scholarly journals Effect of meglumine acridonacetate on growth of experimental colon adenocarcinoma and tumor-associated changes in the blood of BALB/c mice

2019 ◽  
pp. 51-61
Author(s):  
А.П. Трашков ◽  
А.Л. Коваленко ◽  
Е.И. Дрогомирецкая ◽  
Я.Д. Бараков ◽  
М.Г. Хотин ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Therapeutic Effect ◽  
Malignant Tumors ◽  
Treatment Plan ◽  
Colon Adenocarcinoma ◽  
Inhibitory Effect ◽  
Blood System ◽  
Tumor Growth Rate ◽  
Tumor Dissemination ◽  
Organ Systems

По мере своего роста злокачественные новообразования оказывают выраженное токсическое воздействие на работу всех органов и тканей организма, способствуя развитию разнообразной сопутствующей патологии, изменяя тактику лечения и ухудшая прогноз заболевания. Дополнительным фактором, усиливающим степень тяжести сопутствующей патологии или провоцирующим обострение хронических заболеваний, являются проводимые лечебные процедуры, в том числе, цитостатическая терапия. Это определяет актуальность комплексной оценки лекарственных препаратов, применяющихся в онкологии, в отношении влияния и на опухолевый процесс, и на работу систем жизнеобеспечения организма. Цель исследования: комплексный анализ влияния на развитие экспериментальной опухоли и состояние системы крови потенциального противоопухолевого средства - меглюмина акридонацетата, в том числе, на фоне цитостатической терапии. Материалы и методы. Исследование проведено на 256 самцах мышей линии BALB/c. В качестве модели опухолевого процесса использовали аденокарциному толстой кишки (АКАТОЛ). Экспериментальную химиотерапию проводили на 2-е и 5-е сутки после трансплантации опухоли препаратом циклофосфан в дозе 175 мг/кг массы тела. Меглюмина акридонацетат применяли ежедневно в дозе 100 мг/кг на протяжении 5 суток после трансплантации АКАТОЛ. Оценивали динамику роста опухоли и её метастатическую активность. Осуществляли общий клинический анализ крови. Результаты. Циклофосфан оказал выраженное ингибирующее действие на рост первичного опухолевого узла АКАТОЛ и процесс распространения новообразования в организме животного. При этом наблюдалось сильное гемотоксическое действие цитостатической терапии, имеющее временный, краткосрочный характер. Включение в экспериментальную схему лечения меглюмина акридонацетата потенциировало терапевтические эффекты циклофосфана и в значительной степени нивелировало его токсическое действие в отношении системы крови. На фоне монотерапиии новообразования меглюмина акридонацетатом наблюдалось выраженное ингибирование метастазирования АКАТОЛ и увеличение продукции форменных элементов крови. Выводы. Включение меглюмина акридонацетата в схему терапии циклофосфаном экспериментальной модели колоректального рака усиливает эффективность цитостатика и улучшает профиль его безопасности в отношении влияния на состояние системы крови. Монотерапия новообразования меглюмина акридонацетатом показала умеренный терапевтический эффект в отношении роста опухолевого узла и клинически значимый эффект в отношении ингибирования интенсивности метастазирования опухоли. Growing malignant tumors exert a pronounced toxic effect on all organs and tissues. Thereby, they contribute to various concomitant pathology, change the treatment tactics, and aggravate prognosis for the disease. The treatment itself, specifically a cytotoxic therapy, may also worsen the associated pathology and provoke exacerbation of chronic conditions. These factors determine a need for complex assessment of the drugs used in oncology, both regarding their effect on the neoplasm and side effects on functioning of vital organ systems. Aim: Complex evaluation of the effect of a candidate antitumor drug, meglumine acridonacetate, on experimental tumor growth and the blood system, including the effect on the background of cytostatic therapy. Material and methods. The study was performed on 256 male BALB/c mice. Colon adenocarcinoma (CAC) was used as an experimental model of tumor growth. The experimental chemotherapy with cyclophosphane (175 mg/kg) was administered on days 2 and 5 of tumor implantation. Meglumine acridonacetate (100 mg/kg) was administered daily for 5 days after the CAC implantation. The studied parameters included the tumor growth rate and metastatic activity. Clinical blood tests were also performed. Results. Cyclophosphane exerted a pronounced inhibitory effect on the growth of CAC primary node and tumor dissemination. The cytotostatic therapy produced a severe but brief hemotoxic effect. Addition of meglumine acridonacetate to the experimental treatment plan potentiated the therapeutic effect of cyclophosphane and considerably compensated for its hemotoxic effect. The monotherapy with meglumine acridonacetate significantly inhibited CAC metastasis and stimulated hematopoiesis. Conclusion: Supplementation of the cyclophosphane treatment plan with meglumine acridonacetate enhanced the cytostatic efficacy and improved its safety with respect of the blood system. The meglumine acridonacetate monotherapy exerted a moderate therapeutic effect on tumor growth and a clinically significant inhibitory effect on tumor metastasis.

