Natalia Ignatenko

Interests

Teaching

Although I am not currently involved in formal teaching, I would be interested in participation in formal academic curriculum to enrich students' training with my research experiences and broad background in cancer biology . The possible themes are: biochemistry and molecular biology of polyamines in colon carcinogenesis, the molecular mechanisms of gastrointestinal malignancies and development of novel strategies for prevention, detection and treatment of these malignancies.

Research

For the past 20 years I have been involved in colorectal cancer (CRC) research with the focus on the molecular mechanisms of detection and prevention. My research activity include identification and validation of downstream effectors of Adenomatous Polyposis Coli (APC) tumor suppressor gene and K-ras protooncogene within polyamine and prostaglandin pathways and study the luminal and dietary risk factors of colonic inflammation and colorectal carcinogenesis. I also have an expertise in developing Genetically Engineered Mouse (GEM) models of gastrointestinal cancer for studying different steps of carcinogenesis.Current research in my laboratory is focused on regulation and pathophysiological functions of kallikrein-related peptidase 6 (KLK6) in cancer with the focus on cancer cells invasion and metastasis. KLK6 is a secreted serine protease with the specific function to cleave components of the extracellular matrix and activate latent growth factors involved in epithelial-to-mesenchymal transition (EMT) pathways. Our recent findings indicate that KLK6 expression in colon cancer cells is determined by the tumor subtype and the genetic mutations developed during the colon cancer progression. KLK6 protein will be useful for imaging purposes and an appropriate target for evaluation as a colon biomarker.

Courses

Scholarly Contributions

Journals/Publications

• Maar, K. D., Ignatenko, N., Warfel, N. A., Batai, K., Cress, A. E., Pollock, G., Wong, A. C., & Lee, B. R. (2023). Digital Image analysis using Video microscopy of human-derived prostate cancer vs normaprostate organoids to assess migratory behavior on extracellular matrix proteins.. Frontiers in Oncology.
• Bouzid, H., Soualmia, F., Oikonomopoulou, K., Soosaipillai, A., Walker, F., Louati, K., Lo Dico, R., Pocard, M., El Amri, C., Ignatenko, N. A., & Darmoul, D. (2022). Kallikrein-Related Peptidase 6 (KLK6) as a Contributor toward an Aggressive Cancer Cell Phenotype: A Potential Role in Colon Cancer Peritoneal Metastasis. Biomolecules, 12(7).
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  Kallikrein-related peptidases (KLKs) are implicated in many cancer-related processes. KLK6, one of the 15 KLK family members, is a promising biomarker for diagnosis of many cancers and has been associated with poor prognosis of colorectal cancer (CRC) patients. Herein, we evaluated the expression and cellular functions of KLK6 in colon cancer-derived cell lines and in clinical samples from CRC patients. We showed that, although many KLKs transcripts are upregulated in colon cancer-derived cell lines, KLK6, KLK10, and KLK11 are the most highly secreted proteins. KLK6 induced calcium flux in HT29 cells by activation and internalization of protease-activated receptor 2 (PAR2). Furthermore, KLK6 induced extracellular signal-regulated kinases 1 and 2 (ERK1/2) phosphorylation. KLK6 suppression in HCT-116 colon cancer cells decreased the colony formation, increased cell adhesion to extracellular matrix proteins, and reduced spheroid formation and compaction. Immunohistochemistry (IHC) analysis demonstrated ectopic expression of KLK6 in human colon adenocarcinomas but not in normal epithelia. Importantly, high levels of KLK6 protein were detected in the ascites of CRC patients with peritoneal metastasis, but not in benign ascites. These data indicate that KLK6 overexpression is associated with aggressive CRC, and may be applied to differentiate between benign and malignant ascites.
• Chen, H., Henkhaus, R. S., Sells, E., Pandey, R., Abril, E. R., Hsu, C., Krouse, R. R., Nagle, R. B., Pampalakis, G., Sotiropoupou, G., & Ignatenko, N. A. (2019). Kallikrein 6 protease advances colon tumorigenesis via induction of the high mobility group A2 protein. Oncotarget, 10(58), 6062-6068.
