Objective: In this study, the protective effects of vitamin E (Vit E) and alpha-lipoic acid (LA) against the hepatotoxicity of dimethoate, a widely used organophosphate pesticide, were investigated.Material and Method: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test was applied to evaluate cell viability at 24 and 48 hours. The dichlorofluorescein diacetate test was used to evaluate reactive oxygen species (ROS) formation.Result and Discussion: Half maximum inhibitory concentration (IC50) values were calculated as 412 µM and 181 µM for 24 and 48 h, respectively. Dimethoate significantly decreased cell viability in HepG2 cells at 250 µM for 24 hours of exposure and at 50 µM for 48 hours of exposure. Cell viability decreased in a dose-dependent manner. Vit E was observed to increase cell viability significantly at 250 µM concentration (p<0.05) at 24 h. On the other hand, according to the 48-hour exposure results, Vit E was found to be protective against 100 and 250 µM dimethoate (p<0.01). Furthermore, at 4 h exposure, Vit E and LA significantly decreased the ROS levels induced by 100 µM dimethoate treatment (p<0.05 and p<0.001, respectively). In 24 h exposure, it was observed that only Vit E significantly decreased (p<0.05) the ROS levels formed by 100 µM and 250 µM dimethoate treatment. The findings showed that Vit E could be a hepatoprotective agent against possible dimethoate toxicity.

Hydroxychloroquine is an aminoquinoline derivative drug widely used in the treatment of autoimmune diseases, rheumatoid arthritis, and malaria. In 2020, it was approved by the FDA for the treatment of COVID-19, despite a lack of clear evidence of efficacy/safety based solely on in vitro data. In our previous study, we demonstrated that orally administered hydroxychloroquine in rats impaired bone fracture healing, attributing this to increased oxidative stress in the blood. In this study, based on our previous results, we aimed to investigate the effects of the drug on oxidative stress and DNA damage that may develop over time in liver, kidney, and brain tissues in the same model. In the study, antioxidant enzyme activities and lipid peroxidation were measured as parameters of oxidative stress, and the Comet assay was used to determine potential DNA damage in rat tissues. While a dose-independent increase was observed in MDA levels in the liver and brain, the level of MDA in the kidney increased dose-dependently. DNA damage results were also consistent with MDA levels. Although oxidative damage due to bone fracture formation in the control groups showed a time-dependent change, it was not statistically significant. Our findings clearly demonstrate that hydroxychloroquine causes oxidative stress and DNA damage in the liver, kidney, and brain tissues of rats with bone fracture.

Since there are few studies on the toxicity of Physalis peruviana L., its adverse effects on human health are not fully known. Its unripe fruit contains a solanine toxin, which causes gastrointestinal toxicity, and neurological problems such as headaches, and hallucinations. Case studies have reported that the use of preparations containing fruit for weight loss caused adverse effects such as hypertension, ventricular tachycardia, and manic attack. In the acute oral toxicity study, the LD50 value of the fruit was found to be more than 5000 mg/kg for rats. In the subchronic toxicity, the fruit applied for 90 days caused cardiotoxicity in male rats at a dose of 5000 mg/kg. Low amounts of toxic metals have been detected in both the leaves and fruits, even below the permissible levels set by Food and Agriculture Organization/World Health Organization. This chapter aimed to give information about the toxic element content and toxic effects of P. peruviana.

The purpose of the study was to investigate the cytotoxic effects of carnosic acid alone and in combination with cisplatin on human liver cancer cells and their capacity to scavenge reactive oxygen species induced in the presence or absence of hydrogen peroxide.Cytotoxic effects of agents on human liver cancer cells for 24 and 48 hours were evaluated by methyl-thiazol tetrazolium-bromide assay. Mitochondrial membrane potential were detected JC-1 kit. The intracellular reactive oxygen species levels were determined using 2’-7’dichlorofluorescin diacetateassay. According to our findings, both carnosic acid alone and in combination with cisplatin showed cytotoxic effects in human liver cancer cells at 24 and 48 hours of exposure. In particular, it was seen that the cell viability significantly decreased in a dose-dependent manner at 48 hours of exposure, and the combined treatment was found to have a more pronounced cytotoxic effect. In addition, all carnosic acid concentrations alone and in combination with cisplatin were identified to significantly reduce mitochondrial membrane potential. We observed that both carnosic acid alone and in combination with cisplatin lowered intracellular reactive oxygen species levels in the presence or absence of hydrogen peroxide. The results suggested that carnosic acid alone or in combination with cisplatin might be a promising agent in the treatment of liver cancer.

