Testimonial By Nasim Sarrami

Read what our Authors have to say about publishing in our Journal

Nasim Sarrami


Journal Name: Anti-Cancer Agents In Medicinal Chemistry

Contributed Article:  LHRH Targeted Chonderosomes Of Mitomycin C In Breast Cancer: An In Vitro/ In Vivo Study

Press Release | Frontiers in clinical drug research — Anti-cancer agents, now in its 5th edition


This eBook is authored by Dr. Ata-ur-Rahman, published on June 12, 2019.

For Further Details, Please visit https://ebooks.benthamscience.com/book/9789811405150/


Frontiers in Clinical Drug Research – Anti-Cancer Agents brings updated and critical information about developing clinical trials and research in anti-cancer research. Reviews in each volume are written by experts in medical oncology and clinical trials research and compile the latest information available on special topics of interest to oncology researchers.

The fifth volume of the series features reviews on biochemical inhibitors (second-generation protein kinase Inhibitors, histone deacetylase inhibitors, immune checkpoint inhibitors, EGFR Tyrosine Kinase inhibitors, non-coding RNAs), apoptosis, and physical exercise therapy for cancer patients undergoing chemotherapy. The treatment strategies in this volume cover neoplasms such as acute myeloid leukemia, gastrointestinal cancer, breast cancer and lung cancer. Read full press release to find out more at: https://www.eurekalert.org/pub_releases/2019-06/bsp-fic062019.php

Press Release | Impact of a psycho-educational team in early breast cancer patients’ coping strategies


Cancer is a psychologically traumatic experience for affected individuals. Chemotherpautic medications can also be painful to the same patients. Researchers at Fondazione Poliambulanza, Brescia, Italy conducted a psycho-educational study on early stage breast cancer patients. The main objective of the study was to help women to cope with the physical emotional, and lifestyle changes after the diagnosis of breast cancer by evaluating the effect of group action on the participating women. A total of 97 women, participated in the study and were grouped into in 13 psycho-educational groups. All the groups consisted of female patients suffering from breast cancer with no recurrence or metastasis.

All the patients were evaluated using the Hospital Anxiety and Depression Scale (HADS) and the Body Image Scale (BIS). No significant effect on anxiety and body image was found by the researchers. They, however, noted a statistical difference between the results of the HADS depression test at T0 (first evaluation) and T1 (second evaluation) intervals. Read full press release to find out more at: https://www.eurekalert.org/pub_releases/2018-12/bsp-ioa122718.php




This article by Dr. Fausto Meriggi et al. is published in Reviews on Recent Clinical Trials, Volume 13, Issue 4, 2018. To obtain the article, please visit: http://www.eurekaselect.com/161134


Press Release | Fighting to Find Relief: A new study shows decrease in depression in cancer patients


A New Study Published by Bentham Science Shows Support Groups and Educational Resources Can Decrease Depression in Breast Cancer Patients


1 in 8 women in the US will be diagnosed with breast cancer in their lifetime.

In 2018 alone, an estimated 266,120 new cases of breast cancer were diagnosed nationwide. As the numbers of new cases grow, the support network of women who suffer from breast cancer grows. In their ever-increasing numbers, the many women diagnosed with this disease face an arduous physical and emotional journey on their road to recovery, and along the way, many suffer from depression, anxiety, and body image issues.

Regardless of the prevalence of body image issues, anxiety, and depression in women who are suffering from breast cancer, there aren’t a lot of resources available for those afflicted. A recent study suggests it’s time to right that wrong. The study, published by Bentham Science, focused on Dr. Fausto Meriggi and his team at Fondazione Poliambulanza di Brescia who studied the effects of psychotherapeutic and educational groups on depression, anxiety, and body image issues among women suffering from breast cancer.


This study was published in Reviews on Recent Clinical Trials, a journal published by Bentham Science.  Bentham Science continues their work in the Middle East and North Africa, bringing education materials and increased accessibility to the region.


Read full press release to find out more at: http://bit.ly/2E6ZBah

Press Release | Estrogen is a much more effective anticancer agent than antiestrogens


This article by Prof. Zsuzsanna Suba is published in Recent Patents on Anti-Cancer Drug Discovery, Volume 12, Issue 2, 2017

Antiestrogen treatment was introduced into breast cancer therapy based on the presumed carcinogenic capacity of endogenous estrogen hormones. In antiestrogen resistant breast cancers, increased expression and activity of estrogen receptors (ERs) is regarded as a survival technique, presuming that increased estrogen signaling is an absolutely proliferative stimulus. Unexpectedly, among certain circumstances, estrogen treatment is capable of inducing apoptotic death in tumors, even in antiestrogen resistant ones justifying the strong apoptotic capacity of estrogen. Analysis of the results of studies on both estrogen and antiestrogen treated tumors may clarify the associations among artificial ER blockade, compensatory restoration of ER signaling and the clinical behavior of cancers.

