Journal articles: '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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Roller, Monika, Angelo Pietro Femia, Giovanna Caderni, Gerhard Rechkemmer, and Bernhard Watzl. "Intestinal immunity of rats with colon cancer is modulated by oligofructose-enriched inulin combined with Lactobacillus rhamnosus and Bifidobacterium lactis." British Journal of Nutrition 92, no. 6 (December 2004): 931–38. http://dx.doi.org/10.1079/bjn20041289.

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Probiotics (PRO) are known to modulate immunity in animals and human subjects and to inhibit colon carcinogenesis in experimental models, but the effects of synbiotics (SYN) are not well understood. Therefore, the effects of PRO (Lactobacillus rhamnosus GG and Bifidobacterium lactis Bb12), PRE (inulin-based enriched with oligofructose, 100g/kg) and SYN (combination of PRO and PRE) on the immune system of rats were investigated in the azoxymethane (AOM)-induced colon cancer model. After 33 weeks, rats with and without AOM treatment were killed and immune cells were isolated from spleen, mesenterial lymph nodes (MLN) and Peyer's patches (PP). AOM treatment significantly reduced natural killer (NK) cell-like cytotoxicity in control rats and in PRO- and PRE-supplemented rats. SYN supplementation prevented the AOM-induced suppression of NK cell-like cytotoxicity in PP compared with control rats (P<0·01). SYN and PRE supplementation stimulated IL-10 production in PP in these rats (P<0·01) and in MLN of rats not treated with AOM (P<0·05). Interferon-γ production in PP was decreased by PRO supplementation (PRO and SYN groups combined; P<0·05). Proliferative responsiveness of lymphocytes (PP) from AOM-treated rats was suppressed in SYN-supplemented rats (P<0·01). Overall, SYN supplementation in carcinogen-treated rats primarily modulated immune functions in the PP, coinciding with a reduced number of colon tumours. PRE and PRO provided in combination as SYN may contribute to the suppression of colon carcinogenesis by modulating the gut-associated lymphoid tissue.

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Novianry, Virhan, Yulhasri Yulhasri, and Kusmardi Kusmardi. "Serum cell-free DNA concentration in BALB/c mice with azoxymethane-dextran sodium sulfate-induced colorectal cancer." Medical Journal of Indonesia 24, no. 1 (March 22, 2015): 3–7. http://dx.doi.org/10.13181/mji.v24i1.730.

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Background: Colorectal cancer is the third most common cancer in the United States with a mortality rate ranked second in 2012. Early diagnosis such as detection of DNA in serum or faeces at the polyp stage, will reduce colorectal cancer mortality. This study was conducted to analyze the concentration of cell-free DNA (cfDNA) as a tumor marker in colorectal carcinogenesis by using blood serum samples from BALB/c mice previously induced by azoxymethane (AOM) and promoted by dextran sodium sulfate (DSS).Methods: This experimental animal study used 6 BALB/c mice which had serial intervention in a certain time frame. The first serum samples were taken before induction of carcinogenesis (week-0); then AOM induction of carcinogenesis followed and the second sampling one week after AOM intervention (week-1). Subsequently, promotion of carcinogenesis followed with DSS and the third sampling one week after this intervention (week-2). The fourth sampling was 5 weeks after AOM-DSS intervention (week-6). Quantification of the serum cfDNA was performed with SYBR-Green II fluorescence using Rotor Gene 6000 as a reference. Histopathological examination verified induction of carcinogenesis. For statistical analysis paired T-test was used.Results: Concentration of serum cfDNA showed significant difference between sampling group at week-0 (1238.49 ± 674.84 pg/µL) and sampling group at week-6 (2244.04 ± 726.57 pg/µL) the latter group showing pre-cancerous histopathology. Slightly increased cfDNA at week-1 with AOM induction (1358.57 ± 803.81 pg/µL) and week-2 after DSS promotion (1317.23 ± 735.92 pg/µL) were not significantly different from week-0 samples.Conclusion: The concentration of cfDNA in the serum of BALB/c mice 5 weeks after AOM induction of carcinogenesis and DSS promotion is significantly higher than before induction.

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VIRGONE, C., G. CECCHETTO, V. BESUTTI, A. FERRARI, P. BUFFA, R. ALAGGIO, L. ALESSANDRINI, and P. DALL'IGNA. "Bowel parasitosis and neuroendocrine tumours of the appendix. A report from the Italian TREP project." Epidemiology and Infection 143, no. 7 (September 12, 2014): 1552–55. http://dx.doi.org/10.1017/s0950268814002404.

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SUMMARYFive children with a neuroendocrine tumour (NET) of the appendix associated with a parasitic bowel infection are described, and the possibility of inflammation-triggered carcinogenesis is discussed. Schistosoma haematobium is linked primarily to bladder cancer but it has been reported in association with several other histotypes, including NETs of the gastrointestinal tract. Conversely, Enterobius vermicularis has not yet been claimed to participate in the onset of pre-cancerous conditions or tumours. The rare occurrence of contemporary appendiceal NETs and parasitic infection, raises the intriguing hypothesis of an inflammation-related carcinogenesis, although a cause–effect relationship cannot be established. Larger international series of childhood appendiceal NETs, which also include countries with higher prevalence of parasitic bowel infections, are needed to further clarify this possible cause–effect relationship.

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Nakano-Narusawa, Yuko, Masanao Yokohira, Keiko Yamakawa, Juanjuan Ye, Misa Tanimoto, Linxuan Wu, Yuri Mukai, Katsumi Imaida, and Yoko Matsuda. "Relationship between Lung Carcinogenesis and Chronic Inflammation in Rodents." Cancers 13, no. 12 (June 10, 2021): 2910. http://dx.doi.org/10.3390/cancers13122910.

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Lung cancer remains the leading cause of cancer-related deaths, with an estimated 1.76 million deaths reported in 2018. Numerous studies have focused on the prevention and treatment of lung cancer using rodent models. Various chemicals, including tobacco-derived agents induce lung cancer and pre-cancerous lesions in rodents. In recent years, transgenic engineered rodents, in particular, those generated with a focus on the well-known gene mutations in human lung cancer (KRAS, EGFR, and p53 mutations) have been widely studied. Animal studies have revealed that chronic inflammation significantly enhances lung carcinogenesis, and inhibition of inflammation suppresses cancer progression. Moreover, the reduction in tumor size by suppression of inflammation in animal experiments suggests that chronic inflammation influences the promotion of tumorigenesis. Here, we review rodent lung tumor models induced by various chemical carcinogens, including tobacco-related carcinogens, and transgenics, and discuss the roles of chronic inflammation in lung carcinogenesis.