AIM:To examine the effect of cerebellar damage on the process of fracture healing.MATERIAL AND METHODS:A total of forty-two male rats were selected at random and subsequently allocated into three distinct groups. The experimentals were divided into two subgroups within each group, with the intention of sacrificing them during the third and sixth weeks. Group 1 had isolated femoral fracture, Group 2 had femoral fracture after craniotomy, and Group 3 had femoral fracture accompanying cerebellar injury after craniotomy. Left femoral fractures in rats in all groups were treated using an intramedullary Kirschner wire. Radiological, histological, and biochemical evaluations were conducted at 3 and 6 weeks to assess the processes of fracture healing. To determine the effects of fracture healing and cerebellar injury on oxidant-antioxidant systems, catalase (CAT), malondialdehyde, superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities were measured.RESULTS:Between the time frame of 3 to 6 weeks, Group 3 had higher radiography scores, alkaline phosphatase levels, callus/ diaphyse ratio, callus improvement, and bone mineral density in comparison to the other groups. The activity of SOD was found to be statistically negligible in all groups, suggesting that SOD does not have a substantial impact on fracture healing in cerebellar injury. However, notable increases in the activity of GPx and CAT enzymes were observed, showing their considerable involvement in the process of fracture healing.CONCLUSION:Cerebellar injury reduces the oxidative stress in the fracture area and contributes positively to fracture healing by means of radiologically, biochemically and histopathologically.

Pitavastatin (PITA) is a 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitor to treat hypercholesterolemia and in recent studies is focused that its potential anti-cancer effect. This study was aimed to elucidate the effect of PITA alone and in combination with cisplatin on cervical cancer cells (HeLa) in vitro. Cytotoxicity of PITA (5-200 μM) was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and neutral red uptake (NRU) assays for 24, 48, and 72 h. Cell apoptosis and cell cycle analyses were performed in flow cytometry (0.1-100 μM). The evaluation of genotoxic effects and oxidative DNA damage of PITA (2-200 μM) were performed with standard comet assay, formamidopyrimidine glycosylase (fpg)-modified comet assay, and reactive oxygen species (ROS) activation in HeLa cells. PITA alone reduced cell viability in a dose-dependent manner (20-200, 20-200, and 5-200 μM for 24, 48, and 72 h, respectively, in MTT). The combined treatment of PITA with cisplatin resulted in significantly greater inhibition of cell viability. ROS and DNA damage increased significantly at 100 μM for 4 h and 20 μM for 24 h, respectively. PITA-induced apoptosis, an increased proportion of sub G1 cells, was monitored, and also, it increased the expression of active caspase-9 and caspase-3 and upregulated cleaved poly adenosine diphosphate ribose polymerase (PARP) by western blotting and caspase 3/8/9 multiple assay kit. We conclude that PITA can be used to efficiently cervical cancer studies, and promising findings have been obtained for further studies.

Perfluorooctanoic acid (PFOA) is a persistent compound which is associated with many negative effects on human health.In this study, possible oxidative stress inducing effects of PFOA and protective effects of taurine and coenzyme Q10 (CoQ10) in lung, heart and testes of mice were investigated.Animals were administered 15 and 30 mg/kg doses of PFOA orally for 10 days.All three organ weights were found to be affected in response to PFOA while taurine seemed to be effective against absolute heart weight reduction.PFOA was also found to induce histopathological changes in lung tissue.15 mg/kg of PFOA reduced catalase (CAT) activity in lung; increased malondialdehyde (MDA) and total glutathione (GSH) levels, activities of superoxide dismutase (Cu-Zn SOD) and CAT in heart; and increased GSH levels and reduced Cu-Zn SOD and CAT activities in testes.On the other hand, 30 mg/kg PFOA treatment led to Cu-Zn SOD activity increase in lung; GSH level and Cu-Zn SOD activity increase in heart; and reduction of all three enzyme activities in testes.Taurine was found to be protective against Cu-Zn SOD activity increase in both lung and heart tissues, as well as against reduction of glutathione peroxidase (GPx) and CAT activities in the testes.CoQ10 seemed to protect against PFOA-induced increases in MDA levels in the heart tissue.These results suggest the oxidative stress involvement in the toxicity mechanism of an important environmental pollutant, PFOA, in lung, heart and testes of mice.Moreover, taurine and CoQ10 have protective role to some extent against PFOA-induced toxicity.