Inherited BRCA1/2 mutations may be regarded as pathologic models of defective estrogen signaling. In BRCA mutation carriers, the liganded activation of ERs is weak, while an increase in unliganded ER activation results in a more or less compensatory upregulation of ER signaling. Mutation carriers exhibit failure in their ovarian functions, while their risk for cancer is strongly increased (for breast cancer in particular). In cases carrying BRCA mutation, an increase in estrogen levels via either endogenous estrogen synthesis in pregnancy or exogenous estrogen administration via contraceptive use may reduce the risk of cancer development.

Estrogen activated ERs are the principal initiators and organizers of DNA stabilization. ERs work in an upregulative circuit with CYP19 aromatase enzyme and genome safeguarding proteins including BRCAs. The upregulative circuit ensures a strong DNA protection during the proliferation of healthy cells, whilst inducing apoptotic death in spontaneously initiated malignant cells in a Janus faced manner. By contrast, malignant cell proliferation exhibits a downregulative circuit between the low and/or defective expressions of ER and BRCA proteins. The malfunction of ER signaling is coupled with a damaged control of DNA replication resulting in an unrestrained proliferation of poorly differentiated tumor cells. In conclusion, in patients with cancer, estradiol induced upregulation of ER signaling may be an excellent means for the restoration of genome stabilizer machinery and for inducing apoptotic death in cancer cells.

Estrogen treatment upregulates the remnants of genome stabilizer machinery in breast cancer cell lines so as to induce an apoptotic death. Estrogen administration increases the expression and transcriptional activity of ERs in tumor cells, via both liganded and unliganded pathways. In patients, of all examined tumor markers, an increased expression of ERs in their breast cancer defines the prolonged survival. Moreover, the activation of ER-alpha at Ser 167 in tumors is indicative of longer disease free and overall survival in breast cancer patients.

Estrogen treatment induces ESR1 gene amplification resulting in higher expression levels of ERs in breast cancers. Patients exhibiting ESR1 gene amplification in their tumors, experience longer disease free survival than those without it.

Estradiol treatment mediates an increased expression of long non coding RNAs (lncRNAs) including HOTAIR in breast cancer cells. HOTAIR is capable of epigenetic gene modifications resulting in necessary activating mutations in the ESR1 gene. Patients with increased HOTAIR expression in their tumors were found to have lower risks for relapse and mortality than those showing low HOTAIR expression.

Estradiol treatment increases aromatase expression and activity in breast cancer cells in a dose dependent manner. Estradiol activated ERs strongly upregulate the estrogen synthesis of aromatase enzyme so as to increase estrogen signaling and to induce consequential DNA restoration and apoptotic death. Among breast cancer cases, a direct correlation was experienced between the aromatase activity of removed tumors and the patient’s survival time after surgery. Moreover, among young women with breast cancer, the absence of CYP19 aromatase activity in their surgically removed tumors carried a high risk for local cancer recurrence.

Estrogen treatment induces an upregulated expression of DNA safeguarding BRCA1 protein in breast cancer cell lines. In turn, it was found that the BRCA1 protein promotes ESR1 gene activation and transcriptionally upregulates ER-alpha expression in tumor cells. These correlations justify that ER-alpha and BRCA1 protein work in close partnership in the DNA stabilization process which provides apoptotic stimuli for breast cancer cells.

In conclusion, treatment with estrogen may strongly upregulate both estrogen signaling and DNA safeguarding in breast cancers promoting tumor responses. In antiestrogen responsive tumors, the blockade of liganded ER activation via either tamoxifen or aromatase inhibitor, provokes compensatory overexpression and hyperactivity of both ERs and aromatase enzyme via unliganded activations of partially blocked ERs. This compensatory activation of estrogen signaling may restore DNA stability promoting tumor responses. By contrast, in antiestrogen resistant tumors, a long term, exhaustive tamoxifen or aromatase inhibitor treatment induces a compensatory extreme upregulation of ER signaling; however, it may be insufficient to break through the near complete, artificially induced ER blockade. Antiestrogen resistant tumors exhibit a rapid growth in spite of the continuous administration of antiestrogens.


Browse the Article at: Activating Mutations of ESR1, BRCA1 and CYP19 Aromatase Genes Confer Tumor Response in Breast Cancers Treated with Antiestrogens

Article by Disease | Design, Synthesis, and Biological Evaluation of New Azole Derivatives as Potent Aromatase Inhibitors with Potential Effects against Breast Cancer

Bentham Oncology Collection | Oncology | Breast Cancer


Graphical Abstract:


Purpose: Some aromatase inhibitors are FDA-approved agents as first-line therapy in the treatment of endocrine-responsive breast cancer. In this study, we aimed to develop new azole derivatives with higher specificity and potency.

