance of malignancy. Considering the relationship of polyamines and rapidly proliferating tissues (especially cancers), there is a need for better investigation of the relationship between the ingestion of high amounts of folic acid in food supplementation and polyamine metabolism, related to malignant processes in the human body.

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12

Zaletaev, Dmitry V., Vladimir V. Strelnikov, Tatiana V. Kekeeva, Valeria V. Zemliakova, Ekaterina B. Kuznetsova, and Dmitri S. Mikhaylenko. "Methylation anomalies in cancerogenesis: search for new genes, development of methods and DNA-markers for diagnosis." Ecological genetics 9, no. 3 (September 15, 2011): 27–32. http://dx.doi.org/10.17816/ecogen9327-32.

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The report considers the epigenetic defects and their diagnostics in tumors. Aberrant methylation of the promoter or regulatory region of a gene results in its functional inactivation, which is phenotypically similar to structural deletion. Cancerogenesis-associated genes are often methylated in tumors. Tumors differ in methylation frequencies, allowing differential diagnostics. Aberrant methylation of tumor suppressor genes occurs in early cancerogenesis, and its detection may be employed in presymptomatic and noninvasive diagnostics of tumors.

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13

Revazova, Yulia A., and Nataliya A. Ilyushina. "On the issue of nongenotoxic cancerogenes." Toxicological Review 29, no. 4 (August 30, 2021): 51–55. http://dx.doi.org/10.36946/0869-7922-2021-29-4-51-55.

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Introduction. Chemical, physical or biological factors that can cause the formation and expansion of cancer cells are diverse in terms of both activity and mechanisms of action, which leads to the complexity of assessing the risk of developing malignant neoplasms. The aim. Discussion of the classification of carcinogens based on their ability to interact with DNA cell and possible mechanisms of genetic control of carcinogenesis processes induced by non-genotoxic carcinogens. Core content. The article draws attention to some controversial points related to the attribution of factors acting on the body to genotoxic or non-genotoxic carcinogens. The terminology used in the literature to describe genotoxic (mutagenic) and carcinogenic factors is presented. The mechanisms of action of non-genotoxic carcinogens are discussed. The important role of experts determining the danger to public health of factors with potential genotoxicity and carcinogenicity is noted. Conclusion. Non-genotoxic carcinogens are capable of inducing malignant growth through mechanisms not associated with direct damage to genetic structures in the cell. However, the realization of carcinogenic effects caused by such factors is determined by various mechanisms of genetic control.

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14

Hall, Andrew B., Alan Dukes, and Jacob Anderson. "Enterobacter cancerogenus in Trauma." American Surgeon 78, no. 9 (September 2012): 1016–18. http://dx.doi.org/10.1177/000313481207800949.

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15

Katarzyna, Wójcik-Krowiranda. "The Role of The ?klotho Gene, Fgf21 and Fgfr1 in Cancerogenesis." Women Health Care and Issues 1, no. 1 (December 14, 2020): 01–07. http://dx.doi.org/10.31579/2642-9756/003.

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Klotho was discovered in 1997 as an anti-aging gene that, when overexpressed, may extend the life span, but when it is disrupted, it may be a factor responsible for premature aging syndrome. The structure and the role of αKlotho and βKlotho genes from Klotho family in malignant tumors is described. The expression profile of the βKlotho gene is significantly different from the expression of the αKlotho gene. Analysis of Klotho expression in breast cancer, cervical cancer as well as endometrial cancer are discussed. The available data indicate the involvement of βKlotho in the neoplastic transformation of the endometrium. More advanced disease is related to negative expression of βKlotho gene. Fibroblast growth factors (FGFs) are a large family of proteins characterized by different functions in the cell development and metabolism. The FGF signaling is also associated with cancerogenesis. The relation between some FGF subfamilies and endometrial cancer clinical data is reported. The interaction between FGF subfamilies and the Klotho subfamily proteins acting as a co-receptor is stressed. Disorders in signaling of the FGF / FGFR pathway have been confirmed in gynecology. It can be assumed that increased expression of FGF21 might be a suppressor factor in endometrial cancer. The FGF21 factor, like the βKlotho protein, achieves its biological effect via the FGFR1 receptor. High expression of the FGFR1 gene inhibits further tumor growth. FGFR1 has the potential to perform both a suppressor and promoter role in the oncogenesis process.