scholarly journals Hyperprogressive Disease Caused by PD-1 Inhibitors for the Treatment of Pan-Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Shiyun Chen ◽  
Miaomiao Gou ◽  
Huan Yan ◽  
Mengjiao Fan ◽  
Yuting Pan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Tumor Markers ◽  
Malignant Tumors ◽  
Hepatic Metastases ◽  
Lactate Dehydrogenase Level ◽  
Tumor Growth Rate ◽  
Hyperprogressive Disease ◽  
Metastatic Sites ◽  
Pan Cancer

Background. Nowadays, PD-1/PD-L1 inhibitors are widely used to treat various malignant tumors. However, during the immunotherapy in a few patients, a flare-up of tumor growth occurred. This new pattern of progression is called hyperprogressive disease (HPD). Patients and Methods. The retrospective study included 377 patients with various malignant tumors treated with PD-1 inhibitors (nivolumab or pembrolizumab) in the Chinese PLA General Hospital from January 2015 to January 2019. Clinicopathologic variables, tumor growth rate (TGR), and treatment outcomes were analyzed in patients with pan-cancer treated with PD-1 inhibitors. HPD was defined as the difference of TGR before and during immunotherapy exceeding 50%. Results. In 38 of 377 patients (10.08%), HPD occurred after treatment with PD-1 inhibitors. Patients with HPD had lower overall survival (OS) than those without HPD (median OS, 3.6months (95% CI, 3.0–4.2) vs. 7.3 months (95% CI, 5.9–8.7); P < 0.01 ). Factors related to HPD include more than 2 metastatic sites, ECOG performance status ≥ 2 , hepatic metastases, and lactate dehydrogenase level greater than normal upper limit. KRAS status was significantly associated with HPD in patients with colorectal cancer. In the exploratory predictors’ analysis, the rapid increase of characteristic tumor markers (such as CEA in colorectal cancer, CA199 in pancreatic cancer and cholangiocarcinoma) within one month was found to be associated with the occurrence of HPD. Conclusions. HPD was developed with different rates in a variety of malignant tumor patients treated with PD-1 inhibitors and related to some clinicopathological features and poor prognosis. Tumor markers, especially CA199, might be served as early predictors of HPD.

miR-151-3p Inhibits Proliferation and Invasion of Colon Cancer Cell by Targeting Close Homolog of L1

2020 ◽  
Vol 16 (6) ◽  
pp. 876-884
Author(s):  
Chaochi Yue ◽  
Xiaochao Chen ◽  
Jun Li ◽  
Xiangdong Yang ◽  
Yuanzhi Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Malignant Tumors ◽  
Colon Adenocarcinoma ◽  
Tumor Growth Rate ◽  
Normal Tissues ◽  
The Past ◽  
Potential Impact ◽  
Dramatic Growth ◽  
Proliferation And Invasion ◽  
Close Homolog

