جستجوی مقالات مرتبط با کلیدواژه "doxorubicin" در نشریات گروه "پزشکی"

 Doxorubicin (DOX), in addition to its anti-cancer properties, causes toxicity and increases the apoptosis of healthy tissues. The objective of the current research was to explore the concurrent influence of an eight-week aerobic training regimen combined with crocin supplementation on the apoptosis induced by DOX within the soleus muscle tissue of male rodents.

 In this study, a cohort of 40 male Wistar rats, each weighing between 200 and 220 g and approximately 8 weeks old, were systematically distributed into five distinct experimental clusters, including a healthy control (normal saline) and a patient control (intraperitoneal injection of 2 mg/kg of DOX ). The other clusters were DOX-exercise (intraperitoneal injection of 2 mg/kg of DOX with eight weeks of treadmill/5 days a week), DOX-crocin (intraperitoneal injection of 2 mg/kg) 2 kg of DOX along with 10 mg/kg of crocin extract/8 weeks), and DOX-exercise-crocin.

 The administration of DOX was associated with a notable elevation in Bax and a reduction in Bcl-2 expression (P=0.001 and P=0.001). In contrast, engaging in eight weeks of aerobic exercise, ingesting crocin, or a synergistic approach combining both interventions resulted in a marked upregulation of Bcl-2 expression (P=0.001). This combined treatment also led to a significant diminution in the Bax mRNA (P=0.006) and a decrease in the Bax/Bcl-2 ratio (P=0.001) within the soleus muscle tissue of male rodents subjected to DOX exposure.

 Aerobic exercise with crocin supplementation could inhibit apoptosis caused by DOX in the soleus muscle of male rats.

Doxorubicin chemotherapy is a widely used treatment for various cancers, including breast, ovarian, and uterine cancers, among others. However, long-term use can cause nephrotoxicity side effects. Some citrus flavonoids have demonstrated nephroprotective activity; therefore, this study aimed to test the nephroprotective effectiveness of Citrus aurantifolia peel extract in protecting and reducing kidney damage caused by doxorubicin.

Experimental approach: 

Citrus aurantifolia peel was dried, ground, and extracted by ultrasonication (70% ethanol), then the extract was dried. Twenty-five female Sprague-Dawley rats were divided into 5 groups including the normal group (control), positive control (doxorubicin) group receiving doxorubicin at the repeated intraperitoneal (i.p.) dose of 4 mg/kg/day on days 2, 6, 10, and 14, and treatment groups receiving Citrus aurantifolia peel extract (CPE) with the doses of 100, 200, and 400 mg/kg/day orally for 14 days, and doxorubicin (4 mg/kg/day, i.p.) on days 2, 6, 10 and 14. On day 15, the rats were euthanized for the measurements of MDA, superoxide dismutase (SOD), catalase, kidney function (measuring blood urea nitrogen (BUN), creatinine, albumin serum levels), and renal histopathology.

The CPE yield was 16.13%. CPE could significantly reduce the levels of MDA, and increase SOD and catalase activities compared with the doxorubicin-induced nephrotoxic model. CPE could increase renal function by reducing BUN and creatinine levels, increasing albumin, and improving the histopathology of the kidney.

Conclusion and implications:

 CPE has a potential effect as nephroprotective against doxorubicin-induced toxicity in renal through antioxidant capacities and increased renal function.