• De Vita, E., Smits, N., van den Hurk, H., Beck, E. M., Hewitt, J., Baillie, G., Russell, E., Pannifer, A., Hamon, V., Morrison, A., McElroy, S., Jones, P., Ignatenko, N. A., Gunkel, N., & Miller, A. (2019). Synthesis and structure–activity relationships of N-(4-benzamidino)- oxazolidinones–potent and selective inhibitors of kallikrein-related peptidase 6. ChemMedChem., Epub2019.
• Rice, P. F., Ehrichs, K. G., Jones, M. S., Chen, H., Hsu, C. H., Abril, E. R., Nagle, R. B., Besselsen, D. G., Barton, J. K., & Ignatenko, N. A. (2018). Does Mutated Oncogene Attenuate the Effect of Sulindac in Colon Cancer Chemoprevention?. Cancer prevention research (Philadelphia, Pa.), 11(1), 16-26.
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  The NSAID sulindac has been successfully used alone or in combination with other agents to suppress colon tumorigenesis in patients with genetic predisposition and also showed its efficacy in prevention of sporadic colon adenomas. At the same time, some experimental and clinical reports suggest that a mutant oncogene may negate sulindac antitumor efficacy. To directly assess sulindac activity at suppressing premalignant lesions carrying K-RAS mutation, we utilized a novel mouse model with an inducible colon-specific expression of the mutant oncogene ( ). Tumor development and treatment effects were monitored by minimally invasive endoscopic Optical coherence tomography. Expression of the mutant allele accelerated azoxymethane (AOM)-induced colon carcinogenesis in C57BL/6 mice, a strain otherwise resistant to this carcinogen. Sulindac completely prevented AOM-induced tumor formation in wild-type ( wt) animals. In -mutant mice, a 38% reduction in tumor number, an 83% reduction in tumor volume ( ≤ 0.01) and an increase in the number of adenoma-free mice ( = 0.04) were observed. The partial response of animals to sulindac treatment was evident by the decrease in mucosal thickness ( < 0.01) and delay in progression of the precancerous aberrant crypt foci to adenomas. Molecular analyses showed significant induction in cyclooxygenase 2 (COX-2), cleaved caspase-3 (CC3), and Ki-67 expression by AOM, but not sulindac treatment, in all genotypes. Our data underscore the importance of screening for mutations in individuals with colon polyps to provide more personalized interventions targeting mutant signaling pathways. .
• Sinharay, S., Randtke, E. A., Howison, C. M., Ignatenko, N. A., & Pagel, M. D. (2018). Detection of enzyme activity and inhibition during studies in solution, in vitro, and in vivo with catalyCEST MRI. Molec. Imaging Biol, 20, 240-248.
• Ignatenko, N. A., Cui, H., Skovan, B. A., Chen, H., Pandey, R., & Sells, E. (2017). Specific microRNA-mRNA regulatory network of colon cancer invasion regulated by tissue kallikrein-related peptidase 6. Neoplasia.
• LeGendre-McGhee, S., Rice, P. S., Wall, R. A., Sprute, K. J., Bommireddy, R., Luttman, A. M., Nagle, R. B., Abril, E. R., Farrell, K., Hsu, C. H., Roe, D. J., Gerner, E. W., Ignatenko, N. A., & Barton, J. K. (2015). Time-serial Assessment of Drug Combination Interventions in a Mouse Model of Colorectal Carcinogenesis Using Optical Coherence Tomography. Cancer growth and metastasis, 8(Suppl 1), 63-80.