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Rizzi, Renato, Francesco Re, and Enzo Chiesara. "Computerised Image Analysis of Nuclear Enlargement Assay in HeLa Cells." Alternatives to Laboratory Animals 19, no. 1 (February 1991): 41–47. http://dx.doi.org/10.1177/026119299101900109.

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It has been observed that cells often respond to carcinogens by nuclear enlargement. For this reason, new morphometric approaches have been developed to evaluate cell modifications in pre-carcinogenesis assays. Morphometric computerised automatic analysis, with original software, was performed on HeLa cells treated with various compounds (hydroxyurea, dimethylnitrosamine, N-methyl- N’-nitro-nitrosoguanidine and cyclophosphamide) to evaluate nuclear size changes.

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Okada, Seiji, Tarou Irié, Junichi Tanaka, Rika Yasuhara, Gou Yamamoto, Tomohide Isobe, Chie Hokazono, Tetsuhiko Tachikawa, Yohko Kohno, and Kenji Mishima. "Potential role of hematopoietic pre-B-cell leukemia transcription factor-interacting protein in oral carcinogenesis." Journal of Oral Pathology & Medicine 44, no. 2 (July 24, 2014): 115–25. http://dx.doi.org/10.1111/jop.12210.

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Chen, Chien-Chang, Wei-Chuan Lin, Man-Shan Kong, Hai Ning Shi, W. Allan Walker, Chun-Yen Lin, Ching-Tai Huang, Yung-Chang Lin, Shih-Ming Jung, and Tzou-Yien Lin. "Oral inoculation of probioticsLactobacillus acidophilusNCFM suppresses tumour growth both in segmental orthotopic colon cancer and extra-intestinal tissue." British Journal of Nutrition 107, no. 11 (September 30, 2011): 1623–34. http://dx.doi.org/10.1017/s0007114511004934.

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Modulation of the cellular response by the administration of probiotic bacteria may be an effective strategy for preventing or inhibiting tumour growth. We orally pre-inoculated mice with probioticsLactobacillus acidophilusNCFM (La) for 14 d. Subcutaneous dorsal-flank tumours and segmental orthotopic colon cancers were implanted into mice using CT-26 murine colon adenocarcinoma cells. On day 28 after tumour initiation, the lamina propria of the colon, mesenteric lymph nodes (MLN) and spleen were harvested and purified for flow cytometry and mRNA analyses. We demonstrated thatLapre-inoculation reduced tumour volume growth by 50·3 %, compared with untreated mice at 28 d after tumour implants (2465·5 (sem1290·4)v. 4950·9 (sem1689·3) mm3,P < 0·001). Inoculation withLareduced the severity of colonic carcinogenesis caused by CT-26 cells, such as level of colonic involvement and structural abnormality of epithelial/crypt damage. Moreover,Laenhanced apoptosis of CT-26 cells both in dorsal-flank tumour and segmental orthotopic colon cancer, and the mean counts of apoptotic body were higher in mice pre-inoculated withLa(P < 0·05) compared with untreated mice.Lapre-inoculation down-regulated the CXCR4 mRNA expressions in the colon, MLN and extra-intestinal tissue, compared with untreated mice (P < 0·05). In addition,Lapre-inoculation reduced the mean fluorescence index of MHC class I (H-2Dd, -Kd and -Ld) in flow cytometry analysis. Taken together, these findings suggest that probioticsLamay play a role in attenuating tumour growth during CT-26 cell carcinogenesis. The down-regulated expression of CXCR4 mRNA and MHC class I, as well as increasing apoptosis in tumour tissue, indicated thatLamay be associated with modulating the cellular response triggered by colon carcinogenesis.

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Kato, Junichi, Yohei Shirakami, Taku Mizutani, Masaya Kubota, Hiroyasu Sakai, Takashi Ibuka, and Masahito Shimizu. "Alpha-Glucosidase Inhibitor Voglibose Suppresses Azoxymethane-Induced Colonic Preneoplastic Lesions in Diabetic and Obese Mice." International Journal of Molecular Sciences 21, no. 6 (March 23, 2020): 2226. http://dx.doi.org/10.3390/ijms21062226.

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Type 2 diabetes mellitus and its related insulin resistance are known to increase the risk of cancer. Anti-diabetic agents can improve insulin resistance and may lead to the suppression of carcinogenesis. This study aimed to investigate the preventive effects of the alpha-glucosidase inhibitor voglibose on the development of azoxymethane-induced colorectal pre-neoplastic lesions in obese and diabetic C57BL/KsJ-db/db mice. The direct effects of voglibose on the proliferation of colorectal cancer cells were also evaluated. Mice were injected with azoxymethane to induce colorectal pre-malignancy and were then administered drinking water with or without voglibose. At the end of the study, the administration of voglibose significantly suppressed the development of colorectal neoplastic lesions. In voglibose-treated mice, serum glucose levels, oxidative stress, as well as mRNA expression of the insulin-like growth factor-1 in the colon mucosa, were reduced. The proliferation of human colorectal cancer cells was not altered by voglibose. These results suggested that voglibose suppressed colorectal carcinogenesis in a diabetes- and obesity-related colorectal cancer model, presumably by improving inflammation via the reduction of oxidative stress and suppressing of the insulin-like growth factor/insulin-like growth factor-1 receptor axis in the colonic mucosa.

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Melis, Marta, Tuo Zhang, Theresa Scognamiglio, and Lorraine J. Gudas. "Mutations in long-lived epithelial stem cells and their clonal progeny in pre-malignant lesions and in oral squamous cell carcinoma." Carcinogenesis 41, no. 11 (March 2, 2020): 1553–64. http://dx.doi.org/10.1093/carcin/bgaa019.