Photothermal therapy (PTT) is one of the effective and non-invasive strategies which hold great promise for improving the treatment of cancer cells. PTT is based on activating a photosensitizer by infrared light irradiation and producing heat and reactive species and apoptosis in the tumor area. The aim of this study was to investigate the effect of photothermal/chemotherapy on melanoma cancer cells using poly (2-amino phenol)/gold (P2AO/AuNPs) and doxorubicin (DOX). In this experimental study, nanoparticles of P2AO/AuNPs were synthesized, and their mixture with DOX was applied as a photosensitizer for photothermal/chemotherapy of a C540 (B16-F10) melanoma cell line. P2AO/AuNPs generated heat and cytotoxic responsive oxygen species (ROS) upon 808-nm light irradiation with simultaneous intensifying DOX therapeutic effect under domination of synergism effects between light irradiation, P2AO/AuNPs, and doxorubicin. Cell treatment with both P2AO/AuNPs and DOX resulted in a considerable increase in necroptotic cells to 61% with a significant decrease in the living cells (39%).   P2AO/AuNPs provided a platform for light absorption and intensifying DOX therapeutic effect. This study approved the applicability of a new photothermal/chemotherapy by domination of synergistic effects attained by combination of laser light, P2AO, AuNPs, and DOX.

Nowadays, herbal medicine has been utilized to treat various diseases such as cancer, which showed successful therapeutic efficacy in previous studies. This study for the first time evaluated the cytotoxic potential of cinnamaldehyde (CIN) alone and in combination with doxorubicin (DOX), a well-known potent anti-tumor agent, on the proliferation of prostatic cancer cell line (PC3).

Experimental approach: 

The cytotoxicity and apoptotic activities of CIN and DOX, either separately or together, were determined on PC3 cells by the MTT test and Annexin V/PI assay, respectively. To further investigate which apoptotic pathway participated in cell death a collection of prominent markers of apoptosis induction including caspase-3/7 activations, mitochondrial membrane potential (MMP), and phosphatidyl serine translocation were detected.

The different concentrations of CIN and DOX significantly inhibited the proliferation of PC3 cells in a concentration-dependent way within a 24-h treatment. In addition, the induction of apoptosis by CIN was accompanied by an increase in the activation of caspase-3/7 in PC3 cells with IC50 concentrations of 12.5 and 10 μg/mL for CIN and DOX, respectively. Moreover, the morphological observations obtained from flow cytometry MMP and caspase-3/7 activity assays, altogether, revealed the potential effect of CIN on apoptosis induced in PC3 cells by DOX.

Conclusions and implications: 

Taken together, the current study concluded that the combination of CIN and DOX could lead to the production of a potential therapeutic agent for prostate cancer. However, further in vivo and clinical studies are still needed to validate this combination in prostate cancer therapy.

Cerium oxide nanoparticles (Ceo2 NPs) are considered one of the most effective nanomaterials for drug delivery. The current study aimed to investigate the anticancer activities of doxorubicin-loaded Ceo2 NPs (DOX-Ceo2 NPs) against the MDA-MB-231 human breast cancer cell line.

Ceo2 NPs were synthesized using the GREEN synthesis method and loaded with DOX (DOX-Ceo2 NPs). The physicochemical properties of the Ceo2 NPs were evaluated using FTIR, XRD, DLS, zeta potential, and electron microscopy (SEM/TEM). Cultured MDA-MB-231 cells were treated with different concentrations of bare Ceo2 NPs, free DOX, and DOX-Ceo2 NPs. In addition, HDF cells were treated with different concentrations of Ceo2 NPs. MTT, wound healing, and flow cytometry assays were performed to determine the cell viability, migration, and apoptosis, respectively. qPCR was performed to investigate the expression of genes involved in apoptosis, including caspase (CASP) 3, 8, 9, and Bcl-2. 

The XRD and FTIR results confirmed the synthesis of pure and crystalline structured- Ceo2 NPs. The average size, PDI, and zeta potential of the Ceo2 NPs were approximately 239.1 nm, 0.074, and -9.04 mV, respectively. In vitro assays showed that DOX-Ceo2 NPs exhibited higher cell proliferation inhibition, migration suppression, and apoptosis induction through the upregulation of CASP3, CASP8, and CASP9 genes and downregulation of Bcl-2. 

Our data demonstrate the potential of Ceo2 NPs for the efficient delivery of DOX and, subsequently, the improvement of its anticancer activities. Therefore, DOX-Ceo2 NPs have the potential to be proposed as promising anticancer agents for breast cancer.