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  Optical coherence tomography (OCT) is a high-resolution, nondestructive imaging modality that enables time-serial assessment of adenoma development in the mouse model of colorectal cancer. In this study, OCT was utilized to evaluate the effectiveness of interventions with the experimental antitumor agent α-difluoromethylornithine (DFMO) and a nonsteroidal anti-inflammatory drug sulindac during early [chemoprevention (CP)] and late stages [chemotherapy (CT)] of colon tumorigenesis. Biological endpoints for drug interventions included OCT-generated tumor number and tumor burden. Immunochistochemistry was used to evaluate biochemical endpoints [Ki-67, cleaved caspase-3, cyclooxygenase (COX)-2, β-catenin]. K-Ras codon 12 mutations were studied with polymerase chain reaction-based technique. We demonstrated that OCT imaging significantly correlated with histological analysis of both tumor number and tumor burden for all experimental groups (P < 0.0001), but allows more accurate and full characterization of tumor number and burden growth rate because of its time-serial, nondestructive nature. DFMO alone or in combination with sulindac suppressed both the tumor number and tumor burden growth rate in the CP setting because of DFMO-mediated decrease in cell proliferation (Ki-67, P < 0.001) and K-RAS mutations frequency (P = 0.04). In the CT setting, sulindac alone and DFMO/sulindac combination were effective in reducing tumor number, but not tumor burden growth rate. A decrease in COX-2 staining in DFMO/sulindac CT groups (COX-2, P < 0.01) confirmed the treatment effect. Use of nondestructive OCT enabled repeated, quantitative evaluation of tumor number and burden, allowing changes in these parameters to be measured during CP and as a result of CT. In conclusion, OCT is a robust minimally invasive method for monitoring colorectal cancer disease and effectiveness of therapies in mouse models.
• LeGendre-McGhee, S., Rice, P. S., Wall, R. A., Sprute, K. J., Bommireddy, R., Luttman, A. M., Nagle, R. B., Abril, E. R., Farrell, K., Hsu, C. H., Roe, D. J., Gerner, E. W., Ignatenko, N. A., & Barton, J. K. (2015). Time-serial Assessment of Drug Combination Interventions in a Mouse Model of Colorectal Carcinogenesis Using Optical Coherence Tomography. Cancer growth and metastasis, 8, 63-80.
• Padavano, J., Henkhaus, R. S., Chen, H., Skovan, B. A., Cui, H., & Ignatenko, N. A. (2015). Mutant K-RAS Promotes Invasion and Metastasis in Pancreatic Cancer Through GTPase Signaling Pathways. Cancer growth and metastasis, 8, 95-113.
• Yee, N. S., Ignatenko, N., Finnberg, N., Lee, N., & Stairs, D. (2015). ANIMAL MODELS OF CANCER BIOLOGY. Cancer growth and metastasis, 8(Suppl 1), 115-8.
• Banerjee, B., Mckeown, K. R., Skovan, B., Ogram, E., Ingram, P., Ignatenko, N. A., Paine-Murrieta, G., Witte, R., Matsunaga, T., Ignatenko, N. A., & Gerner, E. W. (2013). Ultrasound imaging of the mouse pancreatic duct using lipid microbubbles; Get the fat out!. Cancer prevention research (Philadelphia, Pa.), 832018; 6, 161-164.
• Ignatenko, N., Basu Roy, U. K., Henkhaus, R. S., Loupakis, F., Cremolini, C., Gerner, E. W., & Ignatenko, N. -. (2013). Caveolin-1 is a novel regulator of K-RAS-dependent migration in colon carcinogenesis. International journal of cancer. Journal international du cancer, 133(1).
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  Caveolin-1 is an essential component of membrane caveolae. It is an important regulator of cellular processes such as signal transduction and endocytosis. We report here, for the first time, that caveolin-1 is a target of the K-RAS oncogene in colon carcinogenesis. Caveolin-1 is induced in colon cancer cells and in human colon tumor samples, in response to K-RAS activating mutations. An activated K-RAS oncogene transcriptionally induces caveolin-1 expression in human colon cancer cells and this effect is not restricted to the type of activating K-RAS mutation. Inhibition of the P-I3 Kinase-AKT pathway, but not the ERK MAPK pathway, both important K-RAS effectors, leads to a decrease in caveolin-1 expression indicating that the AKT pathway is involved in caveolin-1 expression in response to an activated K-RAS. Increased AKT signaling induces caveolin-1 expression by increasing the activity of the transcription factor, Sp1. Interestingly; caveolin-1 depletion alters K-RAS-dependent signaling by decreasing Grb2-SOS activity. Consistent with these finding, caveolin-1-depleted cells shows decreased migration in vitro. However, caveolin-1 overexpression by itself does not increase migration whereas an activated Src can increase migration in a caveolin-1-dependent manner. This increased migration is highly dependent on the RhoA GTPase, indicating that an activated K-RAS modulates migration in part via caveolin-1 induction, and increasing RhoA activity via phospho-caveolin-1. Our findings indicate that K-RAS regulates both caveolin-1 expression and other factors affecting caveolin-1 functions in colon cancer-derived cell migration.