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16

Grubelnik, Gašper, Emanuela Boštjančič, Ana Pavlič, Marina Kos, and Nina Zidar. "NANOG expression in human development and cancerogenesis." Experimental Biology and Medicine 245, no. 5 (February 10, 2020): 456–64. http://dx.doi.org/10.1177/1535370220905560.

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NANOG is an important stem cell transcription factor involved in human development and cancerogenesis. Its expression is complex and regulated on different levels. Moreover, NANOG protein might regulate hundreds of target genes at the same time. NANOG is crucial for preimplantation development phase and progressively decreases during embryonic stem cells differentiation, thus regulating embryonic and fetal development. Postnatally, NANOG is undetectable or expressed in very low amounts in the majority of human tissues. NANOG re-expression can be detected during cancerogenesis, already in precancerous lesions, with increasing levels of NANOG in high grade dysplasia. NANOG is believed to enable cancer cells to obtain stem-cell like properties, which are believed to be the source of expanding growth, tumor maintenance, metastasis formation, and tumor relapse. High NANOG expression in cancer is frequently associated with advanced stage, poor differentiation, worse overall survival, and resistance to treatment, and is therefore a promising prognostic and predictive marker. We summarize the current knowledge on the role of NANOG in cancerogenesis and development, including our own experience. We provide a critical overview of NANOG as a prognostic and diagnostic factor, including problems regarding its regulation and detection. Impact statement NANOG has emerged as a key stem cell transcription factor in normal development and cancerogenesis. It is generally regarded as a good prognostic and predictive factor in various human cancers. It is less known that it is expressed already at precancerous stages in various organs, suggesting that finally an ideal candidate diagnostic marker has been discovered, enabling to distinguish between true dysplasia and reactive atypia. NANOG regulation is complex, and new insights into our understanding of its regulation might provide important information for future development in a broad field of two entirely different processes, i.e. normal development and cancerogenesis, showing how a physiologic mechanism can be used and abused, transforming itself into a key mechanism of disease development and progression.

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17

Chojnicki, Michał, Mariola Pawlaczyk, Celina Helak-Łapaj, Jakub Żurawski, and Krzysztof Wiktorowicz. "The role of viruses in the cancerogenesis." Journal of Medical Science 83, no. 2 (June 30, 2014): 152–55. http://dx.doi.org/10.20883/medical.e60.

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It is estimated that seven key viruses such as Hepatitis B virus (HBV), Hepatitis C virus (HCV), Human T-lymphotropic virus (HTLV), Human papilloma viruses (HPV), Kaposi’s sarcoma-associated herpes-virus (KSHV), Epstein-Barr virus (EBV) and Merkel cell polyomavirus (MCV), are responsible for about 11% of cancers all over the world. Viruses however are not only associated with cancerogenesis process. Scientific researches from recent years emphasize the possible use of the microorganisms as antitumor therapy. Oncoviruses, also defined as tumor viruses cause cancers whereas oncolytic viruses infect the host’s cancer cells leading to destruction of tumor and due to that they are described as cancer killing viruses. It offers the potential application of viral infections to the cancer therapy.

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18

Bernegger, Sabine, Miroslaw Jarzab, Silja Wessler, and Gernot Posselt. "Proteolytic Landscapes in Gastric Pathology and Cancerogenesis." International Journal of Molecular Sciences 23, no. 5 (February 22, 2022): 2419. http://dx.doi.org/10.3390/ijms23052419.

