The combination of cytotoxics, hormonal agents or radiotherapy with new molecular-targeted therapies represents one of the main strategies to improve survival in solid cancers. A clinical perspective of these agents as monotherapy or combination therapy will be presented in this paper. Copyright Future Drugs Ltd.
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What are drug targeting strategies in cancer treatment?
Drug targeting strategies in cancer treatment: an overview Classic chemotherapy his little or no specificity for cancer cells, normally resulting in low accumulation at the tumor region (inefficacy), and in severe side effects (toxicity).
How can we prevent cancer drug resistance?
1 Combining Cancer Drugs. Researchers believe one possible way to overcome or delay the development of resistance is to treat patients with combinations of different drugs. 2 Keeping Cancer Drugs inside Cells. ... 3 Erasing Reversible Modifications. ... 4 Altering the Tumor Microenvironment. ... 5 Simultaneously Testing Combinations. ...
Which cancer treatments have increased the most in the last 10 years?
In particular, radiomics, immunotherapy and exosomes are the entries whose number has increased the most in the last 10 years. Open in a separate window Figure 2. Cancer clinical trials.
Is cancer medicine becoming more effective and precise?
In recent years, research into cancer medicine has taken remarkable steps towards more effective, precise and less invasive cancer treatments (Figure 1).
What are the treatment strategies for cancer?
Cancer treatment options include:Surgery. The goal of surgery is to remove the cancer or as much of the cancer as possible.Chemotherapy. Chemotherapy uses drugs to kill cancer cells.Radiation therapy. ... Bone marrow transplant. ... Immunotherapy. ... Hormone therapy. ... Targeted drug therapy. ... Cryoablation.More items...•
How can you improve the effectiveness of chemotherapy?
The study suggests that exercise improved blood supply to the tumor tissue, which in turn increased oxygen delivery to the tumors. Increase in blood flow to the tumors could increase drug delivery to the cancers and improve the effectiveness of the chemotherapy drug.
What are the five major forms of effective cancer treatment?
The most common treatments are surgery, chemotherapy, and radiation. Other options include targeted therapy, immunotherapy, laser, hormonal therapy, and others. Here is an overview of the different treatments for cancer and how they work. Surgery is a common treatment for many types of cancer.
What are the 3 primary treatments for cancer in modern medicine?
Some people with cancer will have only one treatment. But most people have a combination of treatments, such as surgery with chemotherapy and/or radiation therapy. You may also have immunotherapy, targeted therapy, or hormone therapy. Clinical trials might also be an option for you.
What is the effectiveness of chemotherapy?
Chemotherapy is a powerful treatment that involves taking medications to damage cancerous cells. The goal is to prevent these cells from dividing and multiplying....Lung cancer.N-SC lung cancer stageTreatment choiceEarly stage (1 & 2)Late stage (3 & 4)Surgery plus chemo and/or radiotherapy16%7%Chemo alone1%18%2 more rows
Which of the method is useful especially treatment of cancer?
Chemotherapy. Chemotherapy is a type of cancer treatment that uses drugs to kill cancer cells.
What are newer strategies being researched to cure or treat cancer?
Personalized vaccines, cell therapy, gene editing and microbiome treatments are four technologies that will change the way cancer is treated. Curing cancer is certainly one of the big challenges of the 21st century.
Where is the best treatment for cancer?
The Top 5 Countries For Cancer TreatmentAustralia. Whilst Australia suffers high levels of certain types of cancers, such as skin, prostate, lung, bowel and breast, it has the lowest cancer mortality rate in the world3 – which is a huge achievement. ... The Netherlands. ... USA. ... Canada. ... Finland.
Which among the following is used in treatment of cancer?
cis−[PtCl2(NH3)2] also known as cisplatin is very effective against treating cancer-causing tumor while the trans isomer, trans−[PtCl2(NH3)2], exhibited little antitumor activity.
Why is cancer treatment so varied?
Over the years, the treatment of patients with cancer has varied widely as much because of recent advancements in science and medicine as the philosophies that belie their use. This paper briefly describes many of the prevailing approaches in use today with an attempt to offer some perspective of how to apply these disparate methodologies so that they may be more effectively integrated, resulting in consistently better clinical responses.
How do supplements help cancer patients?
As a starting point to help my patients who are fighting cancer, there are a few supplements one can use until lab tests and genetic studies are completed. Once the tests and studies are finalized and returned, a more specific treatment strategy can be formulated to address the above hallmarks. Each of these supplements has a multitude of beneficial effects, but chief among them is their ability to stabilize genetics, creating the foundation of an integrative anticancer strategy. During the course of oncogenesis and tumor progression, cancer cells constitutively upregulate signaling pathways relevant to cell proliferation as a result of any number of genetic mutations. It is that genetic instability that leads to cancer being cancer in the first place and it is those mutations which account for the multiple cell lines that compose every tumor.