• Ignatenko, N. A., Gerner, E. W., & Besselsen, D. G. (2011). Defining the role of polyamines in colon carcinogenesis using mouse models. Journal of carcinogenesis, 10, 10-3163.79673. Epub 2011 Apr 16.
• Paz, E. A., Garcia-Huidobro, J., & Ignatenko, N. A. (2011). Polyamines in cancer. Advances in Clinical Chemistry, 54, 45-70.
• Ignatenko, N. A., Yerushalmi, H. F., Pandey, R., Kachel, K. L., Stringer, D. E., Marton, L. J., & Gerner, E. W. (2009). Gene expression analysis of HCT116 colon tumor-derived cells treated with the polyamine analog PG-11047. Cancer genomics & proteomics, 6, 161-175.
• Zell, J. A., Ziogas, A., Ignatenko, N., Honda, J., Qu, N., Bobbs, A. S., Neuhausen, S. L., Gerner, E. W., & Anton-Culver, H. (2009). Associations of a polymorphism in the ornithine decarboxylase gene with colorectal cancer survival. Clinical cancer research : an official journal of the American Association for Cancer Research, 15, 6208-6216.
• Henkhaus, R. S., Gerner, E. W., & Ignatenko, N. A. (2008). Kallikrein 6 is a mediator of K-RAS-dependent migration of colon carcinoma cells. Biological chemistry, 389, 757-764.
• Henkhaus, R. S., Roy, U. K., Cavallo-Medved, D., Sloane, B. F., Gerner, E. W., & Ignatenko, N. A. (2008). Caveolin-1-mediated expression and secretion of kallikrein 6 in colon cancer cells. Neoplasia (New York, N.Y.), 10, 140-148.
• Ignatenko, N. A., & Gerner, E. W. (2008). HuRrying colon cancer progression. Cancer biology & therapy, 7, 428-429.
• Ignatenko, N. A., Besselsen, D. G., Stringer, D. E., Blohm-Mangone, K. A., Cui, H., & Gerner, E. W. (2008). Combination chemoprevention of intestinal carcinogenesis in a murine model of familial adenomatous polyposis. Nutrition and cancer, 60 Suppl 1, 30-35.
• Ignatenko, N., Henkhaus, R. S., Gerner, E. W., & Ignatenko, N. -. (2008). Kallikrein 6 is a mediator of K-RAS-dependent migration of colon carcinoma cells. Biological chemistry, 389(6).
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  Kallikrein 6 (KLK6) is a trypsin-like serine peptidase whose relevance in various types of cancers is currently being explored. Previous studies have shown that KLK6 mRNA is upregulated in colon and gastric cancers; however, the regulatory mechanisms and phenotypic consequences of this upregulation are largely unknown. Activating K-RAS mutations are common in colon cancer, occurring in approximately 50% of cases. We have recently reported the upregulation of KLK6 mRNA in Caco2 human colon cancer cells stably transfected with a mutant K-RAS allele (K-RAS(G12V)). In this study we examined the pattern of K-RAS-dependent KLK6 expression and secretion in colon cancer cells. Using pharmacological inhibitors of pathways downstream of K-RAS, we could show that the PI3K and p42/44 MAPK pathways play an important role in the induction of KLK6 in mutant K-RAS-expressing colon cancer cells. Increased KLK6 expression enhanced colon cancer cell migration through laminin and Matrigel. Inhibition of KLK6 using small interference RNA treatment or a specific KLK6 antibody in Caco2 cells stably expressing the mutant K-RAS and in SW480 cells carrying a mutation in the K-RAS oncogene resulted in a reduction in invasiveness through cell culture inserts. These data support the oncogenic role of KLK6 in colorectal cancer.