OBJECTIVES:The aim of this study was to investigate whether hydroxychloroquine sulfate (HCQS) induced oxidative stress and how it affected the union of bone fractures in an experimental rat model.MATERIALS AND METHODS:A total of 48 Wistar albino male rats were used. The rats were divided into six groups. To investigate the effects of oral administration of HCQS at varying doses between the third and sixth weeks, fracture healing processes were evaluated using radiography, histopathology, biochemistry, and dual-energy X-ray absorptiometry. The activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA) were measured to analyze the relationship between HCQS and oxidative stress.RESULTS:Radiographic scores, alkaline phosphatase levels, callus/diaphysis ratio, callus development, and bone mineral density were significantly lower in rats given HCQS at three and six weeks compared to the control group (p<0.005). When oxidative stress parameters were compared among the groups, all antioxidant parameters were statistically significant, indicating that antioxidant systems played a role in peripheral blood, when HCQS was used (p<0.005).CONCLUSION:Oral HCQS intake impairs the fracture healing process by causing oxidative stress in rats. However, further biomolecular researches are needed to understand the underlying mechanism of these effects.

Objective: In this study, toxic effects of Roundup, one of the most common glyphosate-based herbicides (GBHs), were assessed on human bronchial epithelial cells (BEAS-2B). Material and Method: MTT and neutral red uptake assays were implemented for evaluation of cell viability at 24 and 48 h. Apoptosis detection was made by Muse analyzer while Hoechst staining was employed to detect apoptotic nuclear changes. In addition, dichlorofluorescein diacetate assay was used for the assessment of reactive oxygen species (ROS) formation. Result and Discussion: Similar half maximal inhibitory concentrations (IC50) were obtained from cytotoxicity assays. Results showed that significant reduction in the viability of BEAS-2B cells started to occur from 200 µM at 24 h and 50 µM at48 h treatment times. Roundup treatments for both time points were found to dose-dependently cause apoptosis and were also observed to induce cellular ROS formation. These findings suggest that GBHs can stimulate ROS production, as well as apoptosis on healthy human lung cells which is important considering inhalation is one of the primary exposure routes to these group of chemicals.

The aim of this study was to investigate oxidative stress induced by perfluorooctanoic acid (PFOA) in the brain and liver tissues of Balb/c mice as well as protective effects of taurine and coenzyme Q(10) (CoQ(10)) in both organs. For this purpose, animals were treated with PFOA (15 and 30 mg/kg) orally and their lipid peroxidation, total glutathione levels (GSH), and antioxidant enzyme activities measured and both tissues analysed for histopathological changes. Our results showed a dose-dependent decrease in body weight and increase in relative brain and liver weights, PFOA-induced lipid peroxidation and reduced glutathione peroxidase (GPx) activity in the brain tissue, and changes in GSH levels, GPx, superoxide dismutase (Cu-Zn SOD), and catalase (CAT) activities in the liver tissue. Pre-treatment with taurine or CoQ(10) provided protection against PFOA-induced Cu-Zn SOD reduction in the liver tissue. Our findings evidence the depleting effect of PFOA on antioxidative systems and confirm that PFOA exerts its (neuro)toxicity through oxidative stress, but further research is needed to identify the exact toxicity mechanisms, especially in the brain.