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Gastric cancer is a leading cause of cancer-related death, and a large proportion of cases are inseparably linked to infections with the bacterial pathogen and type I carcinogen Helicobacter pylori. The development of gastric cancer follows a cascade of transformative tissue events in an inflammatory environment. Proteases of host origin as well as H. pylori-derived proteases contribute to disease progression at every stage, from chronic gastritis to gastric cancer. In the present article, we discuss the importance of (metallo-)proteases in colonization, epithelial inflammation, and barrier disruption in tissue transformation, deregulation of cell proliferation and cell death, as well as tumor metastasis and neoangiogenesis. Proteases of the matrix metalloproteinase (MMP) and a disintegrin and metalloproteinase domain-containing protein (ADAM) families, caspases, calpain, and the H. pylori proteases HtrA, Hp1012, and Hp0169 cleave substrates including extracellular matrix molecules, chemokines, and cytokines, as well as their cognate receptors, and thus shape the pathogenic microenvironment. This review aims to summarize the current understanding of how proteases contribute to disease progression in the gastric compartment.

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19

Poczęta, Marta, Ewa Nowak, Dominik Bieg, and Ilona Bednarek. "Epigenetic modifications and gene expression in cancerogenesis." Annales Academiae Medicae Silesiensis 72 (April 30, 2018): 80–89. http://dx.doi.org/10.18794/aams/77013.

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20

Marchi, Saverio, Veronica Angela Maria Vitto, Alberto Danese, Mariusz R. Wieckowski, Carlotta Giorgi, and Paolo Pinton. "Mitochondrial calcium uniporter complex modulation in cancerogenesis." Cell Cycle 18, no. 10 (May 10, 2019): 1068–83. http://dx.doi.org/10.1080/15384101.2019.1612698.

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21

Dvorská, M., D. Driak, I. Švandova, B. Sehnal, and M. Halaska. "P1006 Significance of apoptosis in endometrial cancerogenesis." International Journal of Gynecology & Obstetrics 107 (October 2009): S695. http://dx.doi.org/10.1016/s0020-7292(09)62492-9.

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22

Appel, K. E., G. Fürstenberger, H. J. Hapke, E. Hecker, A. G. Hildebrandt, W. Koransky, F. Marks, H. G. Neumann, F. K. Ohnesorge, and R. Schulte-Hermann. "Chemical cancerogenesis: Definitions of frequently used terms." Journal of Cancer Research and Clinical Oncology 116, no. 3 (May 1990): 232–36. http://dx.doi.org/10.1007/bf01612896.

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23

Hensel, Frank, Constanze Kn�rr, Ralph Hermann, Veit Krenn, Hans Konrad M�ller-Hermelink, and H. Peter Vollmers. "Mitogenic autoantibodies inHelicobacter pylori-associated stomach cancerogenesis." International Journal of Cancer 81, no. 2 (April 12, 1999): 229–35. http://dx.doi.org/10.1002/(sici)1097-0215(19990412)81:2<229::aid-ijc11>3.0.co;2-u.

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24

Yufang, Zhong, Chen Cen, Wang Xiu, Guo Panpan, Zhang Xinyu, Yu Zhiqiang, and An Jing. "HBCD and PCBs enhance the cell migration and invasion of HepG2 via the PI3 K/Akt pathway." Toxicology Research 4, no. 3 (2015): 677–85. http://dx.doi.org/10.1039/c4tx00108g.

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25

Konjevic, Gordana. "STAT proteins in cancerogenesis and therapy of malignancies." Srpski arhiv za celokupno lekarstvo 137, no. 1-2 (2009): 98–105. http://dx.doi.org/10.2298/sarh0902098k.

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Signal transducers and activators of transcription (STAT) proteins are a 7-member family of cytoplasmic transcription fators that participate in signal transduction by cytokines, hormones, and growth factors. STAT proteins control the most important cellular processes, including survival, proliferation and differentiation. A great number of cytokines and other factors in different cell types activate STAT1, STAT3 and STAT5 and in this manner regulate processes such as cellular proliferation, differentiation and survival. STATs such as STAT4 and STAT6 have a more specific effect and are engaged in the differentiation of T helper cell populations. Given the critical roles of STAT proteins it has been established in many studies that STAT3 and STAT5 are oncogenes that can contribute to cellular transformation by increasing proliferation and slowing-down apoptosis. On the other hand, STAT1 is a tumour suppressor gene and its inactivation contributes to malignant transformation. Initially STAT proteins were extensively studied in leukaemias, but later their role in the development of different solid tumours has been also shown. Aside from their role in the development of tumours, STAT1, STAT3 and STAT5 can be considered as molecular markers for early detection of certain types of tumours, as well as prognostic factors in the determination of tumour aggressiveness and predictors of response to various types of therapy. Evidence of the deregulation of STAT signalling pathway can serve as a basis for designing novel targeted molecular therapeutic strategies that carry a great potential in the therapy of solid tumours and leukaemias.