• Ignatenko, N., Henkhaus, R. S., Roy, U. K., Cavallo-Medved, D., Sloane, B. F., Gerner, E. W., & Ignatenko, N. -. (2008). Caveolin-1-mediated expression and secretion of kallikrein 6 in colon cancer cells. Neoplasia (New York, N.Y.), 10(2).
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  Kallikreins are secreted proteases that may play a functional role and/or serve as a serum biomarker for the presence or progression of certain types of cancers. Kallikrein 6 (KLK6) has been shown to be upregulated in several types of cancers, including colon. The aims of this study were to elucidate pathways that influence KLK6 gene expression and KLK6 protein secretion in the HCT116 human colon cancer cells. Our data indicate a central role for caveolin-1 (CAV-1), the main structural protein of caveolae, in both KLK6 gene expression and protein secretion. Sucrose gradient subcellular fractionation reveals that CAV-1 and KLK6 colocalize to lipid raft domains in the plasma membrane of HCT116 cells. Furthermore, we show that CAV-1, although it does not directly interact with the KLK6 molecule, enhances KLK6 secretion from the cells. Deactivation of CAV-1, through SRC-mediated phosphorylation, decreased KLK6 secretion. We also demonstrate that, in colon cancer cells, CAV-1 increased the amount of phosphorylated AKT in cells by inhibiting the activity of the AKT-negative regulators PP1 and PP2A. This study demonstrates that proteins such as CAV-1 and AKT, which are known to be altered in colon cancer, affect KLK6 expression and KLK6 secretion.
• Roy, U. K., Henkhaus, R. S., Ignatenko, N. A., Mora, J., Fultz, K. E., & Gerner, E. W. (2008). Wild-type APC regulates caveolin-1 expression in human colon adenocarcinoma cell lines via FOXO1a and C-myc. Molecular carcinogenesis, 47, 947-955.
• Bernstein, H., Holubec, H., Bernstein, C., Ignatenko, N. A., Gerner, E., Dvorak, K., Besselsen, D., Blohm-Mangone, K. A., Padilla-Torres, J., Dvorakova, B., Garewal, H., & Payne, C. M. (2007). Deoxycholate-induced colitis is markedly attenuated in Nos2 knockout mice in association with modulation of gene expression profiles. Digestive diseases and sciences, 52, 628-642.
• Hariri, L. P., Qiu, Z., Tumlinson, A. R., Besselsen, D. G., Gerner, E. W., Ignatenko, N. A., Povazay, B., Hermann, B., Sattmann, H., McNally, J., Unterhuber, A., Drexler, W., & Barton, J. K. (2007). Serial endoscopy in azoxymethane treated mice using ultra-high resolution optical coherence tomography. Cancer biology & therapy, 6, 1753-1762.
• Zell, J. A., Ignatenko, N. A., Yerushalmi, H. F., Ziogas, A., Besselsen, D. G., Gerner, E. W., & Anton-Culver, H. (2007). Risk and risk reduction involving arginine intake and meat consumption in colorectal tumorigenesis and survival. International journal of cancer.Journal international du cancer, 120, 459-468.
• Bernstein, H., Holubec, H., Bernstein, C., Ignatenko, N., Gerner, E., Dvorak, K., Besselsen, D., Ramsey, L., Dall'Agnol, M., Blohm-Mangone, K. A., Padilla-Torres, J., Cui, H., Garewal, H., & Payne, C. M. (2006). Unique dietary-related mouse model of colitis. Inflammatory bowel diseases, 12, 278-293.
• Ignatenko, N. A., Besselsen, D. G., Roy, U. K., Stringer, D. E., Blohm-Mangone, K. A., Padilla-Torres, J. L., Guillen-R, J. M., & Gerner, E. W. (2006). Dietary putrescine reduces the intestinal anticarcinogenic activity of sulindac in a murine model of familial adenomatous polyposis. Nutrition and cancer, 56, 172-181.
