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Relevant bibliographies by topics / Pre-carcinogenesis

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Academic literature on the topic 'Pre-carcinogenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Pre-carcinogenesis"

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Schnell, David M., Aaron K. Holley, Sanjit K. Dhar, Teresa WM Fan, and Daret K. St. Clair. "MnSOD Deficiency Triggers Pre-Carcinogenesis Metabolic Switch." Free Radical Biology and Medicine 76 (November 2014): S131. http://dx.doi.org/10.1016/j.freeradbiomed.2014.10.209.

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Cunha, Gerald R., Y. Z. Wang, Simon W. Hayward, and Gail P. Risbridger. "Estrogenic effects on prostatic differentiation and carcinogenesis." Reproduction, Fertility and Development 13, no. 4 (2001): 285. http://dx.doi.org/10.1071/rd01010.

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Estrogens, alone or in combination with androgens, can induce aberrant growth and/or malignancy of the prostate gland. Squamous metaplasia is an abnormal form of prostatic epithelial differentiation elicited by exogenous estrogen alone. Estrogens elicit their effects via estrogen receptors (ER) in the prostate. Experiments using ERα and ERβ null mice demonstrated that ERα, but not ERβ is essential in the induction of prostatic squamous metaplasia. To determine the respective roles of epithelial versus stromal ERα in this response, the following tissue recombinants were constructed with prostatic epithelium (PRE) and stroma (S) from wild-type (wt) and ERα knockout (αERKO) mice: wt-S + wt-PRE, · αERKO-S + αERKO-PRE, wt-S + αERKO-PRE and αERKO-S + wt-PRE. A metaplastic response to diethylstilbestrol (DES) was only observed in wt-S + wt-PRE tissue recombinants. Tissue recombinants containing αERKO-PRE and/or αERKO-S (ERKO-S + αERKO-PRE, wt-S + αERKO-PRE and αERKO-S + wt-PRE) failed to respond to DES. Therefore, full and uniform epithelial squamous metaplasia requires ERα in both the epithelium and stroma. Estradiol (E2) in combination with testosterone (T) was shown to be effective in inducing prostatic carcinogenesis in a tissue recombinant model composed of rat urogenital sinus mesenchyme plus mouse prostatic epithelium. A particularly efficient model of prostatic carcinogenesis in mice involves T + E2 treatment of mice bearing grafts of wild-type rat urogenital mesenchyme (rUGM) plus retinoblastoma gene (Rb) knockout (Rb-KO) prostatic epithelium (rUGM + Rb-KO-PRE). Such rUGM + Rb-KO-PRE tissue recombinants developed hyperplasia, atypical hyperplasia and invasive prostatic carcinoma with high efficiency. During carcinogenesis in rUGM + Rb-KO-PRE tissue recombinants, epithelial E-cadherin almost totally disappeared and epithelial PCNA labeling was elevated. These epithelial changes were associated with almost total loss of smooth muscle cells in the stroma. The results of this study demonstrate that the absence of the Rb tumor suppressor gene predisposes prostatic epithelial cells to hormonal carcinogenesis.

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Gomes, Maria Fernanda Pereira Lavieri, Cristina de Oliveira Massoco, José Guilherme Xavier, and Leoni Villano Bonamin. "Comfrey (Symphytum officinale. L.) and Experimental Hepatic Carcinogenesis: A Short-Term Carcinogenesis Model Study." Evidence-Based Complementary and Alternative Medicine 7, no. 2 (2010): 197–202. http://dx.doi.org/10.1093/ecam/nem172.