Colorectal cancer (CRC) is one of the most common malignant tumors in the world. Cases of colon cancer have experienced dramatic growth for the past few decades in China, while the rate of rectal cancer descends 3% every year in the West. The purpose of this study is to reveal the potential impact of miR-21-5p on the occurrence process of CRC and its connection with a close homolog of L1 (CHL1). In this study, the expression level of the miR-151-3p was found to be significantly higher in colon adenocarcinoma tissue compared with adjacent normal tissues, while the CHL1 was lower in colon adenocarcinoma tissues. The expression of miR-151-3p was inversely correlated with the expression of CHL-1, as it was confirmed with correlation analysis. miR-151-3p deregulates the expression of CHL1. CHL1 overexpression can restrain the proliferation and invasion of CRC. Tumorigenesis experiments showed that the tumor growth rate of CHL1-OV was significantly reduced in mice, and its effect could be reversed by miR-151-3p mimics. Taken together, our study may provide new insights into the potential mechanisms of progression of CRC, and may provide a theory for targeted drug therapy.

scholarly journals A TLR4 agonist improves immune checkpoint blockade treatment by increasing the ratio of effector to regulatory cells within the tumor microenvironment

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
A. Farias ◽  
A. Soto ◽  
F. Puttur ◽  
C. J. Goldin ◽  
S. Sosa ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Therapeutic Effect ◽  
Immune Cells ◽  
Immune Checkpoint ◽  
Combined Treatment ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
Regulatory Cells ◽  
Ifn Γ

AbstractBrucella lumazine synthase (BLS) is a homodecameric protein that activates dendritic cells via toll like receptor 4, inducing the secretion of pro-inflammatory cytokines and chemokines. We have previously shown that BLS has a therapeutic effect in B16 melanoma-bearing mice only when administered at early stages of tumor growth. In this work, we study the mechanisms underlying the therapeutic effect of BLS, by analyzing the tumor microenvironment. Administration of BLS at early stages of tumor growth induces high levels of serum IFN-γ, as well as an increment of hematopoietic immune cells within the tumor. Moreover, BLS-treatment increases the ratio of effector to regulatory cells. However, all treated mice eventually succumb to the tumors. Therefore, we combined BLS administration with anti-PD-1 treatment. Combined treatment increases the outcome of both monotherapies. In conclusion, we show that the absence of the therapeutic effect at late stages of tumor growth correlates with low levels of serum IFN-γ and lower infiltration of immune cells in the tumor, both of which are essential to delay tumor growth. Furthermore, the combined treatment of BLS and PD-1 blockade shows that BLS could be exploited as an essential immunomodulator in combination therapy with an immune checkpoint blockade to treat skin cancer.

245 Human TLR8 knock-in mice potentiate immunotherapy responses of MC38 syngeneic tumors

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A264-A264
Author(s):  
Shanshan Qi ◽  
Hongjuan Zhang ◽  
Ruilin Sun ◽  
Annie An ◽  
Henry Li ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Growth ◽  
Cancer Immunotherapy ◽  
Tumor Regression ◽  
Tumor Growth Rate ◽  
Tumor Growth Inhibition ◽  
List Type ◽  
Rna Recognition ◽  
Ethical Guidelines ◽  
Ifn Γ

