Mitch McVey, Assistant Professor of Biology, and his team of researchers report that PolQ (DNA polymerase theta) could promote a wrong repair process, supposed to be the cause of mutations, cell death and even cancer. The research has been published in the open-access PLoS Genetics journal, the 1st of July edition.

Scientists have been aware for many years that the DNA polymerase theta is in a way related to cancer development, but the exact cellular role it has is difficult to reveal, according to McVey. It is known that its action during incorrect DNA repair might have implications for those biologists who analyze genomic modifications associated with cancer.

The DNA molecule is double stranded and shaped in the form of a spiral staircase. The two strands are connected together by nucleotides like adenine, cytosine, guanine and thymine, which naturally complement each other. Under normal circumstances, a guanine nucleotide corresponds to a cytosine, while an adenine corresponds to a thymine.

During a cell’s life, it may occur that the staircase is cut off into two molecules. The breaks are to be repaired if cells are supposed to replicate accurately and transmit their genetic material. An important part of these breaks is fixed fast and accurately during a process named HR (homologous recombination). This process uses for repair a template formed of an intact DNA copy. There is, however, a second process, named end-joining repair, which is susceptible of errors. It stitches back together the broken stranded ends without considering the original sequence. Thus, the ends of the strands may be modified by addition or removal of little DNA segments that could alter the genomic architecture.

Mitch McVey and Amy Marie Yu, a doctoral student, have demonstrated an alternative structure of end-joining after studying how repair goes on when DNA ligase 4 is absent. DNA ligase 4 is an important protein which connects together two broken ends of DNA.

Two things have been observed during the analysis of breaks inaccurately repaired in Drosophila melanogaster, the fruit fly. One thing was that extra nucleotides were added to the DNA strands were the breaks were present. Secondly, the insertions were tightly related to the DNA original sequences that were adjacent to the breaks.

The authors have shown that polymerase theta has a dominant role to play in the alternative repair process. It reads first the genetic material present in the DNA neighboring the break and constructs a copy of its structure. The copy of the DNA is then used as a molecular sliver which holds together the ends of the broken strand until they are able to join permanently. The PolQ protein is also believed to be able to unwind the sequences of DNA in the neighborghood of a break and this way facilitates alternative end-joining.

Levels of the protein have been demonstrated to be higher in many types of tumors present at the human, as other groups of researchers have previously shown. McVey’s team is currently working to find out if an alternative type of end-joining depending on the PolQ protein is eventually involved in human cancer. If this is found to be true, then there would be a new target for developing new cancer drugs and this would be the PolQ protein. The first goal of the team is to establish which parts of the protein are playing an active role in alternative end-joining. This could give the team a road map for studying how the activity of the protein has to be altered in order to achieve the expected results.

The National Science Foundation together with the Ellison Medical Foundation has funded the work of McVey’s team.

The investigation was released in the Cancer Research journal in its October edition. The investigators from the University of Texas Southwestern Medical Center discovered that if they gave the mice the BEZ235 medication prior to undergoing harmless radiation in order to counteract the cancerous cell development of DNA, the BEZ235 would counteract the activity of the PI3K protein which typically acts as a guardian of the tumor cells. This protein maintains the cancerous cells in life in the moment they are attacked and try to heal their broken DNA.

Besides the leading author, the team of investigators from the University of Texas comprised: doctor Erik Bey from the Harold C. Simmons Comprehensive Cancer Center, doctor Andrea Rabellino, doctor Katja Schuster, doctor Adi Gazdar, professor within the University of Texas Southwestern, Jake Hamon from the Center for Therapeutic Oncology Research, doctor David Boothman from the Simmons Comprehensive Cancer, researchers coming from the University of Camerino in Italy and Novartis Pharma in Switzerland. Their investigation was financed by funds coming from National Institutes of Health, American Cancer Society, Concern Foundation, Gibson Foundation, Leukemia of Texas, United States Department of Energy and the American Italian Cancer Foundation.