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Comfrey orSymphytum officinale(L.) (Boraginaceae) is a very popular plant used for therapeutic purposes. Since the 1980s, its effects have been studied in long-term carcinogenesis studies, in which Comfrey extract is administered at high doses during several months and the neoplastic hepatic lesions are evaluated. However, the literature on this topic is very poor considering the studies performed under short-term carcinogenesis protocols, such as the ‘resistant hepatocyte model’ (RHM). In these studies, it is possible to observe easily the phenomena related to the early phases of tumor development, since pre-neoplastic lesions (PNLs) rise in about 1–2 months of chemical induction. Herein, the effects of chronic oral treatment of rats with 10% Comfrey ethanolic extract were evaluated in a RHM. Wistar rats were sequentially treated withN-nitrosodiethylamine (ip) and 2-acetilaminofluorene (po), and submitted to hepatectomy to induce carcinogenesis promotion. Macroscopic/microscopic quantitative analysis of PNL was performed. Non-parametric statistical tests (Mann–Whitney and χ2) were used, and the level of significance was set atP≤ 0.05. Comfrey treatment reduced the number of pre-neoplastic macroscopic lesions up to 1 mm (P≤ 0.05), the percentage of oval cells (P= 0.0001) and mitotic figures (P= 0.007), as well as the number of Proliferating Cell Nuclear Antigen (PCNA) positive cells (P= 0.0001) and acidophilic pre-neoplastic nodules (P= 0.05). On the other hand, the percentage of cells presenting megalocytosis (P= 0.0001) and vacuolar degeneration (P= 0.0001) was increased. Scores of fibrosis, glycogen stores and the number of nucleolus organizing regions were not altered. The study indicated that oral treatment of rats with 10% Comfrey alcoholic extract reduced cell proliferation in this model.

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Sadlonova, V., P. Kubatka, K. Kajo, D. Ostatnikova, G. Nosalova, K. Adamicova, and J. Sadlonova. "Side effects of anastrozole in the experimental pre-menopausal mammary carcinogenesis." Neoplasma 56, no. 2 (2009): 124–29. http://dx.doi.org/10.4149/neo_2009_02_124.

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Newberne, Paul M., Doug Bueche, Vora Suphiphat, Thomas F. Schrager, and Somphong Sahaphong. "The influence of pre‐ and postnatal caloric intake on colon carcinogenesis." Nutrition and Cancer 13, no. 3 (January 1990): 165–73. http://dx.doi.org/10.1080/01635589009514057.

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C., Onuoha, Chukwudoruo C.S., Ezenwaka C.O., and Ujowundu F.N. "Investigating the Efficacy of Potential Diet-Derived Phytochemicals on LNCaP Cell Lines Under Physiological Conditions." African Journal of Biology and Medical Research 4, no. 3 (June 2, 2021): 1–8. http://dx.doi.org/10.52589/ajbmr-df4a8vsk.

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Prostate cancer (PCa) is increasingly prevalent in Nigeria and chemoprevention has a potential role to stem the initiation, promotion and progression of prostate carcinogenesis. The in vivo efficacy of phytochemicals depends on bioavailability, as the concentration of the compounds reaching target sites are known to reduce tremendously. With lower concentrations being achieved in target organs, the outcome on key players of carcinogenesis needs to be understood. The effect of curcumin, 3,3’-Diindolylmethane and epigallocatechin-3-gallate were interrogated on LNCaP cell lines by imitating in vivo conditions. The LNCaP cell lines were firstly, treated with low doses of curcumin, DIM and EGCG respectively. Subsequently, to investigate chemopreventive potentials of selected phytochemicals, cell lines were pre-treated and subsequently stimulated with testosterone. Lastly, to investigate the therapeutic potential of selected phytochemicals, cell lines were pre-stimulated before receiving respective treatments. From results, the effect of low dose treatments on the androgen receptor (AR) was dose-dependent. AR inhibition was observed more with cell lines that received a pre-treatment than cell-lines that received a pre-stimulation. All findings indicate that the investigated phytochemicals are potential chemopreventive regimens than curative regimens, since inhibitory effects on AR were enhanced more with a pre-treatment than a pre-stimulation. Furthermore, increased bioavailability of chemopreventive regimens will enhance efficacy.

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Tanaka, C., K. Uzawa, T. Shibahara, H. Yokoe, H. Noma, and H. Tanzawa. "Expression of an Inhibitor of Apoptosis, Survivin, in Oral Carcinogenesis." Journal of Dental Research 82, no. 8 (August 2003): 607–11. http://dx.doi.org/10.1177/154405910308200807.