BackgroundToll-like receptors (TLRs) serve critical roles in mediating innate immune responses against many pathogens. However, they may also bind to endogenous ligands and lead to the pathogenesis of autoimmunity. Although TLR8 belongs to the same TLR family as TLR7, its role in inflammation and tumor progression is not yet fully understood due to the lack of suitable animal models. In humans, both TLR7 and TLR8 recognize single-stranded self-RNA, viral RNA, and synthetic small molecule agonists.1, 2 However, mouse Tlr8 is non-functional due to the absence of 5 amino acids necessary for RNA recognition. In order to create a mouse model with functional TLR8, we replaced exon 3 of mouse Tlr8 with human TLR8, therefore developing a hTLR8 knock-in (KI) model. Both heterozygous and homozygous hTLR8 KI mice are viable with inflammatory phenotypes, i.e. enlarged spleens and livers, and significantly higher IL-12 p40 levels under TLR8 agonist treatment. In this study, we evaluated the potential use of hTLR8 mice for cancer immunotherapy studies.MethodshTLR8 mice, together with naïve C57BL/6 mice, were inoculated with MC38 syngeneic tumor cells. Tumor bearing mice were grouped at a mean tumor volume of approximately 100 mm3 for treatment with PBS or 10 mg/kg anti-PD-1 (RMP1-14) antibody. At the efficacy endpoint, spleens and tumors were collected for flow cytometry profiling.ResultsAnti-PD-1 treatment of MC38 tumors in naïve C57BL/6 led to moderate tumor growth inhibition (TGI = 54%). Interestingly, anti-PD-1 treatment showed improved efficacy in hTLR8 mice (TGI = 79%), including 2/10 tumors with complete tumor regression. In comparison, non-treated MC38 tumor growth rate was slower in hTLR8 mice than in naïve mice. Anti-PD-1 treated hTLR8 mice also had significantly increased IFN-γ and TNF-a positive CD4+ T cells in the spleen, along with higher numbers of differentiated effector T cells. In addition, hTLR8 mice have activated dendritic cells and macrophages, acting as critical steps in initiation of the inflammatory process, with higher levels of pro-inflammatory cytokines, such as IL-6, IFN-γ, TNF-a, and IL-1β, which may promote Th1 priming and differentiation of T cells into IFN-γ or TNF-a producing cells.ConclusionshTLR8 mice offer a great tool to model cancer immunotherapy in an inflammatory/autoimmunity prone background. Moreover, hTLR8 mice can be effectively used to shift a ‘cold’ tumor phenotype to ‘hot’ tumors in a syngeneic setting.Ethics ApprovalAnimal experiments were conducted in accordance with animal welfare law, approved by local authorities, and in accordance with the ethical guidelines of CrownBio (Taicang).ReferencesKugelberg E. Making mice more human the TLR8 way. Nat Rev Immunol 2014;14:6.Guiducci C, Gong M, Cepika A-M, et al. RNA recognition by human TLR8 can lead to autoimmune inflammation. J Exp Med 2013;210:2903–2919.

scholarly journals Investigating New Therapeutic Strategies Targeting Hyperinsulinemia's Mitogenic Effects in a Female Mouse Breast Cancer Model

Endocrinology ◽  
2013 ◽  
Vol 154 (5) ◽  
pp. 1701-1710 ◽  
Author(s):  
Ran Rostoker ◽  
Keren Bitton-Worms ◽  
Avishay Caspi ◽  
Zila Shen-Orr ◽  
Derek LeRoith
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Experimental Studies ◽  
Tumor Development ◽  
Treated Group ◽  
Tumor Growth Rate ◽  
Breast Cancer Patients ◽  
Mitogenic Effect

Abstract Epidemiological and experimental studies have identified hyperinsulinemia as an important risk factor for breast cancer induction and for the poor prognosis in breast cancer patients with obesity and type 2 diabetes. Recently it was demonstrated that both the insulin receptor (IR) and the IGF-IR mediate hyperinsulinemia's mitogenic effect in several breast cancer models. Although IGF-IR has been intensively investigated, and anti-IGF-IR therapies are now in advanced clinical trials, the role of the IR in mediating hyperinsulinemia's mitogenic effect remains to be clarified. Here we aimed to explore the potential of IR inhibition compared to dual IR/IGF-IR blockade on breast tumor growth. To initiate breast tumors, we inoculated the mammary carcinoma Mvt-1 cell line into the inguinal mammary fat pad of the hyperinsulinemic MKR female mice, and to study the role of IR, we treated the mice bearing tumors with the recently reported high-affinity IR antagonist-S961, in addition to the well-documented IGF-IR inhibitor picropodophyllin (PPP). Although reducing IR activation, with resultant severe hyperglycemia and hyperinsulinemia, S961-treated mice had significantly larger tumors compared to the vehicle-treated group. This effect maybe secondary to the severe hyperinsulinemia mediated via the IGF-1 receptor. In contrast, PPP by partially inhibiting both IR and IGF-IR activity reduced tumor growth rate with only mild metabolic consequences. We conclude that targeting (even partially) both IR and IGF-IRs impairs hyperinsulinemia's effects in breast tumor development while simultaneously sparing the metabolic abnormalities observed when targeting IR alone with virtual complete inhibition.

scholarly journals Increased Tumor Growth in Mice with Diet-Induced Obesity: Impact of Ovarian Hormones