The scientists observed this treatment opportunity in mice that underwent a transplant process with non-small cell lung cancer tumors from human beings.

During their observation process, the researchers discovered that the malignant tumors developing in the mice which were treated with just the BEZ235 has a decrease in size compared to those affecting mice which were not undergoing any type of treatments. Even though the malignant tumors did not grow in size, their life was not ended by administering the specific medication.

On the other hand, mice undergoing the BEZ235 treatment combined with low-dose radiation recorded many cases of total elimination of the malignant tumors.

The leading investigator was doctor Pier Paolo Scaglioni who is assistant professor of the internal medicine department within the University of Texas Southwestern. He stated that the findings of his research team regarding the combination of medication and low-dose radiation may prove to become an efficient treatment for counteracting non-small cell lung cancer in human beings.

The non-small cell lung cancer represents one of the main causes of cancer connected mortality on the whole Globe. The malignant cells usually favor transformations in the K-RAS which is a gene. People suffering from mutations of the K-RAS usually present an increased resistance to therapies comprising irradiation. This is the cause for which their life perspectives are unfavorable.

The K-RAS transformations trigger the networks or different pathways of various proteins that act as signals to activate. This signaling represents a key element in the development and growth of a malignant tumor. The PI3K represents just one of these proteins. At the moment of activation, it acts as a guardian which aids the cells in maintaining living functions even after their DNA was damaged and they try to heal it.

Some of the elements forming the signal networks comprising also the PI3K protein have been explored as various medication targets for counteracting malignant tumors. The clinical tested medication BEZ235 has been recently in experiments comprising clinical tests for counteracting the activity of the PI3K and the mTOR which represents a signaling protein, also.

As the leading investigator states there is no efficient treatment counteracting the non-small cell lung cancer which hosts transformations of the K-RAS.

Medical doctor Pier Paolo Scaglioni conducted the first tests in order to identify the efficacy of the BEZ235 drug and thus, they tested it alone. The team of investigators discovered that the BEZ235 stops the evolution and growth of the lung cancer malignant cells that were developed in the laboratory and the malignant lung cells that affect the mice.

As the leading author of this first research, doctor Georgia Konstantinidou states the findings of the investigators were shocking. However, they strived to discover a way for a faster malignant cell deterioration. They found put that by combining the tested medication with low-dose radiation, the success of their mission was assured. Doctor Georgia Konstantinidou is a post-doctoral scientist within the University of Texas Southwestern.

Doctor Pier Paolo Scaglioni`s research group observed that the malignant cells which were treated with the BEZ235 medication and low-dosed irradiation. The latter triggered slight breaks in the cellular genetic material but did not managed to affect them in a more effective way in order to destroy them. At the moment the DNA of the cell is broken, the malignant cells are aided by the PI3K signaling network in order to assure the cancer cell`s survival while it is healing its genetic material.

The team of investigators explained that the malignant cells needed the PI3K signaling pathway to assure they remain alive and without the protein`s response they were prone to die. This is why in the moment the scientists administered the BEZ235 medication it stopped the action of the PI3K protein and this means that the non-small cell lung cancer cells were starting to die.

As the leading author of the research explains the future stage of the study is that of administering the BEZ235 medication or similar drugs in clinical tests against the non-small cell lung suffering human beings. This could also be applied in clinical trials comprising people suffering from other types of malignant cells such as pancreatic, colon and thyroid cancers. There are the same with the non-small cell lung due to the fact that the PI3K signaling network also acts as an important agent in the malignant cells` evolution.

This environmental report is just a part of the process of taking care of the continuous and newly discovered problems regarding the pollutant agents of the environment and cancer. Moreover, the scope of the report is to shed more light on the principles, mission, values, objectives and various roles of the American Cancer Society on issues such as those mentioned before: pollution and malignant tumors prevention.