This study was done to achieve a new drug delivery system delivering two different chemotherapy molecules to the target tissue simultaneously.Significance: Co-delivery of chemotherapy medicines provides synergistic effects leading to lowering the dose of administered drugs and side effects.

Doxorubicin (DOX) was introduced to water-soluble hyaluronic acid (Hyal) using 1-amino-3,3-diethoxy-propane (ADEP), as a pH-sensitive linker, to develop a new hydrophobic structure, i.e. Hyal-ADEP-DOX. The conjugates were grafted in three ratios (7.5%, 12.5%, and 20%) to Hyal and characterized by Fourier transform infrared (FT-IR) and proton nuclear magnetic resonance (1HNMR). Cannabidiol (CBD) was physically loaded in the core of nano-micelles.

Prepared nano-micelles were analyzed for critical micelle concentration (CMC) particle size stability and drug release before and after loading the CBD. Hyal-ADEP-DOX-12.5 was the optimized ratio and had a mean diameter of 50 nm before loading the CBD and 120 nm after loading (observed by transmission electron microscopy). The release results showed that DOX releases slowly in physiological pH, and CBD has a burst release at acidic pH from Hyal-ADEP-DOX-12.5. These properties altogether make Hyal-ADEP-DOX nano-micelles, as a stimuli-sensitive nano-carrier, a potential candidate for hydrophobic anticancer agents’ co-delivery.

The grafted DOX exhibited pH-sensitive release behavior, i.e. while 22.8% of the drug was released after 24 h at pH 5.5, and 5% was released after 24 h at pH 7.4. Hyal-ADEP-DOX due to its low CMC value, colloidal stability, slow drug release in physiological pH, and burst release in acidic pH Hyal-ADEP-DOX, is an excellent candidate as a carrier to co-deliver hydrophobic therapeutic agents to tumor tissues.

Inflammation contributes to cancer pathobiology through different mechanisms. Higher levels of pro-inflammatory cytokines can lead to hyperinflammation and promote cancer development and metastasis. For cancer treatment, Doxorubicin (DOX) can be encapsulated into the poly-lactic-glycolic acid (PLGA) nanoparticles. This study aimed to investigate the impact of doxorubicin-loaded PLGA nanoparticles (DOX-PLGA NP) on the expression of pro-inflammatory genes TNF-α, IL-6, iNOS, and IL-1β in the MCF-7 cells.

The DOX-PLGA NP was prepared by loading doxorubicin into PLGA and characterized using dynamic light scattering (DLS) and atomic force microscopy (AFM). The cytotoxic effect of the nanoparticles was determined by the MTT assay, and their impacts on the expression of pro-inflammatory genes were assessed by qRT-PCR.

The encapsulation efficiency and loading capacity were 60±1.5 and 1.13±0.21 percent, respectively. The zeta potential and mean DOX-PLGA nanoparticle size were -18±0.550 mV and 172±55.6 nm, respectively. The 50% inhibitory concentration (IC50) of the DOX-PLGA NP on MCF-7 cell viability was 24.55 µg/mL after 72 hours of treatment. The qRT-PCR results revealed that the 20 µg/mL concentration of the DOX-PLGA NP significantly suppressed the expression of the pro-inflammatory genes TNF-α, IL-6, iNOS, and IL-1β compared to DOX alone (20 µg/mL). Additionally, the suppression effect of DOX-PLGA NP on the expression of these pro-inflammatory genes was dose-dependent.

These results show that DOX-PLGA NP efficiently suppressed the expression of pro-inflammatory genes. Furthermore, encapsulation of DOX into PLGA nanoparticles significantly improved the effectiveness of DOX in suppressing pro-inflammatory genes in MCF-7 breast cancer cells.

Doxorubicin, a commonly utilized anthracycline antibiotic and chemotherapeutic agent, has been associated with hepatotoxicity as an adverse effect. This study aimed to evaluate protective effects of zingerone, a bioactive compound derived from ginger renowned for its antioxidative attributes, on oxidative stress in doxorubicin-induced rat hepatotoxicity.