Dimethoate is an organophosphate insecticide which is used globally in a wide scale in agriculture. It was associated with numerous negative health effects in many studies. Brain is one of the target organs for dimethoate exposure. The aim of present study was to evaluate sub-chronic (60 days) toxicity of dimethoate (7 mg/kg b.w.), investigating its oxidative stress, DNA damage, as well as apoptosis inducing effects, and histopathological changes in brain tissue of rats. We also aimed to analyze protective effects of Laurocerasus officinalis Roem. (cherry laurel) fruit extract. To evaluate oxidative stress, malondialdehyde (MDA) levels, as well as superoxide dismutase (Cu-Zn SOD), glutathione peroxidase (GPx) and catalase (CAT) antioxidant enzymes activities were calculated. Experimental results demonstrated that dimethoate treatment increased MDA and depleted Cu-Zn SOD, GPx and CAT enzyme activities, suggesting its potency as an oxidative stress inducer in rat brain tissues. Furthermore, comet and TUNEL assay results showed that dimethoate stimulated DNA damage and apoptosis. Administration of cherry laurel extract protected against dimethoate-induced oxidative stress, DNA damage and apoptosis. Findings of currents study are important in terms of demonstrating the beneficial effects of L. officinalis extract against dimethoate toxicity in brain, considering the sensitivity of this organ to oxidative stress and extensive usage of dimethoate.

Glyphosate-based herbicides (GBHs) are the most widely used herbicides all over the world and has gained more attention in recent years because of health safety concerns. In this study, Roundup, one of the most popular glyphosate formulations, was used to evaluate cytotoxic, oxidative stress and apoptosis inducing effects of GBHs in a human hepatocellular cell line (HepG2). Roundup was shown to significantly increase cellular reactive oxygen species (ROS) levels, which lead to activation of the nuclear factor-erythroid-2-related factor 2 (Nrf2) antioxidant defense pathway including reduced levels of heme oxygenase 1 (HO-1). Furthermore, Roundup was found to induce apoptosis and further analysis confirmed involvement of a mitochondrial-dependent pathway verified by increased Bax/Bcl-2 ratios. Investigation of the protective effects of antioxidants vitamin E (Vit E) and α-lipoic acid (LA) against Roundup toxicity showed that both antioxidants significantly reduced the cytotoxicity, ROS formation, HO-1 downregulation, and apoptosis and that Vit E did so more efficiently than LA. In conclusion, our findings highlight the ROS producing and apoptosis inducing effects associated with GBHs, the activation of Nrf2 pathway as a defense mechanism and the protective effects of Vit E and LA against GBH toxicity.

α-PVP has become one of the most dangerous drugs today. α-PVP is chemically the ketone analog of proline. Physically, it is an odorless, colorless solid crystal form. α-PVP is also chemically called α-pyrrolidinovalerophenone, 1-Phenyl-2- (pyrrolidine-1-yl) pentane-1-one, α-Pyrrolidinopentiophenone. In this study, we focused on a general review of this drug, α-PVP, which has become very popular among young people. The study mainly focused on the chemical (synthesis, analogs) and physicochemical (such as density, viscosity, polarity, surface tension) properties, pharmacodynamics, pharmacokinetics, and toxic effects of α-PVP, as well as psychological effects and preventive studies. α-PVP users often appear to cause loss of consciousness, difficulty breathing, and, worst cases, death. It has high toxicity. It has been understood that such a synthetic chemical can be produced in high amounts in a laboratory environment and chemically. The information in the literature on these issues is generally collected in this overview article. In the conclusion part of the study, the negative effects of α-PVP were mentioned, and suggestions were made.

In the literature, the anticancer potential of flurbiprofen isn't fully understood. In this study, the cytotoxic, genotoxic, and apoptotic effects of flurbiprofen were evaluated in human cervical and liver cancer cells. Cytotoxicity was measured by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, and it was observed that cytotoxicity increased in a concentration‐ and time‐dependent manner. Genotoxicity was determined using alkaline Comet assay. DNA damage increased in a concentration‐dependent manner. Early apoptosis was evaluated using real‐time polymerase chain reaction, and it was found that apoptotic gene levels increased while antiapoptotic gene levels decreased. Late apoptosis and cell cycle analyzes were determined using flow cytometry. No evidence of late apoptosis was observed, and no significant arrest was found in the cell cycle. In conclusion, it seems that flurbiprofen has a cytotoxic, genotoxic, and apoptotic effects in both human cancer cell lines. Moreover, the findings indicate that flurbiprofen is effective at the gene level and induces apoptosis with an intracellular pathway.