Methods: New aromatase inhibitors were designed by Molecular Operating Environment (MOE) software and synthesized in a one-step SN2 reaction. These compounds were characterized by melting point, 1H- and 13CNMR, elemental analysis and mass spectra. The in vitro and in vivo aromatase inhibition of these compounds was evaluated using the Estrone ELISA assay, and by measuring the inhibition of androstenedione-induced uterine hypertrophy. The selectivity of aromatase inhibition was investigated by the inhibition of ACTH stimulation on the plasma concentrations of aldosterone and cortisol.

Results: Docking simulations showed that four new azole derivatives could efficiently interact with enzyme active sites. The in vitro aromatase-inhibition assay showed that the compounds 1,3,5-tris(imidazol-1- ylmethyl)benzene (3b) and 1,3-Bis(imidazole-1- ylmethyl) benzene (3d) effectively inhibited aromatase, with IC50 values of 0.2 nM and 6.8 nM, respectively; these values were similar to known aromatase inhibitor letrozole (IC50 0.3 nM). The in vivo aromatase-inhibitory potency of compound 3b was similar to letrozole, although compound 3b acted more selectively.

Conclusion: This report introduced a new compound that can be considered as a new lead for further investigation to explore more-potent and more-selective aromatase inhibitors.



Read out more at: http://www.eurekaselect.com/node/159088/article

Article by Disease |Design, Synthesis and Anti-breast Cancer Activity of Some Novel Substituted Isoxazoles as Anti-breast Cancer Agent

Bentham Oncology Collection | Oncology | Breast Cancer

Graphical Abstract:




Methods: A novel series of isoxazole (S21-S30) derivatives were designed, synthesized and screened for their anticancer activity against estrogen receptor-positive MCF-7 and negative MDA-MB-435 breast cancer cell lines. The synthesized derivative has the ability to inhibit the growth of the human breast cancer cell line at low concentrations. In vivo anticancer activity was performed on virgin female sprague dawley rats.

Results: The result shows that compound S23 has more selectivity and marked estrogen modulator activity than the standard tamoxifen.


Open Access Articles – Oncolytic Virotherapy for Breast Cancer Treatment

Journal Name: Current Gene Therapy

Author(s): Samia M. O`Bryan, J. Michael Mathis*.


Breast cancer continues to be a leading cause of mortality among women. While at an early stage, localized breast cancer is easily treated; however, advanced stages of disease continue to carry a high mortality rate. The discrepancy in treatment success highlights that current treatments are insufficient to treat advanced-stage breast cancer. As new and improved treatments have been sought, one therapeutic approach has gained considerable attention. Oncolytic viruses are uniquely capable of targeting cancer cells through intrinsic or engineered means. They come in many forms, mainly from four major virus groups as defined by the Baltimore classification system. These vectors can target and kill cancer cells, and even stimulate immunotherapeutic effects in patients. This review discusses not only individual oncolytic viruses pursued in the context of breast cancer treatment but also the emergence of combination therapies with current or new therapies, which has become a particularly promising strategy for treatment of breast cancer. Overall, oncolytic virotherapy is a promising strategy for increased treatment efficacy for advanced breast cancer and consequently provides a unique platform for personalized treatments in patients.

For more details, please visit: http://www.eurekaselect.com/165254

EDITOR’S CHOICE ARTICLE – Arachidonic Acid Induces the Migration of MDA-MB-231 Cells by Activating Raft-associated Leukotriene B4 Receptors

Journal Name: Clinical Cancer Drugs

Author(s): Atasi De Chatterjee, Debarshi Roy, Priscilla Guevara, Rituraj Pal, Mahesh Narayan, Sukla Roychowdhury, Siddhartha Das*.




Graphical Abstract:




Background: The migration of tumor cells is critical in spreading cancers through the lymphatic nodes and circulatory systems. Although arachidonic acid (AA) and its soluble metabolites have been shown to induce the migration of breast and colon cancer cells, the mechanism by which it induces such migration has not been fully understood.

Objective: The effect of AA on migratory responses of the MDA-MB-231 cell line (a triple-negative breast cancer cell) was examined and compared with MCF-7 (estrogen-receptor positive) breast cancer cells to elucidate the mechanism of AA-induced migration.

Methods: Migrations of breast cancer cells were examined with the help of wound-healing assays. AA-induced eicosanoid synthesis was monitored by RP-HPLC. Cellular localizations of lipoxygenase and lipid rafts were assessed by immunoblot and confocal microscopy.

Results: AA treatment stimulated the synthesis of leukotriene B4 (LTB4) and HETE-8, but lowered the levels of prostaglandin E2 (PGE2), prostaglandin D2 (PGD2), and HETE-5 in MDA-MB-231 cells. Further analysis indicated that AA increased the expression of 5-lipoxygenase (5-LOX) in this cell line and inhibiting its expression by small molecule inhibitors lowered the production of LTB4 and reduced migration. In contrast, MCF-7 cells did not show any appreciable changes in eicosanoid synthesis, 5-LOX expression, or cellular migration.