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Abstract Oral squamous cell carcinomas (OSCCs) are the most common cancers of the oral cavity, but the molecular mechanisms driving OSCC carcinogenesis remain unclear. Our group previously established a murine OSCC model based on a 10-week carcinogen [4-nitroquinoline 1-oxide (4-NQO)] treatment. Here we used K14CreERTAM;Rosa26LacZ mice to perform lineage tracing to delineate the mutational profiles in clonal cell populations resulting from single, long-lived epithelial stem cells, here called LacZ+ stem cell clones (LSCCs). Using laser-capture microdissection, we examined mutational changes in LSCCs immediately after the 10-week 4-NQO treatment and >17 weeks after 4-NQO treatment. We found a 1.8-fold ±0.4 (P = 0.009) increase in single-nucleotide variants and insertions/deletions (indels) in tumor compared with pre-neoplastic LSCCs. The percentages of indels and of loss of heterozygosity events were 1.3-fold±0.3 (P = 0.02) and 2.2-fold±0.7 (P = 0.08) higher in pre-neoplastic compared with tumor LSCCs. Mutations in cell adhesion- and development-associated genes occurred in 83% of the tumor LSCCs. Frequently mutated genes in tumor LSCCs were involved in planar cell polarity (Celsr1, Fat4) or development (Notch1). Chromosomal amplifications in 50% of the tumor LSCCs occurred in epidermal growth factor receptor, phosphoinositide 3-kinase and cell adhesion pathways. All pre-neoplastic and tumor LSCCs were characterized by key smoking-associated changes also observed in human OSCC, C>A and G>T. DeconstructSigs analysis identified smoking and head and neck cancer as the most frequent mutational signatures in pre-neoplastic and tumor LSCCs. Thus, this model recapitulates a smoking-associated mutational profile also observed in humans and illustrates the role of LSCCs in early carcinogenesis and OSCCs.

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Svicher, V., M. Neumann-Fraune, C. Mirabelli, R. Salpini, V. Cento, V. C. Di Maio, A. Bertoli, et al. "430 KEY GENETIC SIGNATURES IN THE WHOLE pre-S1/Pre-S2/S GENE CORRELATE WITH HBV-INDUCED CARCINOGENESIS BY AFFECTING HBsAg SECRETION AND RELEASE." Journal of Hepatology 58 (April 2013): S176. http://dx.doi.org/10.1016/s0168-8278(13)60432-8.

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Yeewa, Ranchana, Aya Naiki-Ito, Taku Naiki, Hiroyuki Kato, Shugo Suzuki, Teera Chewonarin, and Satoru Takahashi. "Hexane Insoluble Fraction from Purple Rice Extract Retards Carcinogenesis and Castration-Resistant Cancer Growth of Prostate Through Suppression of Androgen Receptor Mediated Cell Proliferation and Metabolism." Nutrients 12, no. 2 (February 20, 2020): 558. http://dx.doi.org/10.3390/nu12020558.

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Prostate cancer and castration-resistant prostate cancer (CRPC) remain major health challenges in men. In this study, the inhibitory effects of a hexane insoluble fraction from a purple rice ethanolic extract (PRE-HIF) on prostate carcinogenesis and CRPC were investigated both in vivo and in vitro. In the Transgenic Rat for Adenocarcinoma of Prostate (TRAP) model, 1% PRE-HIF mixed diet-fed rats showed a significantly higher percentage of low-grade prostatic intraepithelial neoplasia and obvious reduction in the incidence of adenocarcinoma in the lateral lobes of the prostate. Additionally, 1% PRE-HIF supplied diet significantly suppressed the tumor growth in a rat CRPC xenograft model of PCai1 cells. In LNCaP and PCai1 cells, PRE-HIF treatment suppressed cell proliferation and induced G0/G1 cell-cycle arrest. Furthermore, androgen receptor (AR), cyclin D1, cdk4, and fatty acid synthase expression were down-regulated while attenuation of p38 mitogen-activated protein kinase, and AMP-activated protein kinase α activation occurred in PRE-HIF treated prostate cancer cells, rat prostate tissues, and CRPC tumors. Due to consistent results with PRE-HIF in PCai1 cells, cyanidin-3-glucoside was characterized as the active compound. Altogether, we surmise that PRE-HIF blocks the development of prostate cancer and CRPC through the inhibition of cell proliferation and metabolic pathways.

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Patel, Snehal T., Tina Mistry, James E. P. Brown, Janet E. Digby, Raghu Adya, Ken M. Desai, and Harpal S. Randeva. "A novel role for the adipokine visfatin/pre-B cell colony-enhancing factor 1 in prostate carcinogenesis." Peptides 31, no. 1 (January 2010): 51–57. http://dx.doi.org/10.1016/j.peptides.2009.10.001.

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Teoh, Narci C. "Pre-“EMT”ing key processes in liver carcinogenesis: Growing evidence for how malignant hepatocytes invade and conquer." Hepatology 52, no. 1 (June 25, 2010): 384–88. http://dx.doi.org/10.1002/hep.23777.

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Brücher, Björn L. D. M., and Ijaz S. Jamall. "Synopsis: Special Issue on “Disruption of signaling homeostasis induced crosstalk in the carcinogenesis paradigm Epistemology of the origin of cancer”." 4open 2 (2019): 28. http://dx.doi.org/10.1051/fopen/2019023.

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It is increasingly evident that carcinogenesis, in the vast majority of cancers, cannot be explained simply through an accumulation of somatic mutations, or epigenetics, the stem cell theory, or the Warburg effect. Here, decades of thinking based on incorrect assumptions has resulted in an incorrect hypothesis on the origin of cancer. Many papers studying DNA, genetics, RNA, miRNA, proteomics, and epigenetics have increased our understanding of biology. Our paradigm, though more complex, is more reliable and plausible. It states that cancer originates from a disruption of homeostasis. This essential biological phenomenon, homeostasis, maintains the interrelationships of various signaling pathways and induced crosstalk which modify cellular functions together with the interactions of surrounding cells and structures such that the equilibrium lies towards the optimal health of the organism. This Special Issue “Disruption of signaling homeostasis induced crosstalk in the carcinogenesis paradigm Epistemology of the origin of cancer” provides compelling evidence that carcinogenesis is explained by a six-step sequence of events for the vast majority of cancers. These six steps include, (1) a pathogenic stimulus followed by (2) chronic inflammation, from which develops (3) fibrosis with associated remodeling in the cellular microenvironment. From these changes a (4) pre-cancerous niche develops which triggers the deployment of (5) a chronic stress escape strategy, and when this fails to resolve, and (6) the transition of a normal cell to a cancer cell occurs. This paradigm provides opportunities to move away from a symptom-oriented understanding of cancer and is much closer to a cause-based understanding, which opens the door for early preventative strategies to mitigate cancer as a disease, and to interdict metastases. This is underpinned by the fact that an independent recently published proof of this paradigm showed how a stimulus trigger the proposed multi-sequence cascade of events as abrupt involution-induced chronic inflammation, followed by fibrosis with remodeling, which describes the pre-cancerous niche followed by hyperplasia, metaplasia, and cancer.

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Lao-Sirieix, Pierre, and Rebecca C. Fitzgerald. "Role of the micro-environment in Barrett's carcinogenesis." Biochemical Society Transactions 38, no. 2 (March 22, 2010): 327–30. http://dx.doi.org/10.1042/bst0380327.