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26

Žlajpah, Margareta, Emanuela Boštjančič, and Nina Zidar. "(Epi)genetic regulation of osteopontin in colorectal cancerogenesis." Epigenomics 12, no. 16 (August 2020): 1389–403. http://dx.doi.org/10.2217/epi-2020-0032.

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Aim: To identify (epi)genetic regulators of osteopontin (OPN, encoded by SPP1 gene) from normal colon mucosa to adenoma, adenoma with early carcinoma and advanced carcinoma. Patients & methods: Biopsy samples of 41 patients with different patohistologic diagnosis were used. Using qPCR, pyrosequencing and statistical analysis, we determined the expression level of osteopontin regulatory miRNAs, its copy number and methylation status. Results & conclusion: We showed that hsa-miR-146a-5p expression is inversely proportional to the expression level of SPP1 and that expression might be also controlled by copy number and methylation. These results suggest that not only expression of SPP1 but also its copy number, methylation status and expression of its regulators might be used as a potential biomarker of colorectal cancer.

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27

Stefania Erra and Ennio Nano B D. "Olfactory neuroblastoma: case report and focus on cancerogenesis." World Journal of Biology Pharmacy and Health Sciences 6, no. 3 (June 30, 2021): 035–39. http://dx.doi.org/10.30574/wjbphs.2021.6.3.0060.

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Background: Neuroendocrine neoplasms (NENs) of the nasal cavity, paranasal sinuses and nasopharynx account for a wide spectrum of histotypes. They can range from indolent form to highly aggressive tumors. Olfactory neuroblastoma, like most sino-nasal NENs, represents a rare neoplasm that prompts diagnostic pitfalls. From a morphological perspective, olfactory neuroblastoma can mimic many nasal neoplasms but a proper recognition is mandatory for its aggressive behaviour. Case presentation: A case of olfactory neuroblastoma in a 85 years old woman is reported. The neoplasm has been surgical removed from the nasal cavity with a clinical and radiographic diagnosis of nasal polyp. Correct diagnostic definition has needed a complete histological and immunohistochemical characterization of the tumoral tissue in surgical pathology laboratory. Conclusion: The correct diagnosis of olfactory neuroblastoma directs the clinical management that is unique for this neoplasm in comparison to other nasal ones. Bicranial-facial surgery or a trephination procedure represent the most common approach for the treatment of this malignancy. Their success determine disease prognosis.

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MADEJ, JANUSZ A. "Is a deterministic chaos the way to cancerogenesis?" Medycyna Weterynaryjna 76, no. 04 (2020): 6389–2020. http://dx.doi.org/10.21521/mw.6389.

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On the basis of the 2nd law of thermodynamics, the study presents a probable process in which a neoplastic cell passes into the dissipative state on its thermodynamic branch and self-transforms into a neoplastic cell. The self-transformation is promoted by a long-term unstable, highly unbalanced state in which cells that are sensitive to cancerogenesis obtain their own thermodynamic branch, and their self-organization is probably based on a disturbed relationship between entropy and temperature. Self-organization is related to the progressive imbalance. It promotes mistakes during genetic copies formation , spontaneous mutations and, as a result, cancerogenesis. A deterministic chaos is a creative process because it is the only one capable of generating completely new structures, such as neoplasms. Neoplastic cells succeed only when their environment (extracellular matrix – ECM) is damaged due to e.g. senile inflammation or inflammation caused by the neoplasm itself. This is known as the oncogenesis adaptation theory and it explains the evolution of neoplastic cells. The mutation leading to the neoplastic transformation of a cell is sometimes unfavorable or even harmful to the cell by preventing its proper adaptation to surrounding tissues. This can be useful in adaptive therapy of some neoplasms.

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29

Kasprzak, Aldona, Wojciech Kwasniewski, Agnieszka Adamek, and Anna Gozdzicka-Jozefiak. "Insulin-like growth factor (IGF) axis in cancerogenesis." Mutation Research/Reviews in Mutation Research 772 (April 2017): 78–104. http://dx.doi.org/10.1016/j.mrrev.2016.08.007.

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30

Stolte, M., and A. Meining. "Helicobacter '98 – Epidemiologie und Bedeutung in der Cancerogenese." Der Chirurg 69, no. 3 (March 1998): 234–38. http://dx.doi.org/10.1007/s001040050404.

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31

Wolf, Susann, Cathleen Haase-Kohn, and Jens Pietzsch. "S100A2 in cancerogenesis: a friend or a foe?" Amino Acids 41, no. 4 (June 3, 2010): 849–61. http://dx.doi.org/10.1007/s00726-010-0623-2.

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32

Bizzarri, M., A. Cucina, F. Conti, and F. D’Anselmi. "Beyond the Oncogene Paradigm: Understanding Complexity in Cancerogenesis." Acta Biotheoretica 56, no. 3 (February 21, 2008): 173–96. http://dx.doi.org/10.1007/s10441-008-9047-8.

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33

Adamyan, L. V., Ya O. Martirosyan, and A. V. Asaturova. "Endometriosis and cancerogenesis of the ovaries (a review)." Problemy reproduktsii 24, no. 4 (2018): 7. http://dx.doi.org/10.17116/repro2018240417.

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34

Demir, Tülin, Gamze Baran, Tuncay Buyukguclu, Fikriye Milletli Sezgin, and Haci Kaymaz. "Pneumonia due to Enterobacter cancerogenus infection." Folia Microbiologica 59, no. 6 (June 29, 2014): 527–30. http://dx.doi.org/10.1007/s12223-014-0330-6.

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35

Zhu, Feng. "KSHV Cancerogenesis and the Novel Strategies in Vaccine Design." Highlights in Science, Engineering and Technology 14 (September 29, 2022): 332–37. http://dx.doi.org/10.54097/hset.v14i.1842.

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Kaposi’s sarcoma-associated herpesvirus (KSHV) or human herpesvirus-8 (HHV-8) is an oncogenic virus that is associated with Kaposi’s sarcoma (KS), primary effusion lymphoma (PEL), multicentric Castleman’s disease (MCD), and other immune disorders. During the millions-year-long co-evolution with human, KSHV has developed a sophisticated system to switch and balance its biphasic latent-lytic lifecycle. To date, tons of efforts have been made to unveil its lifecycle and specific cancerogenesis. However, not a single specific, effective, and widely accessible treatment for this virus has been figured out. This article reviews the basis of the KSHV lifecycle and some important factors to generate malignant cancers and then offers a few novel and feasible vaccination strategies.

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36

Todorović-Raković, Nataša, Jelena Milovanović та Dragica Nikolić-Vukosavljević. "TGF-β and its coreceptors in cancerogenesis: an overview". Biomarkers in Medicine 5, № 6 (грудень 2011): 855–63. http://dx.doi.org/10.2217/bmm.11.59.

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Emmert, Steffen, Diana Leibeling, and Thomas M. Rünger. "Syndromes with genetic instability: Model diseases for (skin) cancerogenesis." JDDG 4, no. 9 (September 2006): 721–31. http://dx.doi.org/10.1111/j.1610-0387.2006.06047.x.

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Dvojakovska, Suzana, Danica Popovic-Monevska, Aleksandar Grcev, Goran Pancevski, Alberto Benedetti, Vladimir Popovski, Aleksandar Dimovski, and Aleksandar Stamatoski. "Promotor hypermethylated genes: Prospective diagnostic biomarkers in oral cancerogenesis." Journal of Cranio-Maxillofacial Surgery 46, no. 10 (October 2018): 1737–40. http://dx.doi.org/10.1016/j.jcms.2018.07.019.