Conclusion: Our results suggest that AA treatment activates the BLT1 receptor (present in membrane microdomains) and stimulates the synthesis of LTB4 production, which is likely to be associated with the migration of MDA-MB-231 cells.



For more details, please visit: http://www.eurekaselect.com/161381/article

PRESS RELEASE – Trastuzumab (Herceptin) and the risk factors for its toxic effects on the heart

Research article: Toxicology of Trastuzumab: An Insight into Mechanisms of Cardiotoxicity

This article by Dr. M. Saeed Sheikh and Dr. Jie An is published in Current Cancer Drug Targets, Volume 18, 2018

Trastuzumab (Herceptin) is a monoclonal antibody for the treatment of breast and stomach cancers. Although trastuzumab is a valuable therapeutic, its toxicity on the heart remains a major concern. Trastuzumab mediates such toxic effects via various mechanisms and there are several risk factors for its cardiotoxic effects. Single nucleotide polymorphisms for HER2 gene are of particular interest as risk factors because of their predictive value to improve the utility of trastuzumab via pharmacogenomics and pharmacogenetics approaches.

Trastuzumab (also known as Herceptin) is a humanized monoclonal antibody that is used for the treatment of breast and stomach cancers. Trastuzumab binds to cell surface molecule HER2, a member of the Epidermal Growth Factor Receptor (EGFR) family. Increased levels of HER2 are noted in breast and gastric cancers. Abnormal levels of HER2 send aberrant signals inside cells that contribute to tumor growth, and trastuzumab blocks these signals thereby mediating the anticancer effects. The mechanisms via which trastuzumab mediates these effects are multifaceted and although it has proven to be a valuable agent, its toxicity on the heart is a major concern. In their scholarly article titled, “Toxicology of Trastuzumab: An Insight into Mechanisms of Cardiotoxicity”, Drs. An and Sheikh have reviewed the possible mechanisms by which trastuzumab could potentially mediate its toxic effects on the heart. The authors have also discussed the potential risk factors for trastuzumab-induced cardiac toxicity.

Trastuzumab has a box warning about its toxic effects such as “cardiomyopathy, infusion reactions, embryo-fetal toxicity and pulmonary toxicity”. Congestive heart failure, significant decrease in left ventricular cardiac function, serious infusion reactions, and pulmonary toxicity are the serious situations warranting temporary or complete stoppage of trastuzumab use.

In the heart, HER2 (the trastuzumab’s target) and other members of the EGFR family such as HER4 and HER3 have important physiological functions.  The heart endothelial cells secrete Neuregulin 1 (NRG-1) that binds to HER4 and HER3 and induces their dimerization with HER2, and consequently activates PI3K/Akt, MAPK and Src/FAK pathways. Activation of these signaling pathways serves to confer protective effects on the heart, and trastuzumab by binding to HER2 could potentially disrupt these protective effects. Trastuzumab-mediated cardiotoxic effects may also involve inhibition of anti-apoptotic pathways and increase in angiotensin II (ANGII). ANGII is suggested to inhibit the protective effects of NRG-1. Additional mechanisms appear to involve inhibition of expression of genes associated with DNA repair, cardiac and mitochondrial functions. Inhibition of stem cells and autophagy in the heart is also implicated.

Several risks factors have been implicated in trastuzumab-mediated toxic effects on the heart. Co-treatment with anthracyclines such as doxorubicin or epirubcin, or prior history of their use is associated with enhanced risk of trastuzumab cardiac toxicity. Renal dysfunction, alcohol consumption, hypertension, diabetes, older age and the history of heart disease are also risk factors for the toxic effects of trastuzumab on the heart.

Single nucleotide polymorphisms (SNPs) for HER2 gene are additional risk factors. Two SNPs including rs1136201 and rs1058808 in the coding region of HER2 are of note. The rs1136201 is associated with a change at codon 655 that results in valine residue in place of isoleucine consequently affecting the transmembrane domain of the HER2 receptor. The rs1058808 is linked to a change at codon 1170 that leads to alanine in place of proline thereby affecting the tail region of HER2 protein. These SNPs have the potential to affect the function of HER2 receptor. In certain patients, these polymorphisms are associated with trastuzumab-induced toxic effects on the heart. Additional studies particularly those involving pharmacogenomics and pharmacogenetics approaches are needed to further refine the patient population with these SNPs at risk of developing the toxic effects of trastuzumab. In the future, pharmacogenetic tests can be developed to harness the predictive value of these polymorphisms and to improve the utility of trastuzumab, which is an effective cancer therapeutic.


%d bloggers like this: