Moving Away From Classical Chemotherapeutics

Targeted therapy, which first became available in the late 1990s, has had a significant impact on the treatment of cancer. Currently, because of advancement in the field of technology, various types of therapies are discovered to treat cancer. In this essay, targeted therapy is defined as a therapy in which various drugs or other substances are used to recognize and kill the cancerous cells without harming the normal cell (National cancer institute, 2014). Effectiveness refers to the degree in

A new compound CU466 is a potential potent inhibitor of Dihydrofolate Reductase to treat methotrexate-resistant breast cancer

A team from the Brazilian university says the experimental drug binds with tumor cells and causes the loss of key molecules.

According to the American Society of Clinical Oncology, in a little over a decade, cancer will become the leading cause of death in the United States. The rate of new cases is expected to increase by 45% by 2030. (Wilson, 2014) Undoubtedly, this comes as no surprise to a populace that has seen an increasing number of their friends and family diagnosed with cancer. It seems to have become an epidemic, affecting both young and old, male and female, and rich and poor. For this reason alone, there is a growing interest in new and more effective treatments in the battle against this disease. Cancer research has vastly improved treatments and outcomes over the previous 50 years, starting with only a handful of treatments half a decade ago, to more than 170 FDA-approved anti-cancer drugs today. (Wilson, 2014) Still, new and better treatments that reduce recovery time and increase success rates are constantly pursued. There is promise for new technology called the iKnife, a cancer “sniffing” surgical scalpel; which is said to identify all of a the cancerous parts of a tumor so that it is removed with 100% accuracy. Should the iKnife prove to be what it is promised to be, not only will it improve overall outcomes for patients, it will also revolutionize the treatment of cancer entirely.

Nusrat Epsi, MBA is a PhD student working at the Rutgers University, School of Healthcare Professional with Dr. Antonina Mitrafanova. Prior to beginning the PhD program, Nusrat worked in the Pharmaceutical Industry. She consulted on a variety of projects which involved both qualitative and quantitative analysis to achieve strategic realignments within large pharmaceutical systems. From this work she developed an interest in drug discovery and drug structure. She is currently working on designing possible targeted cancer therapy to interfere with specific AR genes for tumor growth and progression. She also had a primary interest in the invasion of bladder cancer. She is also interested studying other Hormonal carcinogenesis. For her doctoral

This review will provide a brief investigation of current cancer therapies and the lack of effectiveness that these treatments provide while treating the disease. The aim of this review is to discuss the urgent need to develop new and effective cancer therapy options that can bridge the gap between the various types of cancer and effective cancer targeting.

Breast cancer is one of the most common cancers and the second leading cause of cancer-related death among women in the United States. Up to 6% of breast cancers are advanced or metastatic at the time of diagnosis, requiring chemotherapy1, 2. Aberrant, accelerated growth is a hallmark of cancer3, including breast cancer. The rapid expansion of treatments targeted to aberrant cell growth – for example, cell cycle targeted chemotherapies for the treatment of metastatic breast cancer – allows for precise targeting of specific alterations in tumor cell proliferation pathway with the goal of reducing tumor cellular proliferation and increase tumor cell death while minimizing toxicities associated with chemotherapy. The growing application of

Ovarian cancer is the fifth leading cause of cancer-related deaths in females in the United States. It is anticipated that there will be about 22,280 new cases and 14,240 deaths due to ovarian cancer in 2016 [70]. Most patients present with advanced stage disease, contributing to the high death rate. Generally, these patients are treated with surgical resection followed by platinum-based chemotherapy [71]. A significant problem faced in treating these patients is the high rate of recurrence associated with platinum-resistance. Patients with platinum-resistant ovarian cancer carry a poorer prognosis with only 7-20% of them responding to subsequent therapies [72]. This reveals the urgent need for new therapeutic strategies targeted at pathways of tumorigenesis and chemotherapy resistance in the treatment of ovarian cancer.

Despite the numerous advances in recent years, many cancer therapies have retained a focus on cytotoxic chemotherapy or radiotherapy as the main course of treatment in patients with various types of maligancies. This approach is however unspecific in its mechanism, and effects its cytotoxic mechanism on healthy patient cells as well as cancer cells, causing a variety of secondary health problems and side effects in the patients, the most obvious and commonly observed being hair loss and an abnormal Full Blood Count profile (thrombocytopenia, for example).

Cancer is the uncontrolled growth of cells, and is a major cause of death throughout the world. The development of cancer chemotherapeutics began in the 1940s [Shewach, D. and Kuchta, R, 2009] and very early drugs were based on nitrogen mustards, agents similar to mustard gas. Sulphur mustard gas was used as chemical warfare in World War I (WWI), and this led to new approaches for cancer therapeutics. These traditional chemotherapeutic compounds however, can attack cell division in a cancerous, as well as a normal cell, as tumour and normal cells share the same DNA. This leads to several serious side effects. Newer chemotherapeutics, such as the use of monoclonal antibodies, target specific differences between tumour and normal tissue, and therefore do not exhibit such toxicities [Shewach, D. and Kuchta, R, 2009]

Cancer is the main cause of growing mortality all over the world , it is expected that there will be 19.3 million new cancer cases yearly projected for 2025 [1]. Yearly over a million cases of death worldwide is due to breast cancer [2]. Both environmental and genetic factors play an important role in cancer susceptibility [3, 4]. The cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways could produce carcinogenic synergies [5]. Current treatments for cancer include surgery, hormonal therapy, radiotherapy and targeted therapies. Molecular target therapies have a great role in the treatment of cancer, they include inhibitors of the tyrosine kinase enzyme BCR-ABL, inhibitors of vascular endothelial growth factor receptor (VEGFR) and epidermal growth factor receptor (EGFR) inhibitors

Cancer chemotherapy inhibits cancer via several potential mechanisms for example induces cell death, trap cell growth at certain stage, or induce cell differentiation.

In contrast to a decade ago, we’ve seen an explosion of new drugs and virtually all of these drugs are targeted therapies. The substantial increase in the transition of FDA approvals from standard chemotherapeutics to targeted therapies is also equally astounding (Martino et al., 2015). The traditional chemotherapeutic agents are simply not being developed with the same frequency by drug companies any more. While chemotherapeutics have had a real impact and in some diseases a dramatic impact, for most common solid tumours, these impacts have been minimal. Moreover, standard chemotherapy often results in collateral damage to healthy cells causing unwanted side effects while targeted therapies are associated with fewer and less toxic side

Traditional and modern approaches to cancer therapy all act by exploiting some molecular abnormality that distinguishes cancer cells from healthy living cells. Cancer cells often acquire defects in the cell-cycle control systems that normally respond to DNA damage by activating apoptosis (programmed cell death) hence cancerous cells continue to grow and multiply despite containing faulty DNA, making them genetically unstable. Genetic instability may refer to any combination of genome mutations that cause irregularities in the cell cycle, particularly replication, and may include substitutions in the nucleic acid sequence, chromosomal rearrangements and aneuploidy – where the number of chromosomes differs from the standard haploid cell by

For all my life, due to rapid increase in the number of cancer patients and my fear of it, I was thinking about a new way to find a drug that can treat it without major side effects. That's why I planned to study pharmacy to be aware of cancer biology and latest approaches for it's treatment. Then I decided to continue my studies and to get my masters in the field of Molecular Biology so I can perform researches and try to find a new treatment for this disease.