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A novel inhibitor of apoptosis, survivin, plays a role in oncogenesis. To determine the potential involvement of survivin in oral carcinogenesis, we investigated the distribution of survivin protein expression in oral squamous cell carcinomas (OSCCs) and oral pre-malignant lesions. The mRNA expression level and methylation status of the gene also were evaluated in OSCCs and OSCC-derived cell lines. In immunohistochemistry, 58% of tumors and 37% of pre-malignant lesions examined were positive for survivin, while no immunoreaction was observed in corresponding normal tissues. The reverse-transcription/polymerase chain-reaction revealed similar changes in survivin gene expression levels. Furthermore, of the 9 normal oral tissues with no survivin gene expression, 4 showed methylation of the gene, while no methylation was detected in the corresponding tumorous tissues. The results suggest that survivin plays an important role during oral carcinogenesis, and that the gene expression may be regulated by an epigenetic mechanism.

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Businello, Gianluca, Valentina Angerilli, Paola Parente, Stefano Realdon, Edoardo Savarino, Fabio Farinati, Federica Grillo, et al. "Molecular Landscapes of Gastric Pre-Neoplastic and Pre-Invasive Lesions." International Journal of Molecular Sciences 22, no. 18 (September 14, 2021): 9950. http://dx.doi.org/10.3390/ijms22189950.

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Gastric carcinoma (GC) represents one of the most common and most lethal malignancies worldwide. The histopathological characterization of GC precursor lesions has provided great knowledge about gastric carcinogenesis, with the consequent introduction of effective strategies of primary and secondary prevention. In recent years, a large amount of data about the molecular events in GC development is emerging, flanking the histomorphological descriptions. In this review, we describe the landscape of molecular alterations in gastric pre-invasive lesions with a glance at their potential use in the diagnostic and therapeutic decision-making process.

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Wei, Wen-Jun, Yu-Long Wang, Duan-Shu Li, Yu Wang, Xiao-Feng Wang, Yong-Xue Zhu, Ya-jun Yang, et al. "Association between the rs2910164 Polymorphism in Pre-Mir-146a Sequence and Thyroid Carcinogenesis." PLoS ONE 8, no. 2 (February 22, 2013): e56638. http://dx.doi.org/10.1371/journal.pone.0056638.

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Zhu, Z. "Effect of caloric restriction on pre-malignant and malignant stages of mammary carcinogenesis." Carcinogenesis 18, no. 5 (May 1, 1997): 1007–12. http://dx.doi.org/10.1093/carcin/18.5.1007.

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Dissertations / Theses on the topic "Pre-carcinogenesis"

1

Jeon, Jihyoun. "Mathematical modeling of pre-malignant lesions in multistage carcinogenesis /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/6775.

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Mir, Noreen. "Differential expression analysis during pre-neoplastic stages of azoxymethane (AOM) induced colon carcinogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq58832.pdf.

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Lan, Shang-Lun. "Vitamin D in Normal Breast Tissue Correlates to Early Breast Carcinogenesis." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1471623716.

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Neo, Jenq Chyuan, and 梁正權. "The Biological Role of Pre-S1 and Pre-S2 Mutations of the HBV Large Surface Antigen during Liver Regeneration and Carcinogenesis." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/10816094165793442775.

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碩士
國立陽明大學
生命科學暨基因體科學研究所
97
肝癌依然是全球重要的健康議題，特別是在亞洲。肝癌的危險因子除了基因本身，還有環境等其他非基因分子。B型肝炎病毒的感染是其中導致肝癌發生的重要因子。B型肝炎病毒可以透過直接或間接的機制參與在腫瘤的形成過程中。為了了解B型肝炎病毒的致病急轉，其病毒蛋白，包括HBx蛋白、表面抗原也被研究多年。雖然嬰兒時期注射疫苗的措施已經降低了B型肝炎病毒的感染率，但是因為病毒的高突變率，抗病毒治療，以及免疫壓力，一些B型肝炎病毒的突變種也因而出現。大型表面抗原(large surface antigen)涵蓋了Pre-S1、Pre-S2及S區域。臨床上，可以在病人的血清或肝癌組織中發現具有Pre-S區域突變的大型表面抗癌。為了研究具有Pre-S1或Pre-S突變的大型表面抗原在肝癌過程及肝臟再生中所扮演的生理角色，我們使用由台北榮總及國家衛生研究院合作者提供的Pre-S1、Pre-S2突變的大型面抗原的序列，建立了Pre-S突變大型表面抗原的轉殖基因小鼠。為了研究Pre-S突變大型表面抗原與HBx蛋白在肝癌過程中是否有加成作用，我們也建立了同時帶有這兩種基因的轉殖基因小鼠。在肝臟再生的研究中，當切肝48小時後，會發現在Pre-S2(榮總)突變轉基因小鼠中出現M phase延遲的現象。截至目前對丙胺酸轉胺酶(ALT)的檢測，在轉基因小鼠12個月大前依然維持在正常值。但是，在Pre∆S2 (國衛院) A205譜系原源種(founder)中，在21個月的時候發現了丙胺酸轉胺酶上升及肝癌產生的現象。Pre-S突變蛋白及HBx蛋白也被發現對肝癌的形成有加成作用，帶有兩種基因的小鼠比HBx轉基因小鼠更快出現丙胺酸轉胺酶上升及肝癌的產生。在我們的研究中提出了在Pre-S突變轉基因小鼠中，可能透過Pparalpha�悀W升，抑制了微型核醣核酸Let-7C，進而促進C-myc的上升並參與在肝癌產生的過程中。