In this experimental study, a total of 48 male Wistar rats were allocated into six distinct groups. The first group received a control treatment of normal saline. The second group was administered an intraperitoneal dose of 20 mg/kg of doxorubicin on day 5. The third group received an oral dose of 40 mg/kg of zingerone for 8 days. The fourth, fifth, and sixth groups were administered zingerone at doses of 10, 20, and 40 mg/kg, respectively, for the same 8-day period. On day 5, all groups, except the control group, received an intraperitoneal injection of doxorubicin. Following a 72-hour interval, the animals were anesthetized, and blood samples were collected to assess serum factors. Moreover, portions of the liver tissue were subjected to histopathological analysis and assessment of oxidative stress parameters.

The activity levels of serum enzymes, including aspartate transaminase (AST), alanine transaminase (ALT), and liver malondialdehyde (MDA), increased in the doxorubicin group. Conversely, the levels of other parameters such as glutathione peroxidase (GPX), superoxide dismutase (SOD), and glutathione (GSH) decreased. However, the co-administration of zingerone effectively reversed these levels, restoring them back to normal.

These findings suggest that zingerone, particularly at a high dose, exhibit a hepatoprotective effect in the doxorubicin-induced hepatotoxicity model.

This study assessed the cardioprotective properties ofPersicaria maculosa (PME) and Citrus sinensis (CME) hydromethanolic extracts, besides Citrus sinensis aqueous extract(CWE) against doxorubicin (DOX)-induced cardiotoxicity. The extracts were characterized. Micewere divided into eight groups: control (saline), DOX, protected(injected with 200 mg/kg of PME, CWE or CME for 21 days,orally, and DOX), and extracts (PME, CWE or CMEadministration, orally, for 21 days). DOX was injected (5 mg/kg,ip) on days 8, 13 and 18 of the experiment. Cardiac tumor necrosisfactor-alpha (TNF-α), nuclear factor (erythroid-derived 2)-like 2(Nrf2) and carbonyl reductase 1 (CBR1) expression levels, besidessuperoxide dismutase, catalase, malondialdehyde, nitric oxide andtotal protein levels were evaluated. Serum lactate dehydrogenase,creatine phosphokinase cardiac isoenzyme, aspartate transaminase,cholesterol, triglycerides and creatinine levels, as well as thecardiac tissues were examined. Comparing with the control, DOX considerably (p<0.01)up-regulated TNF-α expression, malondialdehyde, nitric oxide,cardiac enzymes, lipids and creatinine levels, while it significantly(p<0.01) down-regulated Nrf2 and CBR1. Additionally, DOXinterfered with antioxidant enzymes' activities (p<0.01).Conversely, protected groups showed a significant (p<0.01)amelioration of DOX-induced cardiotoxic effects. The current study provides a new understanding of P.maculosa and C. sinensis cardioprotective mechanisms. Theextracts' cardioprotective effects may be due to their antioxidantactivities, ability to maintain the redox homeostasis throughregulation of important antioxidant genes and primary antioxidantenzymes, and capability to recover inflammatory cytokines andlipids levels. Noteworthy, the tested extracts showed no toxicchanges on the normal mice.

 Doxorubicin is a widely used antineoplastic agent for the treatment of solid tumors but its use is limited by its several severe tissue and organ toxicities. This study investigated changes in liver and spleen as a result of toxicity produced by Doxorubicin and the protective role of aqueous leaf extract of J. Tanjorensis.