Dimethoate (DM) is one of the most important organophosphate (OP) insecticide that has been frequently used in agriculture against a broad range of insects, mites, and fungal diseases of fruits, vegetables, and field crops. The excessive use of DM causes environmental pollution and toxic effects on human health. The mechanism of the toxic action of DM is one of inhibiting the acetylcholinesterase activity, leading to an accumulation of acetylcholine and subsequent activation of cholinergic, muscarinic, and nicotinic receptors. In addition, acute and subchronic exposure to DM provokes oxidative stress through the generation of free radicals and induction of lipid peroxidation. The toxicity of DM results in deleterious effects on many organs and systems in human and other mammals such as the liver, kidney, pancreas, brain, nervous system, immune system, and reproductive system. This chapter focuses on the role of oxidative stress in the toxic effect of DM on human and experimental animals.

ERα and Wnt/β‐catenin pathways are critical for the progression of most endometrial cancers. We aimed to investigate the cytotoxic and apoptotic effects of tamoxifen and quinazoline derivative drugs of doxazosin and erlotinib, and their roles in ERα and Wnt/β‐catenin signaling pathways in human endometrial cancer RL 95‐2 cell. 3‐(4,5‐Dimethylthiazol‐2yl)−2,5‐diphenyltetrazolium bromide assay and xCELLigence systems were performed to evaluate cytotoxicity. Furthermore, apoptotic induction was tested by Annexin V analysis. Caspase‐3 and ‐9 activity and changes in the mitochondrial membrane potential were evaluated. The level of reactive oxygen species was measured by incubating with dichlorofluorescein diacetate. Protein ratios of p‐ER α /ER α , GSK3 β /p‐GSK3 β , and p‐ β ‐catenin/ β ‐catenin and expression levels of ESR1, EGFR, c‐Myc genes were evaluated to elucidate mechanisms in signaling pathways. We found that the tested drugs showed cytotoxic and apoptotic effects in the cells. Doxazosin significantly reduced ESR1 expression, slightly reduced the p‐ β ‐catenin/ β ‐catenin ratio and c‐Myc expression. Erlotinib significantly increased c‐Myc expression while significantly decreasing the p‐ β ‐catenin/ β ‐catenin and p‐ER α /ER α ratio, and ESR1 expression. However, we observed that the cells develop resistance to erlotinib over a certain concentration, suggesting that ER α, ESR1, EGFR , and c‐Myc may be a new target for overcoming drug resistance in the treatment of endometrial cancer. We also observed that erlotinib and doxazosin play an important role in the ER α signaling pathway and can act as potent inhibitors of PKA and/or tyrosine kinase in the Wnt/ β ‐catenin signaling pathway in RL 95‐2 cell. In conclusion, doxazosin and erlotinib may have a possible therapeutic potential in human endometrial cancer.

Colon cancer is one of the causes of cancer-related mortality. So, more efficient therapy strategies are needed. There is an increasing interest in natural products due to their potential cytotoxic activity in various cancer cell lines. Osthole and imperatorin are major active coumarins found in a variety of plants. The aim of the present study was to assess the cytotoxic effects of osthole and imperatorin administered separately and in combination with 5-fluorouracil (5-FU) in human colon carcinoma cells and to identify the action of mechanism. Therefore, Colo205 cells were treated with imperatorin (200 μM), osthole (400 μM), and 5-FU (64 μM) 24 h after cell seeding. Real-time cell analysis by xCELLigence System was used to continuously monitor the cell proliferation and viability on Colo205 cells. Furthermore, the effects of the compound on p38 MAPK acitivity and Akt mRNA levels were evaluated. As a result, osthole showed considerable anti-proliferative activity in Colo205 cells and increased the efficacy of 5-FU by accelerating the cytotoxic effect and decreasing the Akt mRNA levels and inhibiting the p38 MAPK activity. Additionally, it was observed that osthole was more effective than imperatorin inhibiting cell proliferation. The findings indicate that osthole may be a promising anti-cancer agent in the treatment of colon cancer.