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Most epithelial cancers occur on the background of chronic exposure to damaging agents which is reflected in the long lag phase from development of a pre-invasive lesion to the development of a carcinoma. Luminal refluxate has long been recognized to be associated with Barrett's oesophagus, although causal mechanisms have not been clearly defined. Recently, obesity and dietary nitric oxide have also been implicated in the disease pathogenesis. We have demonstrated that acid can alter cell kinetics and, together with nitric oxide, can induce double-stranded DNA breaks. Aside from exposure to luminal factors, the stromal micro-environment may also be important. There is increasing evidence to suggest that inflammatory pathways such as TGF (transforming growth factor) β may play a role in Barrett's oesophagus carcinogenesis. Hence stromal–epithelial–luminal interactions may influence cell behaviour. As sequelae to this, it is possible that the niches created by the micro-environment may influence genetic epithelial diversity observed within the Barrett's oesophagus segment.

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Imrhan, Victorine L., and Andie M. Hsueh. "Effects of type and level of dietary fat during the pre-initiation phase of mammary carcinogenesis in rats." Nutrition Research 18, no. 3 (March 1998): 543–55. http://dx.doi.org/10.1016/s0271-5317(98)00041-4.

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Babino, Alvaro, Pablo Oppezzo, Stella Bianco, Enrique Barrios, Nora Berois, H�ctor Navarrete, and Eduardo Osinaga. "Tn antigen is a pre-cancerous biomarker in breast tissue and serum inn-nitrosomethylurea-induced rat mammary carcinogenesis." International Journal of Cancer 86, no. 6 (June 15, 2000): 753–59. http://dx.doi.org/10.1002/(sici)1097-0215(20000615)86:6<753::aid-ijc1>3.0.co;2-#.

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Patel, V., C. Ieethanakul, and J. S. Gutkind. "New Approaches To the Understanding of the Molecular Basis of Oral Cancer." Critical Reviews in Oral Biology & Medicine 12, no. 1 (January 2001): 55–63. http://dx.doi.org/10.1177/10454411010120010401.

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Cancers of the oral cavity, salivary glands, larynx, and pharynx, collectively referred to as squamous cell carcinomas of the head and neck (HNSCC), are the sixth most common cancer among men in the developed world. The prognosis of HNSCC patients is still poor, which reflects the fact that although the risk factors for HNSCC are well-recognized, very little is known about the molecular mechanisms responsible for this malignancy. This review describes some of the current efforts and technological advances that have focused on the creation of a complete information infrastructure for genes expressed during squamous cell carcinogenesis. These include: the recently described HNSCC-specific chromosomal alterations (cCAP); the Head and Neck Cancer Genome Anatomy Project (HN-CGAP), whose goal is the systematic identification and cataloguing of known and novel genes expressed during tumor development; and the use of laser-capture microdissection (LCM), which is pivotal for the comprehensive molecular characterization of normal, pre-cancerous, and malignant cells by means of DNA-array technology. The latter provides the means for the analysis of expression patterns of thousands of genes simultaneously. The use of LCM for proteomics and DNA analysis is also included in this review. These revolutionary approaches are likely to have an unprecedented impact on cancer biology, and provide exciting opportunities to unravel the still-unknown mechanisms involved in squamous cell carcinogenesis. They are also expected to provide a molecular blueprint for HNSCC, thus helping to identify suitable markers for the early detection of pre-neoplastic lesions, as well as novel targets for pharmacological intervention in this disease.

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Koiss, Róbert, Imre Boncz, Zoltán Hernádi, and Zoltán Szentirmay. "Javaslat a hazai méhnyakszűrési eljárásrend korszerűsítésére." Orvosi Hetilap 158, no. 52 (December 2017): 2062–67. http://dx.doi.org/10.1556/650.2017.30896.

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Abstract: Two main considerations played roles in creation of new cervical screening system. One was the proven fact that high-risk human papilloma virus infection plays a role in the development of cervical cancer and pre-cancerous lesions. The other was the implementation of the HPV infection’s biological behavior in the new screening strategy. The new screening procedure faithfully reflects the cervical carcinogenesis. An organised, population-based and age differentiated screening method could increase attendance of screening and could decrease the possibility of interval cancer rate due to increased sensitivity. Orv Hetil. 2017; 158(52): 2062–2067.

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Torezan, Luis Antonio Ribeiro, and Cyro Festa-Neto. "Cutaneous field cancerization: clinical, histopathological and therapeutic aspects." Anais Brasileiros de Dermatologia 88, no. 5 (October 2013): 775–86. http://dx.doi.org/10.1590/abd1806-4841.20132300.

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The concept of "field cancerization" was first introduced by Slaughter in 1953 when studying the presence of histologically abnormal tissue surrounding oral squamous cell carcinoma. It was proposed to explain the development of multiple primary tumors and locally recurrent cancer. Organ systems in which field cancerization has been described since then are: head and neck (oral cavity, oropharynx, and larynx), lung, vulva, esophagus, cervix, breast, skin, colon, and bladder. Recent molecular studies support the carcinogenesis model in which the development of a field with genetically altered cells plays a central role. An important clinical implication is that fields often remain after the surgery for the primary tumor and may lead to new cancers, designated presently as "a second primary tumor" or "local recurrence," depending on the exact site and time interval. In conclusion, the development of an expanding pre-neoplastic field appears to be a critical step in epithelial carcinogenesis with important clinical consequences. Diagnosis and treatment of epithelial cancers should not only be focused on the tumor but also on the field from which it developed. The most important etiopathogenetic, clinical, histopathological and therapeutic aspects of field cancerization are reviewed in this article.

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Raimondi, A. R., A. A. Molinolo, and M. E. Itoiz. "Fibroblast growth factor-2 expression during experimental oral carcinogenesis. Its possible role in the induction of pre-malignant fibrosis." Journal of Oral Pathology and Medicine 35, no. 4 (April 2006): 212–17. http://dx.doi.org/10.1111/j.1600-0714.2006.00394.x.

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32

Verlaat, Wina, Robert W. Van Leeuwen, Putri W. Novianti, Ed Schuuring, Chris J. L. M. Meijer, Ate G. J. Van Der Zee, Peter J. F. Snijders, Daniëlle A. M. Heideman, Renske D. M. Steenbergen, and G. Bea A. Wisman. "Host-cell DNA methylation patterns during high-risk HPV-induced carcinogenesis reveal a heterogeneous nature of cervical pre-cancer." Epigenetics 13, no. 7 (July 3, 2018): 769–78. http://dx.doi.org/10.1080/15592294.2018.1507197.