How does antiangiogenesis help cancer?
Over 60% of tumors create and release vascular endothelial growth factor (VEGF) which is a key pathway for the induction and growth of new blood vessels. Some of the principle stimuli for this production are an anoxic environment, inflammatory molecules, and oncogenic mutations. Once stimulated, the angiogenic switch leads to the cancer cell's expression of proangiogenic factors that increase the tumor's vascularization such as angiogenin, VEGF, fibroblast growth factor (FGF), and transforming growth factor-β(TGF-β). Agents that inhibit this response range from ammonium tetrathiomolybdate (ATM), which chelates the copper that these enzymes need as a cofactor, to EGCG, monoclonal antibodies, and genetically modified bacteria, among other things. Research in this area is very important and promising as it affects a key pathway needed for the progression of cancer as clearly demonstrated by 4D ultrasound [93–97].
What is the role of indole-3-carbinol in cancer?
They target multiple aspects of cancer cell cycle regulation and survival including Akt-NFκB signaling, caspase activation, and cyclin-dependent kinase activities, stabilize estrogen metabolism, normalize estrogen receptor signaling, reduce endoplasmic reticulum stress, and limit BRCA gene expression. DNA hypermethylation is a common feature of cancer genetics. When methylation detox pathways start to fail, certain regions of the genome will accumulate too many methyl groups, such as at CpG promoter regions (segments of the DNA involved in DNA and RNA transcription); this can lead to increased mutagenesis and eventual cancer development. Much research has demonstrated how DIM reduced methylation at 5 CpG promoter regions. For example, in split population studies, mice given TRAMP prostate cancer cells were also given DIM. The mice given the DIM showed a much lower incidence of cancer and metastasis than controls, as well as much higher expression of antioxidant/anticarcinogen protective enzymes NQO1 and NFR2 in prostate tissues [8–14].
How does the immune response cascade work?
The first is to recognize that which is foreign and sound the alarm soon enough to thwart the invader. Molecules and cell surfaces that are identified as foreign are referred to as antigens and have the ability to elicit an immunogenic response. The second directive is to respond to the alarm with enough of a counterattack to effectively neutralize the invader quickly. The third directive is to remember what happened so that if the same situation were to arise again, an effective response could be generated faster. The length and efficacy of the immune response depend upon the “intactness” of the underlying biochemistry. The immune response cascade is the ultimate biological information processing and transfer vehicle designed to define, defend, and integrate oneself relative to the environment that surrounds us. When there is a miscommunication, disease ensues due to corruption, misdirection, or a lack of that informational flow. Immunotherapy is designed to correct, stimulate, direct, or reconstitute an effective anticancer response.
What is the best genetic stabilizer?
First on our list of genetic stabilizers is vitamin D. In addition to enhancing DNA repair, vitamin D also induces growth arrest and apoptosis of tumor cells and their nonneoplastic progenitors. Cell-based studies show that the active metabolite 1,25 dihydroxyvitamin D is the biologically active form that works through the vitamin D receptor to regulate gene transcription. Vitamin D (D3) is produced from 7-dehydrocholesterol when skin is directly exposed to UVB light which, in more northern locations, is largely filtered out by the atmosphere. Vitamin D is readily sourced from various foods including fish, eggs, caviar (for the gourmets among us), some mushrooms, beef liver, and cheese. Regardless of whether vitamin D comes from the skin or the diet, vitamin D3is transported through the blood by the vitamin D Binding Protein (DBP). Once delivered to the liver, vitamin D is hydroxylated on its side chain to form 25 hydroxyvitamin D (25OH D). This is a stable metabolite whose serum levels are commonly used to assess vitamin D status. As needed and if available, D3circulates to the kidneys which is the primary site where the active form of vitamin D, 1,25(OH)2D, is produced through the genomic actions of 1α,25(OH)2via the vitamin D receptor (VDR), and its analogs inhibit cell cycle progression and tumor cell growth. Mechanisms of action range from preventing cell proliferation (cell cycle arrest) in cancer cells to inducing apoptosis or suppressing cell adhesion molecules and growth factors that promote cellular homing and metastasis. It also affords important antioxidant protection and serves as an immunomodulatory for both the innate and adaptive arms of the immune system [3–7].
Why is oxidative therapy important?
Oxidative therapies can be an important adjunctive therapy because tumor hypoxia is an adverse factor for a useful clinical response to chemotherapy and radiotherapy and stimulates the activity of cancer stem cells. Oxidative therapies are the subject of research and clinical trials. An example of an oxidative therapy that directly increases, at least, blood oxygen levels is intravenous ozone therapy. Biochemically CoQ10 has been shown to increase oxygen tension in the blood. The effects of both of these and other agents against cancer have been shown to be helpful in a number of clinical trials but many of the details are yet to be worked out [111–117].