In this experimental study, rats were divided into 5 groups as follows: Group 1 served as control and orally received normal saline once daily. Doxorubicin (15 mg/kg) was administered to Group 2  from day 10. Group 3 received J. Tanjorensis (300 mg/kg, orally) once daily for 12 days. Group 4 received J. Tanjorensis (300 mg/kg, orally) once daily for 12 days and Doxorubicin (15 mg/kg) from day 10. Group 5 received Vitamin C (100 mg/kg, orally) once daily for 12 days, and Doxorubicin (15 mg/kg) from day 10. Doxorubicin administration was done intraperitoneally for three consecutive days. Sera samples were collected and used to assess liver function enzymes and synthetic molecules. Liver and spleen tissues were used to examine histopathological analysis. Data were analyzed by SPSS v.20 at a significance level of P<0.05.  

 Administration of Doxorubicin caused significant increase in Alanine Transaminase (ALT), Aspartate Transaminase (AST), Acid Phosphatase (ACP), and total bilirubin (P values below 0.05), and a significant decrease in total protein and albumin compared to the control and J. Tanjorensis administered rats (P values below 0.05). The histopathological evaluation of liver tissue in the Doxorubicin injected rats revealed congestion, hemorrhagic necrosis, sinusoidal dilation, and mononuclear cell infiltration. Similarly, histology of spleen tissue in Doxorubicin administered rats showed degeneration and congestion, disintegrated peri-arteriolar lymphoid sheath, granuloma formation, and necrosis of lymphoid follicles. However, liver and spleen of rats given Doxorubicin and J. Tanjorensis showed reversal of liver function enzymes and synthetic ability towards normalcy, reduced signs of damage as well as recovering peri-arteriolar lymphoid sheath.

 Our study found that J. Tanjorensis is effective in preventing liver and spleen damage caused by Doxorubicin.

Drug resistance is a major challenge in cancer chemotherapy.

By adopting an appropriately timed strategy, we generated MCF-7 cell sublines resistant to serial doses of doxorubicin (DOX). Our higher-dose sublines showed more stability in resistance and were, therefore, subjected to further analyses. We tested the consistency of drug resistance by comparing sublines with control groups for growth and migration capacities. Molecular analyses monitored expression changes, CD44/CD24 ratios, and DOX binding to key molecules. The reverting impact of shikonin (SHKN) and metformin (MTFN) on DOX resistance was examined.

The resistant sublines grew parallel to or even faster than WT MCF-7 cells and showed a larger and more rounded morphology. The consistency of their drug resistance and invasive potential was demonstrated over time using serial doses of DOX. Real-time PCR revealed upregulation of genes involved in cell growth and survival, drug resistance, migration/invasion, and epithelial-mesenchymal transition and, conversely, downregulation of pro-apoptotic, anti-chemoresistance, and tumor suppressor genes. SHKN-MTFN co-treated resistant cells showed significantly lower CD44/CD24 ratios, less aggressiveness, and reduced survival and migration rates but enhanced apoptosis. SHKN’s affinity to CYP1A and TOP2A demonstrated the importance of these interactions and the compounds’ capacity to compete with DOX.

Acquisition of DOX resistance increases tumorigenic properties of cancer cells, whereas synergy between selective anti-tumorigenic compounds re-sensitizes resistant cells by reverting cellular pathways that favor or follow resistance. Our findings suggest that this reversal is supported by competing reactions that deprive DOX of binding to its target molecules.

In the current study, the effects of cerium oxide nanoparticles (nanocerium; NC) on doxorubicin (DOX)-induced cardiomyopathy and its possible underlying mechanisms were addressed.

32 adult male rats were allocated into 4 groups; i) control group, ii) NC group; rats received NC (0.2 mg/kg, i.p., daily), iii) DOX group; rats received DOX 4 mg/kg (2 injections with a 14-day interval), and iv) DOX+NC group as DOX but rats received NC. At the end of the experiment, ECG and ECHO recordings and assessments of the levels of cardiac enzymes (CK-MB, LDH), and myocardial oxidative stress (MDA, catalase, and GSH), the expression of LC3 and beclin1 (markers of autophagy), caspase3 (marker of apoptosis) by immunohistochemistry, the expression of acetyl-CoA carboxylase alpha (ACCA) by PCR, and 5’adenosine monophosphate-activated protein kinase (AMPK) levels in the heart tissues were performed.

The DOX group displayed a prolonged corrected QT interval, an increase in cardiac enzymes (CK-MB and LDH), myocardial oxidative stress (high MDA with low catalase and GSH), expression of ACCA, caspase-3, beclin1, and LC3 in myocardial tissues, with reduction in myocardial AMPK levels, and myocardial contractility (low ejection fraction, and fractional shortening). On the other hand, administration of NC with DOX resulted in significant improvement of all studied parameters.

NC offers a cardioprotective effect against DOX-induced cardiomyopathy. This effect might be due to its antioxidant and antiapoptotic effects as well as to the modulation of autophagy and metabolic dysfunctions induced by DOX in the heart tissues.

Breast cancer is one of the common malignancies in women, for which doxorubicin (DOX) is widely used in its chemotherapy. Recently, it has been found that DOX affects the expression profile of oncogene genes and miRNAs. In this study, the impacts of DOX on the expressions of the STAT3 gene, miR-874-3p, and miR-337-3p were studied in the MCF-7 breast cancer cell line.

After exposure of MCF-7 cells with DOX, the MTT method was applied for evaluating the cell viability. Apoptosis and necrosis percentages were measured using flow cytometry. Also, the levels of ROS and NF-κB were measured in DOX-treated cells. Then, exosomes secreted from these cells were prepared. The shape of exosomes was studied by SEM. Finally, the expression of bax, bcl-2, p53, casp3, STAT3 gene, and miR-874-3p and miR-337-3p in MCF-7 cells as well as exosomes were evaluated using the RT-PCR technique. Data analysis was done by T-test in GraphPad Prism8 software.

The exposure of MCF-7 cells to doxorubicin led to a concentration-dependent decrease in cell viability and increases in apoptosis and necrosis. ROS and NF-κB activity were increased in DOX-treated cells. In DOX-treated cells, decreased expressions of bcl-2 and STAT3 genes and overexpression of bax, p53, casp3, miR-874-3p, and miR-337-3p were observed compared to untreated control cells.

One of the mechanisms of the anti-breast cancer effects of DOX is the induction of changes in the expression of oncogenic genes, mediating by downregulating of STAT3 gene and overexpressing miR-874-3p and miR-337-3p. More studies are needed in this field.

Breast cancer is one of the most common malignancies in women for which no suitable treatment has been found yet. Therefore, the present study studied the cytotoxicity effects of tyrosol (TRY) on the Michigan Cancer Foundation-7 (MCF7) breast cancer cell line and L929 normal cells.

MCF7 and L929 cells were cultured red in DMEM-F12 culture medium after preparation and then exposed to 0, 100, 200, and 300 μM of TRY for 72 hours. Cell viability was evaluated using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay, and apoptotic and necrotic cell percentages were determined by flow cytometry. After designing specific primers, the expression levels of bax, p53, and bcl-2 genes were evaluated by RT-PCR. GraphPad Prism software was used for analyzing the data.

TRY-treated MCF7 cells showed significantly decreased cell viability in a dose-depended manner. Also, the cell treated with high concentrations of TRY (200 and 300 µM) had a high rate of apoptosis and necrosis (P<0.0001). Reactive oxygen species (ROS) content increased in TRY-treated MCF7 cells. Moreover, the overexpression of bax and p53 and downregulation of bcl-2 was seen in TRY-treated MCF7 cells.

TRY has anticancer effects on breast cancer cells by the induction of oxidative stress and apoptosis, as well as the regulation of genes involved in the process of mitochondrial apoptosis.

One of the most potentially hazardous diseases, prostate cancer has a high morbidity and mortality rate. Polymeric matrix drug-eluting implants have become widely employed, and modeling their behavior is becoming more and more prominent. It is always difficult to achieve effective drug delivery and release of it into specific tumor sites. One of the most significant purposes of this investigation, is the enhancement of the anticancer effects of prostate cancer treatment by co-delivering anticancer multi-drugs with PU-PCL films. The films were recognized utilizing SEM  (scanning electron microscopy) while the material was being characterized. In addition, the MTT assay and flow cytometry (Annexin V/PI staining) have been employed to assess cell viability at various times. A dialysis approach was used to investigate the drug release characteristics of DOX and Ezetimibe in films in vitro for 5 days. To optimize pharmacokinetic profiles and reduce systemic toxicity induced by drugs, we loaded polymeric PU-PCL films with ezetimibe (EZ) and doxorubicin (DOX). Co-delivery of EZ and DOX via film-carrier demonstrated improved anticancer effects when compared to free drug delivery. The co-delivery of DOX and EZ drugs by PU-PCL films improved anticancer effects while reducing systemic toxicity, suggesting clinical usage of drug-resistant prostate cancer therapy.

The combination of chemotherapy drugs with angiogenesis inhibitors improves response and survival and reduces the cytotoxic side effects and drug resistance in patients compared to chemotherapy alone. Here, we investigated the efficacy of the concomitant administration of doxorubicin and a peptide derived from the N-terminal domain of Endostatin (called ES-SS) in the 4T1 mammary carcinoma tumor model. Tumor-bearing mice were divided into the control and three treatment groups, including ES-SS, doxorubicin, and the combination. Injections were performed daily for two weeks and tumor volumes were measured during the treatment. Immunohistochemical analysis of Ki-67, CD31, CD34, Bcl-2, p53 expression, and TUNEL assay were performed on tumor tissues at the end of treatment. Besides, molecular dynamics and docking simulations were performed. It was demonstrated that tumor growth was inhibited in mice treated with peptide plus doxorubicin more significantly than in each treatment alone (P<0.05). No weight loss or adverse effects were observed. Moreover, combination therapy was more effective in tumor angiogenesis suppression and apoptosis stimulation (P<0.05). Docking simulations by ClusPro server demonstrated that ES-SS binds to integrin α5β1, Transglutaminase 2, and Matrix metalloproteinase 2 with more negative binding energy and hydrogen bonds compared to the native peptide. Generally, we proposed that ES-SS can augment the therapeutic efficacy of doxorubicin through angiogenesis prevention and apoptosis induction in breast tumor. Owing to the advantages of peptides to recombinant proteins or monoclonal antibodies, further preclinical and clinical evaluations of this combination strategy are worth taking into consideration.

Acute Myeloid Leukemia (AML) is the most common form of acute leukemia among adults. Treatment of acute leukemia has been divided into induction chemotherapy and post-remission therapy. The goal of induction chemotherapy, that consists of anthracycline and cytarabine, is to achieve morphologic complete remission (CR), but the main problem is that it has a high economic burden. Idarubicin is the anthracycline of choice used in AML, while doxorubicin, is mainly used in other types of cancer. The aims of this study were evaluating the use of doxorubicin versus idarubicin in the induction phase for the treatment of AML and analysis the impact of the adoption of this anthracycline in Egypt’s public health system.

A randomized controlled trial was undertaken in 244 patients with AML. A decision tree was developed based on the clinical outcome of the study, safety and efficacy, aiming to get the expected cost of doxorubicin compared with idarubicin in AML management.

In the doxorubicin group, 52.5% had a CR, versus 49.2 % in the idarubicin group (P=0.6). The most common toxicities among the 2 groups were febrile neutropenia, diarrhea and vomiting. Oral mucositis (OM) was higher in the doxorubicin group (70.8% vs 37%, P=0.0001), while invasive fungal infections were greater in the idarubicin group (75% vs 88.7%, P=0.004). Doxorubicin arm had a lower cost than idarubicin arm in treatment success group (39,492 LE vs 44,323 LE).

Doxorubicin provides a treatment option with comparable efficacy, toxicity profile and survival rates at a lower cost compared to the traditional treatment, idarubicin.