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Siddique, Aktarul Islam, Vijay Mani, Senbagarani Renganathan, Rajagopal Ayyanar, Ananthi Nagappan, and Nalini Namasivayam. "Asiatic acid abridges pre-neoplastic lesions, inflammation, cell proliferation and induces apoptosis in a rat model of colon carcinogenesis." Chemico-Biological Interactions 278 (December 2017): 197–211. http://dx.doi.org/10.1016/j.cbi.2017.10.024.

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34

Machackova, Prochazka, Kala, and Slaby. "Translational Potential of MicroRNAs for Preoperative Staging and Prediction of Chemoradiotherapy Response in Rectal Cancer." Cancers 11, no. 10 (October 12, 2019): 1545. http://dx.doi.org/10.3390/cancers11101545.

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Abstract: Colorectal cancer is the third most common cancer and the second cause of cancer-related deaths. Rectal cancer presents roughly one-third of all colorectal cancer cases and differs from it on both anatomical and molecular levels. While standard treatment of colon cancer patients is radical surgery, rectal cancer is usually treated with pre-operative chemoradiotherapy followed by total mesorectal excision, which requires precise estimation of TNM staging. Unfortunately, stage evaluation is based solely on imaging modalities, and they often do not correlate with postoperative pathological findings. Moreover, approximately half of rectal cancer patients do not respond to such pre-operative therapy, so they are exposed to its toxic effects without any clinical benefit. Thus, biomarkers that could precisely predict pre-operative TNM staging, and especially response to therapy, would significantly advance rectal cancer treatment—but till now, no such biomarker has been identified. In cancer research, microRNAs are emerging biomarkers due to their connection with carcinogenesis and exceptional stability. Circulating miRNAs are promising non-invasive biomarkers that could allow monitoring of a patient throughout the whole therapeutic process. This mini-review aims to summarize the current knowledge on miRNAs and circulating miRNAs involved in the prediction of response to treatment and pre-operative staging in rectal cancer patients.

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Payne, Claire M., Cheray Crowley-Skillicorn, Hana Holubec, Katerina Dvorak, Carol Bernstein, Mary Pat Moyer, Harinder Garewal, and Harris Bernstein. "Deoxycholate, an Endogenous Cytotoxin/Genotoxin, Induces the Autophagic Stress-Survival Pathway: Implications for Colon Carcinogenesis." Journal of Toxicology 2009 (2009): 1–14. http://dx.doi.org/10.1155/2009/785907.

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We report that deoxycholate (DOC), a hydrophobic bile acid associated with a high-fat diet, activates the autophagic pathway in non-cancer colon epithelial cells (NCM-460), and that this activation contributes to cell survival. The DOC-induced increase in autophagy was documented by an increase in autophagic vacuoles (detected using transmission electron microscopy, increased levels of LC3-I and LC3-II (western blotting), an increase in acidic vesicles (fluorescence spectroscopy of monodansycadaverine and lysotracker red probes), and increased expression of the autophagic protein, beclin-1 (immunohistochemistry/western blotting). The DOC-induced increase in beclin-1 expression was ROS-dependent. Rapamycin (activator of autophagy) pre-treatment of NCM-460 cells significantly (P<.05) decreased, and 3-MA (inhibitor of autophagy) significantly (P<.05) increased the cell loss caused by DOC treatment, alone. Rapamycin pre-treatment of the apoptosis-resistant colon cancer cell line, HCT-116RC (developed in our laboratory), resulted in a significant decrease in DOC-induced cell death. BafilomycinA1and hydroxychloroquine (inhibitors of the autophagic process) increased the DOC-induced percentage of apoptotic cells in HCT-116RC cells. It was concluded that the activation of autophagy by DOC has important implications for colon carcinogenesis and for the treatment of colon cancer in conjunction with commonly used chemotherapeutic agents.

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SUNDBERG, Kathrin, Bengt JERNSTRÖM, and Stellan SWEDMARK. "Studies on the differential inhibition of glutathione conjugate formation of (+)-anti-benzo[a]pyrene 7,8-dihydrodiol 9,10-epoxide and 1-chloro-2,4-dinitrobenzene in V79 Chinese hamster cells." Biochemical Journal 349, no. 3 (July 25, 2000): 693–96. http://dx.doi.org/10.1042/bj3490693.

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V79 Chinese hamster cells have previously been shown to lack the capacity to detoxify the mutagenic and carcinogenic compound (+)-anti-benzo[a]pyrene 7,8-dihydrodiol 9,10-epoxide [(+)-anti-BPDE] by Pi class glutathione transferase (GSTPi)-catalysed conjugation with GSH, although these cells contain such an enzyme [Romert, Dock, Jenssen and Jernström (1989) Carcinogenesis 10, 1701–1707; Swedmark, Romert, Morgenstern and Jenssen (1992) Carcinogenesis 13, 1719–1723; Swedmark and Jenssen (1994) Gene 139, 251–256]. Previous findings also indicate that these results do not depend on an inactive GSTPi enzyme, since V79 cells conjugate 1-chloro-2,4-dinitrobenzene (CDNB) with GSH, but more likely on (a) factor(s) that inhibit(s) V79 GSTPi selectively [Swedmark, Jernström and Jenssen (1996) Biochem. J. 318, 533–538]. The present study demonstrates that both human and V79 recombinant GSTPi enzymes are inhibited with respect to conjugating (+)-anti-BPDE, but not CDNB, after pre-incubation with V79-cell extract, but not with MCF-7-cell extract. In addition, it was found that the inhibition is dependent on the amount of cell extract present and that the factor(s) is heat-resistant and has a molecular mass of less than 10 kDa, suggesting that the factor(s) is (are) non-proteinaceous in nature.

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Healy, Jasmine, Hélène Bélanger, Patrick Beaulieu, Mathieu Larivière, Damian Labuda, and Daniel Sinnett. "Promoter SNPs in G1/S checkpoint regulators and their impact on the susceptibility to childhood leukemia." Blood 109, no. 2 (September 28, 2006): 683–92. http://dx.doi.org/10.1182/blood-2006-02-003236.