• Ignatenko, N. A., Holubec, H., Besselsen, D. G., Blohm-Mangone, K. A., Padilla-Torres, J. L., Nagle, R. B., Alboranc, I. M., Guillen-R, J. M., & Gerner, E. W. (2006). Role of c-Myc in intestinal tumorigenesis of the ApcMin/+ mouse. Cancer biology & therapy, 5, 1658-1664.
• Ignatenko, N. A., Yerushalmi, H. F., Watts, G. S., Futscher, B. W., Stringer, D. E., Marton, L. J., & Gerner, E. W. (2006). Pharmacogenomics of the polyamine analog 3,8,13,18-tetraaza-10,11-[(E)-1,2-cyclopropyl]eicosane tetrahydrochloride, CGC-11093, in the colon adenocarcinoma cell line HCT1161. Technology in cancer research & treatment, 5, 553-564.
• Yerushalmi, H. F., Besselsen, D. G., Ignatenko, N. A., Blohm-Mangone, K. A., Padilla-Torres, J. L., Stringer, D. E., Cui, H., Holubec, H., Payne, C. M., & Gerner, E. W. (2006). The role of NO synthases in arginine-dependent small intestinal and colonic carcinogenesis. Molecular carcinogenesis, 45, 93-105.
• Yerushalmi, H. F., Besselsen, D. G., Ignatenko, N. A., Blohm-Mangone, K. A., Padilla-Torres, J. L., Stringer, D. E., Guillen, J. M., Holubec, H., Payne, C. M., & Gerner, E. W. (2006). Role of polyamines in arginine-dependent colon carcinogenesis in Apc(Min) (/+) mice. Molecular carcinogenesis, 45, 764-773.
• Gerner, E. W., Ignatenko, N. A., Lance, P., & Hurley, L. H. (2005). A comprehensive strategy to combat colon cancer targeting the adenomatous polyposis coli tumor suppressor gene. Annals of the New York Academy of Sciences, 1059, 97-105.
• Ignatenko, N. A., Babbar, N., Mehta, D., Jr, R. A., & Gerner, E. W. (2004). Suppression of polyamine catabolism by activated Ki-ras in human colon cancer cells. Molecular carcinogenesis, 39, 91-102.
• Ignatenko, N. A., Zhang, H., Watts, G. S., Skovan, B. A., Stringer, D. E., & Gerner, E. W. (2004). The chemopreventive agent alpha-difluoromethylornithine blocks Ki-ras-dependent tumor formation and specific gene expression in Caco-2 cells. Molecular carcinogenesis, 39, 221-233.
• Zaletok, S., Alexandrova, N., Berdynskykh, N., Ignatenko, N., Gogol, S., Orlovsky, O., Tregubova, N., Gerner, E., & Chekhun, V. (2004). Role of polyamines in the function of nuclear transcription factor NF-kappaB in breast cancer cells. Experimental oncology, 26, 221-225.
• Babbar, N., Ignatenko, N. A., Jr, R. A., & Gerner, E. W. (2003). Cyclooxygenase-independent induction of apoptosis by sulindac sulfone is mediated by polyamines in colon cancer. The Journal of biological chemistry, 278, 47762-47775.
• Gerner, E. W., Broome-Powell, M., Erdman, S. H., Ignatenko, N. A., Besselsen, D. G., Gerner, E. W., Ignatenko, N. A., Fultz, K. E., Gerner, E. W., Ignatenko, N. A., & Besselsen, D. G. (2003). COST 917: Biogenically Active Amines in Food; Pharmaceutical Perspectives of Nucleic Acid-Based Therapeutics; Preclinical models for chemoprevention of colon cancer. Recent results in cancer research.Fortschritte der Krebsforschung.Progres dans les recherches sur le cancer, 163, 58-71; discussion 264-6.