As the co-chair of the subcommittee and chairman of the Department of Preventive Medicine within the Keck School of Medicine of University of Southern California, medical doctor Jonathan Samet explains the problems regarding the environmental pollution agents affecting the air, water, food and thus, customer products represent issues on general public care and high unknowns. He also adds that their report aims to put the pollution agents of the environment in a greater relationship with preventing malignant tumors. The relationship focuses on reducing the smoking habit of the population, improving nutritional behavior, increasing the physical activities, maintaining a proper body weight and come up with vaccines that counteract the infections which may cause cancers.

The other co-chair of the subcommittee is also volunteer president of the American Cancer Society. Her name is Elizabeth “Terry” T.H. Fontham and she stated that the exposure levels of the population to chemical and pollution agents affecting the environment are much lower than the levels linked to the showed predisposition to developing malignant tumors in the jobs people have and other daily settings. However, the concern raised by the low exposure levels has to do with the fact that the number and types of pollution substances are increasing and may prove in the future to get out of the population`s control. In addition, the problems related to the fact that even low exposure levels bring some contribution to the cancer developing cases cause more reasons for distress considering the high number of persons who are daily exposed to the environmental pollutants.

The subcommittee`s report states that the scientific problems related to the exposure of people to the environmental pollutants represent complex issues just like increase in the number of landscape technologies which are utilized to analyze the chemical carcinogenicity. In spite of the capability of the nowadays tools used to identify and categorize proves for carcinogenicity, the subcommittee`s article states that there exist three main problems which constrain them from using them because there is a limited quantity of resources which are allotted to function those specific systems and from a scientific point of view, the environmental problems are complex and uncertain.

The report`s concerns about cancer vary and are related to malignant tumors prevention. There is a high need for new stratagems related to the tests done to evaluate the environment`s toxicity, comprising also the evaluation of carcinogenicity. These new strategies could be incorporated in such a manner as to assure a more efficient and effective screening process of a higher number of chemical agents which affect people daily. In addition, exposure to occupational and community settings should be regulated by some standards. The subcommittee draws attention on the need to support investigations aimed at identifying and decreasing the number of hazards provoked by carcinogens. Furthermore, the institutions that determine and implement standards for the environment must meet proper financing and appropriate technology in order to be near the scientific evolution and upgrade their set standards according to the new available data.

Even though some exposure cannot be avoided, this type of exposure must be somehow diminished and even stopped in the cases where it is possible to do so. In addition, the population must receive information about these matters in order to know their health status and risk of cancer or other diseases. Last, but not least, the media communication must make people aware of the situation of the exposure in an accurate manner and not to exaggerate or diminish the importance and level of environmental pollution factors.

The subcommittee’s report states that in order to create and implement this new initiative in order to assure the acquiring of more knowledge regarding the association between the levels of exposure to environmental pollution agents and the predisposition to various types of cancers, the American Cancer Society is going to further develop its long-run commitment to preventing malignant tumors. In addition, the American Cancer Society is also keen on studying these problems more thorough in order to discover new ways in which the initiative could bring more benefits in an effective and efficient manner.

The MASCOT project was financed in part by the European Commission (IST-027652).

This device is the first of its kind because it comprises various significant preparation phases for samples and muxing based detection which was created and implemented in the lab-on chip. An interesting fact is that all the module complexes for investigating and mingling with the samples and the detection feature of the gadget are preparing to be even further minimized in order to be incorporated in just one lab-on-chip device. The researchers desire that this complex would become feasible in a medical manner in the Oslo during the studies of breast cancer treatments.

A great thing is that this circulating cancer diagnosis represents an important methodology for a personalized tracking of people who suffer from malignant tumors both in an early development stage and in an advanced one. This, in turn, would lead to an improvement in the physicians and surgeons` decision-making ability.

Taking into consideration breast cancer, 5 milliliters of blood comprise just two or three cells coming from tumors. In order to find out from the blood tests if someone has developed malignant tumors, the malignant cells circulating in the blood flow have to be isolated, caught and their genetics have to be observed.