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AbstractMutations leading to the alteration of cell-cycle checkpoint functions are a common feature of most cancers. Because of the highly regulated nature of the cell cycle, it seems likely that variation in gene dosage of key components due to functional regulatory polymorphisms could play an important role in cancer development. Here we provide evidence of the involvement of promoter single-nucleotide polymorphisms (pSNPs) in the cyclin-dependent–kinase inhibitor genes CDKN2A, CDKN2B, CDKN1A, and CDKN1B in the etiology of childhood pre-B acute lymphoblastic leukemia (ALL). A case-control study, conducted in 240 patients with pre-B ALL and 277 healthy controls, combined with a family-based analysis using 135 parental trios, all of French-Canadian origin, were used to evaluate single-site genotypic as well as multilocus haplotypic associations for a total of 10 pSNPs. Using both study designs, we showed evidence of association between variants CDKN2A −222A, CDKN2B −593A, and CDKN1B −1608A, and an increased risk of ALL. These findings suggest that variable expression levels of cell-cycle inhibitor genes CDKN2A, CDKN2B, and CDKN1B due to regulatory polymorphisms could indeed influence the risk of childhood pre-B ALL and contribute to carcinogenesis.

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Ku, Mei-Sheng, Chen-Yu Liu, Chen-Yang Hsu, Han-Mo Chiu, Hsiu-Hsi Chen, and Chang-Chuan Chan. "Association of Ambient Fine Particulate Matter (PM2.5) with Elevated Fecal Hemoglobin Concentration and Colorectal Carcinogenesis: A Population-Based Retrospective Cohort Study." Cancer Control 28 (January 2021): 107327482110412. http://dx.doi.org/10.1177/10732748211041232.

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The roles of ambient fine particulate matter (PM2.5) in the prevention of colorectal cancer (CRC) have been scarcely highlighted as there is short of empirical evidence regarding the influences of PM2.5 on multistep carcinogenic processes of CRC. A retrospective cohort design with multistate outcomes was envisaged by linking monthly average PM2.5 concentrations at 22 city/county level with large-scale cohorts of cancer-screened population to study the influences of PM2.5 on short-term inflammatory process and multistep carcinogenic processes of CRC. Our study included a nationwide CRC screening cohort of 4,628,995 aged 50–69 years who attended first screen between 2004 and 2009 and continued periodical screens until 2016. We aimed to illustrate the carcinogenesis of PM2.5 related to CRC by applying both hierarchical logistical and multistate Markov regression models to estimate the effects of air pollution on fecal immunochemical test (FIT) positive (a proxy of inflammatory marker) and pre-clinical and clinical states of CRC in the nationwide cohort. We found a significant association of high PM2.5 exposure and FIT-positive by an increased risk of 11% [95% confidence interval (CI), 10–12]. PM2.5 enhanced the risk of being preclinical state by 14% (95% CI, 10–18) and that of subsequent progression from pre-clinical to clinical state by 21% (95% CI, 14–28). Furthermore, the elevated risks for CRC carcinogenesis were significantly higher for people living in high PM2.5 pollution areas in terms of yearly averages and the number days above 35 µg/m3 than those living in low PM2.5 pollution areas. We concluded that both short-term and long-term PM2.5 exposure were associated with multistep progression of CRC, which were useful to design precision primary and secondary prevention strategies of CRC for people who are exposed to high PM2.5 pollution.

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Tang, Rong, Qinghua Qi, Ruirong Wu, Xinru Zhou, Dongjuan Wu, Huan Zhou, Yong Mao, et al. "The polymorphic terminal-loop of pre-miR-1307 binding with MBNL1 contributes to colorectal carcinogenesis via interference with Dicer1 recruitment." Carcinogenesis 36, no. 8 (May 14, 2015): 867–75. http://dx.doi.org/10.1093/carcin/bgv066.

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40

Sales, K. U., S. Friis, J. E. Konkel, S. Godiksen, M. Hatakeyama, K. K. Hansen, S. R. Rogatto, et al. "Non-hematopoietic PAR-2 is essential for matriptase-driven pre-malignant progression and potentiation of ras-mediated squamous cell carcinogenesis." Oncogene 34, no. 3 (January 27, 2014): 346–56. http://dx.doi.org/10.1038/onc.2013.563.

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41

Sequetto, Priscila L., Tânia T. Oliveira, Izabel R. S. C. Maldonado, Luís Eugênio F. Augusto, Vanessa J. Mello, Virginia R. Pizziolo, Márcia R. Almeida, Marcelo E. Silva, and Rômulo D. Novaes. "Naringin accelerates the regression of pre-neoplastic lesions and the colorectal structural reorganization in a murine model of chemical carcinogenesis." Food and Chemical Toxicology 64 (February 2014): 200–209. http://dx.doi.org/10.1016/j.fct.2013.11.032.

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42

Tiffon, Camille, Julie Giraud, Silvia Elena Molina-Castro, Sara Peru, Lornella Seeneevassen, Elodie Sifré, Cathy Staedel, et al. "TAZ Controls Helicobacter pylori-Induced Epithelial–Mesenchymal Transition and Cancer Stem Cell-Like Invasive and Tumorigenic Properties." Cells 9, no. 6 (June 13, 2020): 1462. http://dx.doi.org/10.3390/cells9061462.

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Helicobacter pylori infection, the main risk factor for gastric cancer (GC), leads to an epithelial–mesenchymal transition (EMT) of gastric epithelium contributing to gastric cancer stem cell (CSC) emergence. The Hippo pathway effectors yes-associated protein (YAP) and transcriptional co-activator with PDZ binding motif (TAZ) control cancer initiation and progression in many cancers including GC. Here, we investigated the role of TAZ in the early steps of H. pylori-mediated gastric carcinogenesis. TAZ implication in EMT, invasion, and CSC-related tumorigenic properties were evaluated in three gastric epithelial cell lines infected by H. pylori. We showed that H. pylori infection increased TAZ nuclear expression and transcriptional enhancer TEA domain (TEAD) transcription factors transcriptional activity. Nuclear TAZ and zinc finger E-box-binding homeobox 1 (ZEB1) were co-overexpressed in cells harboring a mesenchymal phenotype in vitro, and in areas of regenerative hyperplasia in gastric mucosa of H. pylori-infected patients and experimentally infected mice, as well as at the invasive front of gastric carcinoma. TAZ silencing reduced ZEB1 expression and EMT phenotype, and strongly inhibited invasion and tumorsphere formation induced by H. pylori. In conclusion, TAZ activation in response to H. pylori infection contributes to H. pylori-induced EMT, invasion, and CSC-like tumorigenic properties. TAZ overexpression in H. pylori-induced pre-neoplastic lesions and in GC could therefore constitute a biomarker of early transformation in gastric carcinogenesis.