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Hsieh, Yi-Hsuan, and 謝逸璇. "The roles of hepatitis B virus pre-S2 mutant large surface antigen in cellular stress-induced hepatocellular carcinogenesis." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/89944461579709182971.

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博士
國立成功大學
基礎醫學研究所
95
Chronic hepatitis B virus (HBV) infection is a major global cause of hepatocellular carcinoma (HCC). Hepatocytes expressing the HBV large surface antigen (LHBs) pre-S2 mutant, which is partially deleted in the pre-S2 region on HBV surface gene, exhibited nodule formation, clonal expansion and growth advantage. The majority of HBV-related HCC patients harbored pre-S2 mutant LHBs, indicating that pre-S2 mutant LHBsis highly associated with hepatocellular carcinogenesis. It was found that pre-S2 mutant LHBs accumulates in endoplasmic reticulum (ER) inducing ER stress and oxidative DNA damage. In this study, we aim to explore the molecular mechanisms regulated by pre-S2 mutant LHBs and seek potential prophylaxis and therapeutic approaches for pre-S2 mutant LHBs-associated HCC. We found that the oxidative stress and DNA damages induced by pre-S2 mutant LHBs were dependent on ER stress, as the ER stress inhibitors vomitoxin or TMB8 dramatically decreased such oxidative stress. By yeast two-hybrid screening assays, the pre-S2 mutant LHBs was found to directly interact with the Jun activation domain-binding protein 1 (JAB1), a subunit of COP9 signalosome. JAB1 has been shown to interact with p27Kip1 cyclin-dependent kinase inhibitor and target it to cytosolic 26S proteasome for degradation. We found that JAB1 and pre-S2 mutant LHBs enhanced the nuclear translocation of JAB1 and trigger p27Kip1 degradation and Cdk2 activation, resulting in inactivation of the tumor suppressor retinoblastoma (RB), a downstream molecule regulated by Cdk2. In transgenic mice carrying the pre-S2 mutant LHBs, p27Kip1 degradation, Cdk2 activation and RB inactivation were also seen, indicating the pre-S2 mutant LHBs triggers cell cycle progression in vivo and in vitro. These results suggest that cell cycle progression caused by RB inactivation might contribute to HCC associated with pre-S2 mutant LHBs. In the last part of our study, we seek potential targeted prophylaxis and therapeutic approaches for HCC induced by pre-S2 mutant LHBs. Vitamin D3 (VitD3) and the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) have been found to enhance thioredoxin binding protein 2 (TBP2) expression and JAB1-TBP2 interactions, resulting in blockage of JAB1-p27Kip1 interaction and stabilization of p27Kip1. We found VitD3 and the HDAC inhibitors SAHA, trichostatin A and sodium butyrate enhanced p27Kip1 stabilization in the cells expressing the pre-S2 mutant LHBs. We also found that the oxidative DNA damages induced by pre-S2 mutant LHBs were dramatically decreased after treatments with vitD3 and HDAC inhibitors, indicating that HDAC inhibitors are effective targeted drugs to repress p27Kip1 degradation and oxidative stress caused by the pre-S2 mutant LHBs. The HDAC inhibitors might provide a novel therapeutic approach for the pre-S2 mutant LHBs-induced hepatocellular carcinogenesis.