Dimethoate is an organophosphorus pesticide used against agricultural insects, which causes oxidative stress and damage in many organs, including the reproductive ones. Cherry laurel (Laurocerasus officinalis Roem.) fruit is rich in vitamins and phenolic compounds with antioxidant effect. The aim of this study was to investigate how effective its extract would be against dimethoate-induced testis and sperm damage in rats. Sixty animals were divided in six groups of 10. Group 1 (control) received only 1 mL of saline (0.9 % NaCl). Group 2 received 7 mg/kg of dimethoate in 1 mL of saline. Group 3 received 4 mg/kg of extract in 1 mL of saline. Group 4 received the extract 30 min before dimethoate administration. Group 5 received vitamin C (positive control, 100 mg/kg in 1 mL of saline) 30 min before dimethoate administration. Group 6 received only dimethoate for the first four weeks and then a combination of dimethoate and extract for another four weeks. All doses were administered daily by oral gavage. After eight weeks of treatment, the rats were euthanised and their reproductive organs removed. We took their body and reproductive organ weights and evaluated testicular oxidative stress, semen characteristics, sperm DNA damage, testicular apoptosis, and histopathological changes. Dimethoate significantly decreased body and reproductive organ weights, sperm motility and concentration, testicular superoxide dismutase, and glutathione-peroxidase activities and significantly increased lipid peroxidation, abnormal sperm rate, sperm DNA damage, testicular apoptosis, and caused histopathological lesions. Cherry laurel extract significantly countered many dimethoate-induced adverse effects, both as pre- and post-treatment, including reproductive organ weight, semen parameters, oxidant-antioxidant balance, sperm DNA integrity, testicular apoptosis, and histological structure. Our findings clearly suggest that the beneficial effects of the extract are associated with countering oxidative stress, lipid peroxidation in particular.

Natural products are important in prevention and treatment of cancer because of their antitumor effect and reducing side effects of chemotherapeutic drugs. The aim of this study was to investigate the potential cytotoxic effecs of carnosic acid and in combination with cisplatin in liver cancer cells. Cytotoxicity was assessed using MTT assay for 24/48 hours. The intracellular ROS levels were determined using the oxidation‐sensitive fluorescent probes DCFH‐DA. Changes in the mitochondrial membrane potential (MMP) were detected using JC-1 commercial kit. Concentrations were selected for carnosic acid and cisplatin according to IC50 values. As a results, % cell viability decreased with concentration/time dependent and combination treatments showed potentiated effect at 48 hours exposure. According to DCFH-DA assay, it was observed that carnosic acid and combinations with cisplatin reduced intracellular ROS levels in presence of H2O2. Carnosic acid and its combinations reduced MMP. Our results showed that carnosic acid has the potential to inhibit growth in HepG2 cells without increasing ROS production. In conclusion, carnosic acid alone and combination with cisplatin may be promising for the prevention and treatment of liver cancer.

Endometriyum kanseri, Türkiye’de ve dünya genelinde mortalitesi en yüksek olan jinekolojik kanserlerden biridir. Son yıllarda kinazolin türevi maddelerin antikanser etkilerine olan ilgi artmış olmasına rağmen endometriyum kanser üzerine etkileri bilinmemektedir. Bu amaçla, antihipertansif ilaç olarak kullanılan doksazosin ile antineoplastik bir ilaç olan erlotinib’in endometriyum kanser hücrelerinde (RL95-2) olası sitotoksik etkilerini araştırdık. Çalışmamızda, MTT yöntemi ile insan endometriyum kanser (RL95-2) hücresinin doksazosine, erlotinibe ve pozitif kontrol olarak tamoksifene 0,01 µM-100 µM doz aralıklarında 24 ve 48 saatlik maruz bırakılmasını takiben hücrelerin % canlılığında azalmasına göre sitotoksisite belirlendi ve IC50 değerleri hesaplandı. Elde edilen bulgularımıza göre doksazosin, erlotinib ve tamoksifen’in RL95-2 hücreleri üzerinde sitotoksik etkileri gözlendi. 24 saatlik maruziyet için IC50 değerleri sırası ile 50,09 µM, 18,47 µM ve 57,76 µM olarak belirlendi. 48 saatlik maruziyet için IC50 değerleri ise sırası ile 52,52 µM, 9,32 µM ve 50,06 µM olarak belirlendi. Sonuç olarak, doksazosin ve erlotinib ilaçlarının endometriyum kanser tedavisi için potansiyel antikanser ajan olarak umut verici olduğu düşünülmektedir.