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Xie, W. Z., M. Leibl, M. R. Clark, P. Dohrmann, T. Kunze, and F. Gieseler. "Activation of the coagulation system in cancerogenesis and metastasation." Biomedicine & Pharmacotherapy 59, no. 3 (April 2005): 70–75. http://dx.doi.org/10.1016/j.biopha.2005.01.001.

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40

Tripkovic, Ingrid, Andro Tripkovic, Zlatko Ivanisevic, Vesna Capkun, and Ljubinka Zekan. "Insulin increase in colon cancerogenesis: a case-control study." Archives of Medical Research 35, no. 3 (May 2004): 215–19. http://dx.doi.org/10.1016/j.arcmed.2003.12.003.

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41

Costarelli, Leopoldo, Domenico Campagna, Maria Mauri, and Lucio Fortunato. "Intraductal Proliferative Lesions of the Breast—Terminology and Biology Matter: Premalignant Lesions or Preinvasive Cancer?" International Journal of Surgical Oncology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/501904.

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Morphological criteria for the diagnosis of intraductal proliferative lesions of the breast have been an object of research and much controversy, and its terminology is rather confusing. Knowledge of the molecular aspects of this disease probably necessitates further research to clarify if these entities can be identified as breast cancer precursors or as a malignant preinvasive disease. These issues are of great interest not only for their biological implications, but also to the clinician who must understand the disease and direct therapies. Molecular studies have shown that epitheliosis (usual ductal hyperplasia) is not monoclonal, while malignant lesions (atypical ductal hyperplasia, flat epithelial atypia, low-grade and high-grade intraductal carcinoma) constantly show these characteristics. These malignant lesions, classified with a DIN grading system (ductal intraepithelial neoplasia), are not obligate precursors of invasive ductal carcinoma and do not represent different evolving grades in a linear model of cancerogenesis. Breast cancerogenesis probably has different pathways with different morphologic precursors.

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Tena, Daniel, María R. Lago, Juan Antonio Sáez-Nieto, María José Medina, Noelia Lara, and Jesús Oteo. "Surgical Site Infection Caused by Enterobacter cancerogenus." Infectious Diseases in Clinical Practice 23, no. 6 (November 2015): 289–91. http://dx.doi.org/10.1097/ipc.0000000000000307.

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Valko-Rokytovská, Marcela, Peter Očenáš, Aneta Salayová, and Zuzana Kostecká. "Breast Cancer: Targeting of Steroid Hormones in Cancerogenesis and Diagnostics." International Journal of Molecular Sciences 22, no. 11 (May 30, 2021): 5878. http://dx.doi.org/10.3390/ijms22115878.

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Breast cancer is the most common malignancy in women with high mortality. Sensitive and specific methods for the detection, characterization and quantification of endogenous steroids in body fluids or tissues are needed for the diagnosis, treatment and prognosis of breast cancer and many other diseases. At present, non-invasive diagnostic methods are gaining more and more prominence, which enable a relatively fast and painless way of detecting many diseases. Metabolomics is a promising analytical method, the principle of which is the study and analysis of metabolites in biological material. It represents a comprehensive non-invasive diagnosis, which has a high potential for use in the diagnosis and prognosis of cancers, including breast cancer. This short review focuses on the targeted metabolomics of steroid hormones, which play an important role in the development and classification of breast cancer. The most commonly used diagnostic tool is the chromatographic method with mass spectrometry detection, which can simultaneously determine several steroid hormones and metabolites in one sample. This analytical procedure has a high potential in effective diagnosis of steroidogenesis disorders. Due to the association between steroidogenesis and breast cancer progression, steroid profiling is an important tool, as well as in monitoring disease progression, improving prognosis, and minimizing recurrence.

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Kayukova, E. V., T. E. Belokrinitskaya, L. F. Sholokhov, and P. P. Tereshkov. "STUDY THE LOCAL LEVEL OF INFLAMMATORY PROTEINS IN CERVICAL CANCEROGENESIS." Transbaikalian Medical Bulletin, no. 2 (2020): 42–48. http://dx.doi.org/10.52485/19986173_2020_2_42.