• Martinez, J. D., Parker, M. T., Fultz, K. E., Ignatenko, N. A., Gerner, E. W., Ignatenko, N. A., & Gerner, E. W. (2003). Burger's Medicinal Chemistry and Drug Discovery; Regulation of the HIV1 long terminal repeat by mutant heat shock factor. Experimental cell research, 288, 1156; 1-8.
• Qu, N., Ignatenko, N. A., Yamauchi, P., Stringer, D. E., Levenson, C., Shannon, P., Perrin, S., & Gerner, E. W. (2003). Inhibition of human ornithine decarboxylase activity by enantiomers of difluoromethylornithine. The Biochemical journal, 375, 465-470.
• Lawson, K. R., Ignatenko, N. A., Piazza, G. A., Cui, H., & Gerner, E. W. (2000). Influence of K-ras activation on the survival responses of Caco-2 cells to the chemopreventive agents sulindac and difluoromethylornithine. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 9, 1155-1162.
• Taylor, M. T., Lawson, K. R., Ignatenko, N. A., Marek, S. E., Stringer, D. E., Skovan, B. A., & Gerner, E. W. (2000). Sulindac sulfone inhibits K-ras-dependent cyclooxygenase-2 expression in human colon cancer cells. Cancer research, 60, 6607-6610.
• Erdman, S. H., Ignatenko, N. A., Powell, M. B., Blohm-Mangone, K. A., Holubec, H., Guillen-Rodriguez, J. M., & Gerner, E. W. (1999). APC-dependent changes in expression of genes influencing polyamine metabolism, and consequences for gastrointestinal carcinogenesis, in the Min mouse. Carcinogenesis, 20, 1709-1713.
• Ignatenko, N. A., Fish, J. L., Shassetz, L. R., Woolridge, D. P., & Gerner, E. W. (1996). Expression of the human spermidine/spermine N1-acetyltransferase in spermidine acetylation-deficient Escherichia coli. The Biochemical journal, 319 ( Pt 2), 435-440.
• Zaletok, S. P., Lyalyushko, N. M., Berdinskikh, N. K., Ignatenko, N. A., Lidak, M. Y., Baumanis, E. A., Birska, I. A., Zaletok, S. P., Berdinskikh, N. K., Ignatenko, N. A., Baumanis, E. A., Lidak, M. Y., Lyalyushko, N. M., Ignatenko, N. A., & Gerner, E. W. (1996). The influence of polyhexamethyleneguanidine on polyamine methabolism in mongrel rats and on the growth and metastatic spreading of transplantable Lewis lung carcinoma in C57B1 mice; The effect of polyhexamethyleneguanidine on some indices of polyamine metabolism in rats with transplantable hepatoma H-27; Growth arrest- and polyamine-dependent expression of spermidine/spermine N1-acetyltransferase in human tumor cells. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research, 15; 16; 7, 36; 136; 481-41; 139; 486.
• Berdinskikh, N. K., Ignatenko, N. A., Zaletok, S. P., Ganina, K. P., & Chorniy, V. A. (1991). Ornithine decarboxylase activity and polyamine content in adenocarcinomas of human stomach and large intestine. International journal of cancer.Journal international du cancer, 47, 496-498.
• Berdinskikh, N. K., Ignatenko, N. A., & Zaletok, S. P. (1990). Ornithine decarboxylase activity and polyamine contents in 1,2-dimethylhydrazine-induced carcinogenesis of the intestines in rats. Eksperimental'naia onkologiia, 12, 34-36.
• Berdinskikh, N. K., Zaletok, S. P., Bobro, L. I., & Ignatenko, N. A. (1988). Ornithine decarboxylase activity and polyamine content in human adenocarcinomas of the stomach and large intestine. Eksperimental'naia onkologiia, 10, 39-41.
• Berdinskikh, N. K., Zaletok, S. P., Ignatenko, N. A., & Draga, N. V. (1988). Increase in ornithine decarboxylase activity and polyamine levels of the rat liver during an early period of hepatocarcinogenesis. Ukrainskii biokhimicheskii zhurnal (1978), 60, 94-97.