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43

Lebrecht, A., C. Grimm, G. Euller, E. Ludwig, E. Ulbrich, T. Lantzsch, L. Hefler, and H. Koelbl. "Transforming Growth Factor Beta 1 Serum Levels in Patients with Preinvasive and Invasive Lesions of the Breast." International Journal of Biological Markers 19, no. 3 (July 2004): 236–39. http://dx.doi.org/10.1177/172460080401900309.

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Transforming growth factor beta (TGF-β)1 is thought to be involved in breast carcinogenesis. TGF-β1 acts in an antiproliferative manner in the early stages of breast carcinogenesis, but promotes tumor progression and metastases in the advanced stages of the disease. No data have been published on serum TGF-β1 in breast cancer. We investigated TGF-β1 serum levels in patients with breast cancer (n=135), ductal carcinoma in situ (DCIS) I to III (n=67) or fibroadenoma (n=35), and in healthy women (n=40) to determine its value as a differentiation marker between malignant, pre-invasive and benign diseases and as a predictive marker for metastatic spread. Median (range) TGF-β1 serum levels in patients with breast cancer, DCIS I-III or benign breast lesions and in healthy women were 48.8 (18–82.4) pg/mL, 45.3 (26.9–58.3) pg/mL, 47.2 (17.2–80.5) pg/mL and 51.6 (30.9–65.1) pg/mL, respectively (p=0.2). In breast cancer patients TGF-β1 serum levels showed no statistically significant correlation with tumor stage, lymph node involvement, histological grade, estrogen receptor status and progesterone receptor status. Our data fail to indicate any correlation between serum TGF-β1 levels and clinicopathological parameters of breast diseases. Serum TGF-β1 levels do not provide clinical information in addition to established tumor markers.

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Wang, Jin, Yuan Hu, Vicente Escamilla-Rivera, Cassandra L. Gonzalez, Lin Tang, Bingbing Wang, Adel K. El-Naggar, Jeffrey N. Myers, and Carlos Caulin. "Epithelial Mutant p53 Promotes Resistance to Anti-PD-1-Mediated Oral Cancer Immunoprevention in Carcinogen-Induced Mouse Models." Cancers 13, no. 6 (March 23, 2021): 1471. http://dx.doi.org/10.3390/cancers13061471.

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Oral squamous cell carcinoma (OSCC) develops through the multistep malignant progression of squamous epithelium. This process can be prevented by PD-1 blockade in a mouse model for oral carcinogenesis. OSCCs exhibit a high incidence of p53 mutations that confer oncogenic gain-of-function (GOF) activities that promote resistance to standard therapies and poor clinical outcomes. To determine whether epithelial p53 mutations modulate anti-PD-1-mediated oral cancer immunoprevention, we generated mouse models for oral carcinogenesis by exposing mice carrying epithelial-specific p53 mutations to the carcinogen 4NQO. Consistent with the oncogenic functions of mutant p53, mice with OSCCs expressing the p53R172H GOF mutation developed higher metastasis rates than mice with loss-of-function (LOF) p53 deletion or with wild-type p53. Throughout oral cancer progression, pre-invasive and invasive lesions showed a gradual increase in T-cell infiltration, recruitment of immunosuppressive regulatory T-cells (Tregs), and induction of PD-1/PD-L1 immune checkpoint proteins. Notably, while PD-1 blockade prevented the development of OSCCs in mice with wild-type p53 or p53 deletion, GOF p53R172H abrogated the immunopreventive effects of anti-PD-1, associated with upregulation of IL17 signaling and depletion of exhausted CD8 cells in the microenvironment of the p53R172H tumors. These findings sustain a potential role for p53 profiling in personalized oral cancer immunoprevention.

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Santos, Susana, Tiago Ferreira, José Almeida, Maria J. Pires, Aura Colaço, Sílvia Lemos, Rui M. Gil da Costa, et al. "Dietary Supplementation with the Red Seaweed Porphyra umbilicalis Protects against DNA Damage and Pre-Malignant Dysplastic Skin Lesions in HPV-Transgenic Mice." Marine Drugs 17, no. 11 (October 29, 2019): 615. http://dx.doi.org/10.3390/md17110615.

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Some diet profiles are associated with the risk of developing cancer; however, some nutrients show protective effects. Porphyra umbilicalis is widely consumed, having a balanced nutritional profile; however, its potential for cancer chemoprevention still needs comprehensive studies. In this study, we incorporated P. umbilicalis into the diet of mice transgenic for the human papillomavirus type 16 (HPV16), which spontaneously develop pre-malignant and malignant lesions, and determined whether this seaweed was able to block lesion development. Forty-four 20-week-old HPV+/− and HPV−/− mice were fed either a base diet or a diet supplemented with 10% seaweed. At the end of the study, skin samples were examined to classify HPV16-induced lesions. The liver was also screened for potential toxic effects of the seaweed. Blood was used to study toxicological parameters and to perform comet and micronucleus genotoxicity tests. P. umbilicalis significantly reduced the incidence of pre-malignant dysplastic lesions, completely abrogating them in the chest skin. These results suggest that P. umbilicalis dietary supplementation has the potential to block the development of pre-malignant skin lesions and indicate its antigenotoxic activity against HPV-induced DNA damage. Further studies are needed to establish the seaweed as a functional food and clarify the mechanisms whereby this seaweed blocks multistep carcinogenesis induced by HPV.

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Thurman, Joshua M., Jennifer Laskowski, and Raphael A. Nemenoff. "Complement and Cancer—A Dysfunctional Relationship?" Antibodies 9, no. 4 (November 5, 2020): 61. http://dx.doi.org/10.3390/antib9040061.

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Although it was long believed that the complement system helps the body to identify and remove transformed cells, it is now clear that complement activation contributes to carcinogenesis and can also help tumors to escape immune-elimination. Complement is activated by several different mechanisms in various types of cancer, and complement activation fragments have multiple different downstream effects on cancer cells and throughout the tumor microenvironment. Thus, the role of complement activation in tumor biology may vary among different types of cancer and over time within a single tumor. In multiple different pre-clinical models, however, complement activation has been shown to recruit immunosuppressive myeloid cells into the tumor microenvironment. These cells, in turn, suppress anti-tumor T cell immunity, enabling the tumor to grow. Based on extensive pre-clinical work, therapeutic complement inhibitors hold great promise as a new class of immunotherapy. A greater understanding of the role of complement in tumor biology will improve our ability to identify those patients most likely to benefit from this treatment and to rationally combine complement inhibitors with other cancer therapies.