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Books on the topic "Pre-carcinogenesis"

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Mir, Noreen. Differential expression analysis during pre-neoplastic stages of azoxymethane (AOM) induced colon carcinogenesis. Ottawa: National Library of Canada, 2001.

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Book chapters on the topic "Pre-carcinogenesis"

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Khan, Seema A., and Scott Stickles. "Cell Proliferation and Apoptosis in the Normal Breast Epithelium of Pre, Peri, and Postmenopausal Women." In Hormonal Carcinogenesis III, 418–23. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4612-2092-3_42.

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Valentina Caracostea, Gabriela, Alexandru Bucur, Iulia Cristina Micu, Andrada Soanca, Andreea Ciurea, Adriana Objelean, Ada Gabriela Delean, et al. "Periodontal Medicine: Impact of Periodontal Status on Pregnancy Outcomes and Carcinogenesis." In Periodontology - Fundamentals and Clinical Features [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96147.

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Periodontal medicine is a broad term commonly used to define the relationship between periodontitis and systemic health. Periodontitis is a highly prevalent, chronic multifactorial infectious disease, induced by the dysbiotic biofilm that triggers a persistent systemic inflammation and recurrent bacteremia. There is a growing body of scientific evidence that suggests the potential implication of periodontitis in the causation and progression of various systemic disease and conditions, such as diabetes, cardiovascular disease, pulmonary disease, adverse pregnancy outcomes and cancer. Some studies consider periodontitis as an independent risk factor for preterm birth, growth restriction, low birth-weight and pre-eclampsia. However not all studies support the association. Despite sparse scientific data, some studies indicate that individuals with periodontitis are at increased risk for cancer development, due to the increased inflammatory burden sustained by the presence of periodontal pathogens. This chapter emphasis the relationship between periodontitis and adverse pregnancy outcomes and the underlying mechanisms that link peridontitis to oral carcinogenesis.

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Sağnıç, Saliha. "Human Papillomavirus and Cervical Cancer." In Cervical Cancer - A Global Public Health Treatise [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98490.

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Cervical cancer is one of the leading female cancers especially in developing countries and a common cause of death among middle-aged women. The main role of Human Papillomavirus (HPV) in both cervical cancer and pre-invasive lesions of the cervix has been proven in studies. Reducing the incidence of the disease can be achieved by the regular cervical screening of women and vaccination of appropriate age groups. The disease can be better controlled by better elucidating the details of HPV carcinogenesis, the interaction between the host and the virus, and determinants of the systemic and cellular immune response to the viral infection. HPV causes oropharyngeal and anogenital diseases in both men and women and is usually sexually transmitted. Most infections are transient and could be cleared spontaneously by the host immune system. After the first encounter with HPV infection, it takes years to progress to cervical cancer, which gives clinicians a long period to follow these patients in terms of precancerous lesions and to investigate the pathogenesis of the disease. HPV plays a major role in the development of cervical cancer, but histological types have different relationships with HPV genotypes. HPV can remain latent for a long time and the most important thing determining the persistence is the type of HPV. HPV vaccination provides a direct benefit to both men and women by providing safe protection against cancers that may result from persistent HPV infection.

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Conference papers on the topic "Pre-carcinogenesis"

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Backman, V., Y. L. Kim, Y. Liu, R. K. Wali, H. K. Roy, M. J. Goldberg, A. K. Kromine, and K. Chen. "Diagnosis of early pre-dysplastic stages of colon carcinogenesis using light scattering “fingerprints”." In Frontiers in Optics. Washington, D.C.: OSA, 2003. http://dx.doi.org/10.1364/fio.2003.tur3.

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Dhar, Sanjit K., Jibjoy Tangpong, Luksana Chaiswing, Terry D. Oberley, and Daret K. St Clair. "Abstract 1606: Altered regulation of manganese superoxide dismutase is an important pre-carcinogenesis event mediated by p53." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1606.

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Cui, Changxu, Reika Takamatsu, Hiroshi Doguchi, Akiko Matsuzaki, Masanao Saio, and Naoki Yoshimi. "Abstract 4416: The pre-neoplastic lesion, mucin-depleted foci, reveals asde novohigh-grade dysplasia in rat colon carcinogenesis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4416.

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