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Dvořáková, M., I. Weingartová, J. Nevoral, D. Němeček, and T. Krejčová. "Garlic Sulfur Compounds Suppress Cancerogenesis and Oxidative Stress: a Review." Scientia Agriculturae Bohemica 46, no. 2 (June 1, 2015): 65–72. http://dx.doi.org/10.1515/sab-2015-0018.

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Abstract Garlic has long been considered a food with many health benefits. Several studies have confirmed that sulfur compounds are responsible for the positive effects of garlic on organisms. Garlic acts as an antioxidant by increasing antioxidant enzyme activity, reducing reactive oxygen species generation, and protecting proteins and lipids from oxidation. Garlic suppresses carcinogenesis through several mechanisms: (1) it reduces oxidative stress, and therefore, prevents damage to DNA; (2) it induces apoptosis or cell cycle arrest in cancer cells; and (3) it modifies gene expression through histon acetylation. The positive effects of garlic could be mediated by several mechanisms. It influences signalling pathways of gasotransmitters such as hydrogen sulfide. Garlic enhances hydrogen sulfide production both through its direct release and through an increase in activity of enzymes which produce hydrogen sulfide. Hydrogen sulfide acts as a signalling molecule in various tissues and participates in the regulation of many physiological processes. We can presume that garlic, which is able to release hydrogen sulfide, exhibits effects similar to those of this gasotransmitter.

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Buchholz, Malte, and Volker Ellenrieder. "An Emerging Role for Ca2+/Calcineurin/NFAT Signaling in Cancerogenesis." Cell Cycle 6, no. 1 (January 2007): 16–19. http://dx.doi.org/10.4161/cc.6.1.3650.

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Molaei, Mahsa, BabakKhoshkrood Mansoori, Somayeh Ghiasi, Fatemeh Nemati, Shohreh Almasi, SeyedReza Fatemi, AliGhanbari Motlagh, and MohammadReza Zali. "Cancerogenesis in colorectal neoplasms: Evidence from early onset colorectal cancer." Clinical Cancer Investigation Journal 1, no. 2 (2012): 57. http://dx.doi.org/10.4103/2278-0513.99562.

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Martinetz, Dieter. "Chemische Entgiftung wichtiger organischer Cancerogene im Laboratorium." Zeitschrift für Chemie 26, no. 9 (August 31, 2010): 309–15. http://dx.doi.org/10.1002/zfch.19860260902.

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Müller, Th. "Übersichtsartikel Cancerogene und genotoxische Wirkung von Mycotoxinen." Food / Nahrung 31, no. 2 (1987): 117–25. http://dx.doi.org/10.1002/food.19870310205.

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Lai, Lo, Ga Yoon Shin, and Hongyu Qiu. "The Role of Cell Cycle Regulators in Cell Survival—Dual Functions of Cyclin-Dependent Kinase 20 and p21Cip1/Waf1." International Journal of Molecular Sciences 21, no. 22 (November 12, 2020): 8504. http://dx.doi.org/10.3390/ijms21228504.

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The mammalian cell cycle is important in controlling normal cell proliferation and the development of various diseases. Cell cycle checkpoints are well regulated by both activators and inhibitors to avoid cell growth disorder and cancerogenesis. Cyclin dependent kinase 20 (CDK20) and p21Cip1/Waf1 are widely recognized as key regulators of cell cycle checkpoints controlling cell proliferation/growth and involving in developing multiple cancers. Emerging evidence demonstrates that these two cell cycle regulators also play an essential role in promoting cell survival independent of the cell cycle, particularly in those cells with a limited capability of proliferation, such as cardiomyocytes. These findings bring new insights into understanding cytoprotection in these tissues. Here, we summarize the new progress of the studies on these two molecules in regulating cell cycle/growth, and their new roles in cell survival by inhibiting various cell death mechanisms. We also outline their potential implications in cancerogenesis and protection in heart diseases. This information renews the knowledge in molecular natures and cellular functions of these regulators, leading to a better understanding of the pathogenesis of the associated diseases and the discovery of new therapeutic strategies.

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