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Arif, Jamal M., Amal A. Al-Hazzani, Muhammed Kunhi, and Fahad Al-Khodairy. "Novel Marine Compounds: Anticancer or Genotoxic?" Journal of Biomedicine and Biotechnology 2004, no. 2 (2004): 93–98. http://dx.doi.org/10.1155/s1110724304307060.

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In the past several decades, marine organisms have generously gifted to the pharmaceutical industries numerous naturally bioactive compounds with antiviral, antibacterial, antimalarial, anti-inflammatory, antioxidant, and anticancer potentials. But till date only few anticancer drugs (cytarabine, vidarabine) have been commercially developed from marine compounds while several others are currently in different clinical trials. Majority of these compounds were tested in the tumor xenograft models, however, lack of anticancer potential data in the chemical- and/or oncogene-induced pre-initiation animal carcinogenesis models might have cost some of the marine anticancer compounds an early exit from the clinical trials. This review critically discusses importance of preclinical evaluation, failure of human clinical trials with certain potential anticancer agents, the screening tests used, and choice of biomarkers.

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Schwartz, Joel L. "Biomarkers and Molecular Epidemiology and Chemoprevention of Oral Carcinogenesis." Critical Reviews in Oral Biology & Medicine 11, no. 1 (January 2000): 92–122. http://dx.doi.org/10.1177/10454411000110010501.

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Chemopreventives are chemicals that prevent the formation of cancers such as oral cancer. They can take the form of nutrients or synthetic molecules, and their fundamental characteristic is that they do not produce disease processes that would result in debilitating symptoms. Current evidence indicates that they function by modifying the oxidative state of transforming cells. Biomarkers can take the form of genetic and molecular indicators, which characterize the function of chemopreventives and cancer processes such as oral carcinogenesis. Biomarkers cannot provide all the required information for risk assessment or possible activity of the chemopreventives. Other methods, such as epidemiological analyses and techniques, must be used to enhance our understanding of the risk for oral cancer in human populations. One common epidemiologic method, the questionnaire, helps to determine the use and carcinogenic potential of tobacco and alcohol during oral carcinogenesis. Genetic and molecular changes in human patient populations may result in a reduction in the number and function of tumor suppressor genes. If these changes are to be assessed, the tissues ( e. g., buccal mucosa) must be accessible and harvested in a reliable and consistent manner for the acquisition of DNA, mRNA, and protein. Oral tissues provide sufficient quantities of these molecules and, under stringent conditions, the quality required for the isolation of these molecular constituents. In conjunction with epidemiologic techniques, various genotypic polymorphisms, such as glutathione-S-transferase (GSTM 1) or cytochrome P 450 (CYP450Al), have indicated a loss in carcinogen detoxification or the processing of internal growth control signals. Biomarkers are composed of a large diverse group of genetic and molecular structures. Some of these biomarkers are indicators for programmed cell death (PCD), while others describe malignant tumor growth. Many of these classes of molecules are oxidative-responsive ( e.g., tumor suppressor p53, Bcl-2, growth factors, immune-derived proteins, and death-inducing molecules) and induce PCD by triggering a cascade of cysteine proteases and regulators ( e. g., caspases, death receptors). This pathway results in cell-cycle alterations and DNA fragmentation. It is hoped that a detailed knowledge of the processes involved in malignant transformation will better define the biomarker-screening tools for oral cancer. These tools will enhance our ability to predict the incidence of cancer, detect early malignant change, and quantitate chemoprevention during oral carcinogenesis. Chemopreventives such as the retinoids have already demonstrated their ability to suppress potential malignant changes in pre-malignant oral leukoplakias and decrease the incidence of second head-and-neck cancer primaries. It is our hope that this review will increase investigators' interest in developing new screening and detection systems for oral cancer.

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Agahozo, Marie Colombe, Anieta M. Sieuwerts, S. Charlane Doebar, Esther I. Verhoef, Corine M. Beaufort, Kirsten Ruigrok-Ritstier, Vanja de Weerd, et al. "PIK3CA mutations in ductal carcinoma in situ and adjacent invasive breast cancer." Endocrine-Related Cancer 26, no. 5 (May 2019): 471–82. http://dx.doi.org/10.1530/erc-19-0019.

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PIK3CA is one of the most frequently mutated genes in invasive breast cancer (IBC). These mutations are generally associated with hyper-activation of the phosphatidylinositol 3-kinase signaling pathway, which involves increased phosphorylation of AKT (p-AKT). This pathway is negatively regulated by the tumor suppressor PTEN. Data are limited regarding the variant allele frequency (VAF) of PIK3CA, PTEN and p-AKT expression during various stages of breast carcinogenesis. Therefore, the aim of this study was to gain insight into PIK3CA VAF and associated PTEN and p-AKT expression during the progression from ductal carcinoma in situ (DCIS) to IBC. We isolated DNA from DCIS tissue, synchronous IBC and metastasis when present. These samples were pre-screened for PIK3CA hotspot mutations using the SNaPshot assay and, if positive, validated and quantified by digital PCR. PTEN and p-AKT expression was evaluated by immunohistochemistry using the Histo-score (H-score). Differences in PIK3CA VAF, PTEN and p-AKT H-scores between DCIS and IBC were analyzed. PIK3CA mutations were detected in 17 out of 73 DCIS samples, 16 out of 73 IBC samples and 3 out of 23 lymph node metastasis. We detected a significantly higher VAF of PIK3CA in the DCIS component compared to the adjacent IBC component (P = 0.007). The expression of PTEN was significantly higher in DCIS compared to the IBC component in cases with a wild-type (WT) PIK3CA status (P = 0.007), while it remained similar in both components when PIK3CA was mutated. There was no difference in p-AKT expression between DCIS and the IBC component. In conclusion, our data suggest that PIK3CA mutations could be essential specifically in early stages of breast carcinogenesis. In addition, these mutations do not co-occur with PTEN expression during DCIS progression to IBC in the majority of patients. These results may contribute to further unraveling the process of breast carcinogenesis, and this could aid in the development of patient-specific treatment.

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Mistry, T., J. E. Digby, R. Raghu, J. Joe, K. M. Desai, and H. S. Randeva. "A NOVEL ROLE FOR THE ADIPOKINE VISFATIN (PRE-B CELL COLONY-ENHANCING FACTOR 1 (PBEF)/NICOTINAMIDE PHOSPHORIBOSYLTRANSFERASE (NMPRTASE)) IN PROSTATE CARCINOGENESIS." European Urology Supplements 7, no. 3 (March 2008): 312. http://dx.doi.org/10.1016/s1569-9056(08)60961-6.

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Journal articles on the topic 'Pre-carcinogenesis'

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