Indian Biological Sciences and Research Institute, located in NCR, Noida and it is QCI(Quality Council Of India body of Government of India) an ISO 9001-2008 certified institute and it is and unit of Exordior Technical Services Private Limited.IBRI is an institute of its own kind as it is governed and managed by academician and professionals from different fields i.e Bioinformatics, Biotechnology, Pharmacy, IT, Clinical Trials etc. forming the backbone of the institute for its success.
Wednesday, May 21, 2014
Database and Website Development by Ariff at IBRI
DATABASE OF MEDICINAL PLANTS
Welcome to the Cancer Phytotherapy Service.We are here to provide you with all the information
you need about phytotherapy for controlling cancer.This is complementary approach perhaps shows
the future of cancer treament especially when metastasis starts.
Phytotherapy is a form of medical treatment which relies on the use of plants, either whole or in the form of prepared extracts and essences. For thousands of years, plants were a primary source of therapeutic medication for cultures all over the world. With the 20th century came the development of synthesization techniques and totally synthetic drugs, causing phytotherapy to fall out of popularity. However, plants still have a very important place in medicine, and they will continue to do so well into the foreseeable future.
This technique involves the study of plants to determine their properties, and the careful application of plants to treat medical problems. Herbal medicine is a form of phytotherapy, and many of the remedies used in homeopathy are also phytotherapeutic in origin. Extracts of plants are also used in the preparation of some commercial pharmaceuticals, as are synthetic drugs which are based on compounds found in plants. Researchers are also constantly studying plants to find new pharmaceutical compounds and potential applications for them.
Quality and safety are also important issues in phytotherapy. Producers want to make products of high quality and reliability so that practitioners will feel comfortable prescribing them, and patients will feel comfortable using them. Due to the lack of regulation over herbal preparations in many nations, reputable producers must also be able to police themselves to confirm that their products are safe for use.
Chemical companies with a vested interest in finding new drugs have scoured the world seeking for new sources of plant material used by indigenous people or as cottage remedies in the treatment of cancer. There have been hundreds of indigenous plants used in traditional therapies in various countries throughout the world over past centuries. Some of them have been tested and are still being trialled in current efforts to find a way of curing cancer, now recognized as a difficult exercise because of the complex nature of the disease.Modern research proves the efficacy of some plants such as astragalus, eleutherococccus, shisandra and shiitake mushroom and many of the plants used traditionally in herbalism.However, there are many more employed by traditional herbalists that can be included in the range of plant material offering value in therapy, sometimes used in herbal extract, sometimes as food, and sometimes as homoeopathic doses.There are particular plants that affect certain types of cancer by improving specific physiological functions. No magic overall formula has been found so far that is applicable to all types of cancer. However, medical and herbal research continues. The University of Wisconsin, for instance lists 150 plants which they have established as having potential value in the treatment of cancer.
Cancer is a genetic disease characterized by uncontrolled cell growth in the absence of cell cycle regulation. Aberrant cell cycle regulation can arise as a consequence of DNA damage. Under normal physiological conditions the uncontrolled growth of damaged cells is restricted by apoptosis. However these cells can escape the regulatory mechanisms of apoptosis as a result of secondary mutations to genes that regulate apoptosis. This DNA damage can be a result of several environmental factors such as stress, smoking, pollution, diet, toxins and endogenous processes such as errors in replication of DNA and chemical instability of certain DNA bases.
Genetics of Cancer
Only a small number of the approximately 35,000 genes in the human genome have been associated with cancer. Alterations in the same gene often are associated with different forms of cancer. These malfunctioning genes can be broadly classified into three groups. The first group, called proto-oncogenes, produces protein products that normally enhance cell division or inhibit normal cell death. The mutated forms of these genes are calledoncogenes. The second group, called tumor suppressors, makes proteins that normally prevent cell division or cause cell death. The third group contains DNA repair genes, which help prevent mutations that lead to cancer. Proto-oncogenes and tumor suppressor genes work much like the accelerator and brakes of a car, respectively. The normal speed of a car can be maintained by controlled use of both the accelerator and the brake. Similarly, controlled cell growth is maintained by regulation of proto-oncogenes, which accelerate growth, and tumor suppressor genes, which slow cell growth. Mutations that produce oncogenes accelerate growth while those that affect tumor suppressors prevent the normal inhibition of growth. In either case, uncontrolled cell growth occurs.
Oncogenes and Signal Transduction
In normal cells, proto-oncogenes code for the proteins that send a signal to the nucleus to stimulate cell division. These signaling proteins act in a series of steps called signal transduction cascade or pathway. This cascade includes a membrane receptor for the signal molecule, intermediary proteins that carry the signal through the cytoplasm, and transcription factors in the nucleus that activate the genes for cell division. In each step of the pathway, one factor or protein activates the next; however, some factors can activate more than one protein in the cell. Oncogenes are altered versions of the proto-oncogenes that code for these signaling molecules. The oncogenes activate the signaling cascade continuously, resulting in an increased production of factors that stimulate growth. For instance, MYC is a proto-oncogene that codes for a transcription factor. Mutations in MYC convert it into an oncogene associated with seventy percent of cancers. RAS is another oncogene that normally functions as an “on-off” switch in the signal cascade. Mutations in RAS cause the signaling pathway to remain “on,” leading to uncontrolled cell growth. About thirty percent of tumors including lung, colon, thyroid, and pancreatic carcinomas have a mutation in RAS.
The conversion of a proto-oncogene to an oncogene may occur by mutation of the proto-oncogene, by rearrangement of genes in the chromosome that moves the proto-oncogene to a new location, or by an increase in the number of copies of the normal proto-oncogene. Sometimes a virus inserts its DNA in or near the proto-oncogene, causing it to become an oncogene. The result of any of these events is an altered form of the gene, which contributes to cancer. Think again of the analogy of the accelerator: mutations that convert proto-oncogenes into oncogenes result in an accelerator stuck to the floor, producing uncontrolled cell growth. Most oncogenes are dominant mutations; a single copy of this gene is sufficient for expression of the growth trait. This is also a “gain of function” mutation because the cells with the mutant form of the protein have gained a new function not present in cells with the normal gene. If your car had two accelerators and one were stuck to the floor, the car would still go too fast, even if there were a second, perfectly functional accelerator. Similarly, one copy of an oncogene is sufficient to cause alterations in cell growth. The presence of an oncogene in a germ line cell (egg or sperm) results in an inherited predisposition for tumors in the offspring. However, a single oncogene is not usually sufficient to cause cancer, so inheritance of an oncogene does not necessarily result in cancer.
Causes of Cancers
The prevailing model for cancer development is that mutations in genes for tumor suppressors and oncogenes lead to cancer. However, some scientists challenge this view as too simple, arguing that it fails to explain the genetic diversity among cells within a single tumor and does not adequately explain many chromosomal aberrations typical of cancer cells. An alternate model suggests that there are “master genes” controlling cell division. A mutation in a master gene leads to abnormal replication of chromosomes, causing whole sections of chromosomes to be missing or duplicated. This leads to a change in gene dosage, so cells produce too little or too much of a specific protein. If the chromosomal aberrations affect the amount of one or more proteins controlling the cell cycle, such as growth factors or tumor suppressors, the result may be cancer. There is also strong evidence that the excessive addition of methyl groups to genes involved in the cell cycle, DNA repair, and apoptosis is characteristic of some cancers. There may be multiple mechanisms leading to the development of cancer. This further complicates the difficult task of determining what causes cancer.
Posted by:Indian Biological Sciences and Research Institute, NOIDA