What is targeted cancer treatment?
Targeted therapy is another branch of cancer therapy aiming at targeting a specific site, such as tumour vasculature or intracellular organelles, leaving the surroundings unaffected. This enormously increases the specificity of the treatment, reducing its drawbacks [6].
What are the clinical trials of loaded exosomes?
Three clinical trials with loaded exosomes are currently ongoing for the treatment of different tumours [85–87]: a phase I trial is evaluating the ability of exosomes to deliver curcumin to normal and colon cancer tissues [85]; a phase II trial is investigating the in vivoperformance of autologous tumour cell-derived microparticles carrying methotrexate in lung cancer patients [86] and a clinical inquiry is focusing on autologous erythrocyte-derived microparticles loaded with methotrexate for gastric, colorectal and ovarian cancer treatment [87].
How are exosomes used in cancer?
Exosomes could also be exploited as natural, biocompatible and low immunogenic nanocarriers for drug delivery in cancer therapy. They can be passively loaded by mixing purified vesicles with small drugs [78–82], or actively loaded by means of laboratory techniques, such as electroporation and sonication [83, 84]. Superparamagnetic nanoparticles conjugated to transferrin have been tested for the isolation of exosomes expressing transferrin receptor from mice blood. After incubation with doxorubicin, they have been used to target liver cancer cells in response to external magnetic fields, inhibiting cell growth both in vitroand in vivo[80]. Kim et al.[83] engineered mouse macrophage-derived exosomes with aminoethyl anisamide-PEG to target sigma receptor, overexpressed in lung cancer cells and passively loaded them with paclitaxel. These systems acted as targeting agents able to suppress metastatic growth in vivo.
What are superparamagnetic nanoparticles used for?
Superparamagnetic iron oxide nanoparticles (SPIONs) are usually exploited as contrast agents in magnetic resonance imaging (MRI) because they interact with magnetic fields [29, 30]. Five types of SPIONs have been tested for MRI: ferumoxides (Feridex in the US, Endorem in Europe), ferucarbotran (Resovist), ferucarbotran C (Supravist, SHU 555 C), ferumoxtran-10 (Combidex) and NC100150 (Clariscan). Ferucarbotran is currently available in few countries, while the others have been removed from the market [25]. SPIONs have also been studied for cancer treatment by magnetic hyperthermia (see the “Thermal ablation and magnetic hyperthermia” section), and a formulation of iron oxide coated with aminosilane called Nanotherm has been already approved for the treatment of glioblastoma [31].
Is thermal ablation a precision medicine?
Thermal ablation of tumours and magnetic hyperthermia are opening new opportunities for precision medicine, making the treatment localised in very narrow and precise areas. These methods could be a potential substitute for more invasive practices, such as surgery [10, 11].
How do cancer cells resist treatment?
One way cancer cells resist treatment is by expelling cancer drugs. For example, healthy cells have proteins known as transporters that pump out toxic agents. One such group of proteins, called the ATP-binding cassette (ABC) transporters, expels some chemotherapy drugs, including doxorubicin, and some targeted therapies, like imatinib (Gleevec®).
How many drug combinations did the researchers find that killed cancer cells?
For each cell line, the researchers identified an average of 3.4 drug combinations that effectively killed the cancer cells. For many of the effective drug pairs, they realized that the second drug inhibited a signaling pathway that was able to bypass the effect of the original drug.
How does drug resistance arise?
In addition to arising through genetic alterations, drug resistance can also emerge as a result of alterations in cancer cells' epigenetic codes—molecular modifications that , without altering the DNA code, turn genes on or off. A major difference between epigenetics and genetics is that the epigenetic code is reversible and can shift over time.
How long does it take for cancer to develop resistance?
Sometimes resistance develops quickly, within a matter of weeks of starting treatment. In other cases, it develops months, or even years, later. Resistance can occur when cancer cells—even a small group ...
Why do cancer cells have intrinsic resistance?
Resistance can occur when cancer cells—even a small group of cells within a tumor—contain molecular changes that make them insensitive to a particular drug before treatment even begins. Because cancer cells within the same tumor often have a variety of molecular changes, this so-called intrinsic resistance is common.
Can drug combinations overcome cancer?
Scientists are pioneering many different methods to discover and test novel drug combinations that may be able to overcome multiple mechanisms of resistance or delay their emergence. If these efforts are successful, it could potentially transform cancer for many patients.
Can cancer cells adapt to drugs?
In other cases of resistance, cancer cells may adapt to the drug while it is being administered, acquiring molecular changes that allow them to escape its effects.