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5826-5834 ◽  
Author(s):  
Shoshana Yakar ◽  
Nomeli P. Nunez ◽  
Patricia Pennisi ◽  
Pnina Brodt ◽  
Hui Sun ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Tumor Growth ◽  
Glucose Intolerance ◽  
Tumor Development ◽  
Tumor Growth Rate ◽  
Obese Mice ◽  
Female Mice ◽  
Diet Induced Obesity ◽  
Body Adiposity ◽  
Obese Female

Obesity increases the risk of many cancers in both males and females. This study describes a link between obesity, obesity-associated metabolic alterations, and the risk of developing cancer in male and female mice. The goal of this study was to evaluate the relationship between gender and obesity and to determine the role of estrogen status in obese females and its effect on tumor growth. We examined the susceptibility of C57BL/6 mice to diet-induced obesity, insulin resistance/glucose intolerance, and tumors. Mice were injected sc with one of two tumorigenic cell lines, Lewis lung carcinoma, or mouse colon 38-adenocarcinoma. Results show that tumor growth rate was increased in obese mice vs. control mice irrespective of the tumor cell type. To investigate the effect of estrogen status on tumor development in obese females, we compared metabolic parameters and tumor growth in ovariectomized (ovx) and intact obese female mice. Obese ovx female mice developed insulin resistance and glucose intolerance similar to that observed in obese males. Our results demonstrate that body adiposity increased in ovx females irrespective of the diet administered and that tumor growth correlated positively with body adiposity. Overall, these data point to more rapid tumor growth in obese mice and suggest that endogenous sex steroids, together with diet, affect adiposity, insulin sensitivity, and tumor growth in female mice.

scholarly journals Tumor growth characteristics of the Walker 256 AR tumor, a regressive variant of the rat Walker 256 A tumor

2010 ◽  
Vol 53 (5) ◽  
pp. 1101-1108 ◽  
Author(s):  
Fernando Guimarães ◽  
Alessandra Soares Schanoski ◽  
Tereza Cristina Samico Cavalcanti ◽  
Priscila Bianchi Juliano ◽  
Ana Neuza Viera-Matos ◽  
...  
Keyword(s):  
Growth Rate ◽  
Tumor Growth ◽  
Wistar Rats ◽  
Tumor Regression ◽  
Growth Characteristics ◽  
Tumor Growth Rate ◽  
Continuous Growth ◽  
Tumor Bearing ◽  
Walker 256 ◽  
Complete Tumor

The present study aimed at characterizing the subcutaneous development of the Walker 256 (W256) AR tumor, a regressive variant of the rat W256 A tumor. Wistar rats were injected subcutaneously with 4x10(6) W256 A or W256 AR tumor cells. The development of tumors was evaluated daily by percutaneous measurements. None of the W256 A tumors (n=20) regressed, but 62% of the W256 AR tumor-bearing rats (n=21) underwent complete tumor regression within 35 days. Continuous growth of AR tumors was characterized by an increase of the tumor growth rate from day 12, which reached values above 1.0 g/day, and were significantly higher (p<0.05) than those of the regressive AR tumors. Immunosuppression by irradiation before subcutaneous injection of AR cells completely abrogated tumor regression and was associated with severe metastatic dissemination. Daily evaluation of the tumor growth rate enabled the discrimination, in advance, between continuously growing tumors and those that regressed later on.

Targeted Treatment of Experimental Spinal Cord Glioma With Dual Gene-Engineered Human Neural Stem Cells

Neurosurgery ◽  
2015 ◽  
Vol 79 (3) ◽  
pp. 481-491 ◽  
Author(s):  
Alexander E. Ropper ◽  
Xiang Zeng ◽  
Hariprakash Haragopal ◽  
Jamie E. Anderson ◽  
Zaid Aljuboori ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Stem Cells ◽  
Growth Rate ◽  
Neural Stem Cells ◽  
Tumor Growth ◽  
Rat Model ◽  
Weight Bearing ◽  
Tumor Growth Rate ◽  
Intramedullary Spinal Cord ◽  
Human Neural Stem Cells

Abstract BACKGROUND There are currently no satisfactory treatments or experimental models showing autonomic dysfunction for intramedullary spinal cord gliomas (ISCG). OBJECTIVE To develop a rat model of ISCG and investigate whether genetically engineered human neural stem cells (F3.hNSCs) could be developed into effective therapies for ISCG. METHODS Immunodeficient/Rowett Nude rats received C6 implantation of G55 human glioblastoma cells (10K/each). F3.hNSCs engineered to express either cytosine deaminase gene only (i.e., F3.CD) or dual genes of CD and thymidine kinase (i.e., F3.CD-TK) converted benign 5-fluorocytosine and ganciclovir into oncolytic 5-fluorouracil and ganciclovir-triphosphate, respectively. ISCG rats received injection of F3.CD-TK, F3.CD, or F3.CD-TK debris near the tumor epicenter 7 days after G55 seeding, followed with 5-FC (500 mg/kg/5 mL) and ganciclovir administrations (25 mg/kg/1 mL/day × 5/each repeat, intraperitoneal injection). Per humane standards for animals, loss of weight-bearing stepping in the hindlimb was used to determine post-tumor survival. Also evaluated were autonomic functions and tumor growth rate in vivo. RESULTS ISCG rats with F3.CD-TK treatment survived significantly longer (37.5 ± 4.78 days) than those receiving F3.CD (21.5 ± 1.75 days) or F3.CD-TK debris (19.3 ± 0.85 days; n = 4/group; P &lt;.05, median rank test), with significantly improved autonomic function and reduced tumor growth rate. F3.DC-TK cells migrated diffusively into ISCG clusters to mediate oncolytic effect. CONCLUSION Dual gene-engineered human neural stem cell regimen markedly prolonged survival in a rat model that emulates somatomotor and autonomic dysfunctions of human cervical ISCG. F3.CD-TK may provide a novel approach to treating clinical ISCG.

scholarly journals Anti-Cancer Effects of Zotarolimus Combined with 5-Fluorouracil Treatment in HCT-116 Colorectal Cancer-Bearing BALB/c Nude Mice

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4683
Author(s):  
Geng-Ruei Chang ◽  
Chan-Yen Kuo ◽  
Ming-Yang Tsai ◽  
Wei-Li Lin ◽  
Tzu-Chun Lin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Growth ◽  
Nude Mice ◽  
Colorectal Adenocarcinoma ◽  
Transforming Growth Factor ◽  
Colon Adenocarcinoma ◽  
Future Research ◽  
Related Factors ◽  
Hct 116

Zotarolimus is a semi-synthetic derivative of rapamycin and an inhibitor of mammalian target of rapamycin (mTOR) signaling. Currently, zotarolimus is used to prolong the survival time of organ grafts, but it is also a novel immunosuppressive agent with potent anti-proliferative activity. Here, we examine the anti-tumor effect of zotarolimus, alone and in combination with 5-fluorouracil, on HCT-116 colorectal adenocarcinoma cells implanted in BALB/c nude mice. Compared with the control mice, mice treated with zotarolimus or zotarolimus combined with 5-FU showed retarded tumor growth; increased tumor apoptosis through the enhanced expression of cleaved caspase 3 and extracellular signal-regulated kinase (ERK) phosphorylation; reduced inflammation-related factors such as IL-1β, TNF-α, and cyclooxygenase-2 (COX-2) protein; and inhibited metastasis-related factors such as CD44, epidermal growth factor receptor (EGFR), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF). Notably, mice treated with a combination of zotarolimus and 5-FU showed significantly retarded tumor growth, reduced tumor size, and increased tumor inhibition compared with mice treated with 5-FU or zotarolimus alone, indicating a strong synergistic effect. This in vivo study confirms that zotarolimus or zotarolimus combined with 5-FU can be used to retard colorectal adenocarcinoma growth and inhibit tumorigenesis. Our results suggest that zotarolimus may increase the chemo-sensitization of tumor cells. Therefore, zotarolimus alone and zotarolimus combined with 5-FU may be potential anti-tumor agents in the treatment of human colon adenocarcinoma. Future research on zotarolimus may lead to the development of new therapeutic strategies.

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