The nowadays diagnostics done in the labs of the medical facilities are not time- and cost-effective and require a lot of work. This type of diagnosis might ask for a number of processing phases for the sample in various medical tools so the complete analysis of the sample is for sure to take more than 24 hours. On the other hand, the lab-on-chip technology could have many benefits for the entire medical world and the people who are ill. This innovative system is cost-effective, has easy usage and is very fast compared to the past methods. An interesting aspect of this technology is that it does not need medical laboratories and laborious hours. Instead, the tests comprised by the lab-on-chip can be undergone routinely either in the physician`s office or nearby the bed of the sick person. Thus, the lab-on-chip technology represent a time saving opportunity which does not require laborious work do be done in order to get the results to diagnosis tests. Moreover, it provides the minimum of body invasion in order to discover cancer cells and a customized treatment and screening.

The study`s collaborators created a modular platform in which every module performed a specific job and kept its independence. This endowment means that the technology can be utilized in numerous medical tests. The first module of the platform is the incubation one which has the role of mixing the blood under testing with specialized magnetic beads in order to link the tumor cells to one another. The second module has the role to isolate the malignant cells and count them thanks to a magnetic characteristic which can attract each cell and dielectrophoresis function. The third one is entitled the amplification module. It has the role to destroy the wall comprising malignant cells and by doing this the mRNA, the desired genetic material, is taken out from the sample and enhanced by using MLPA (multiplex ligation dependent probe amplification).

In the third module, certain procedures that measure the biochemical substances from the extracted substance enhance approximately twenty markers that are generated in the carcinoma cells of the breast. In the last module used for detection, the enhanced genetic substance is discovered by utilizing a series of electrochemical markers. These modules have been created and are feasible to use on the samples of blood.

The modules are prepared for advanced incorporation in just one lab-on-chip. By minimizing the size and linking the micofluidic and electronic functions of the technology, their accuracy and trustworthy character is enhanced in order to perform tests on sick people. The medical utilization of the lab-on-chip is going to be observed in order to see its similarities and differences compared to the existing methodologies used in the breast cancer treatments. This is going to be accomplished by a new investigation.

In order to complete the research, the multi-organizational group of investigators observed the telomeres of Arabidopsis which is a weed located everywhere around the Globe and found out that it contains a set of proteins that people did not know anything about. After this discovery, the investigators found its human correspondent. This result might prove to be advantageous for comprehending better the nature of cancer and cell`s life span. The investigation`s findings were released in the Molecular Cell journal. The research was financed by the National Institutes of Health.

Professor of biophysics and biochemistry within Texas A&M University, Mrs. Dorothy Shippen and Carolyn Price, her counterpart from the University of Cincinnati College of Medicine, professor of cell biology and cancer, were the co-authors of this investigation.

The telomeres are found in the chromosomes in their every end and comprise DNA and protein. Their primary role is to defend their location and are also essential factors regarding the cellular division process. Scientists also think that telomeres are essential elements in the lifetime duration of the cells.

As Dorothy Shippen states the team of researchers discovered that by removing the telomere proteins from the common weed, its chromosomes would join their ends in an aggressive manner, a process which would trigger significant problems in the Arabidopsis` evolution.

The investigation team proved that by removing just one human protein from the human malignant cells would cause a great DNA defect and the whole loss of some of the telomeres. In addition, the researchers state that they knew that the telomeres were a protective hat for the chromosomes which were a must in inhibiting the chromosomal fusions. Moreover, their length determines the cell`s division number. Nonetheless, the scientists still do not completely comprehend the way the hat structure prevents the chromosomal fusions or how it sets the length of the telomeres. These are considered very important issues due to the fact that if the telomeres are not maintained properly, illnesses like pulmonary fibrosis, premature aging syndromes, aplastic anemia and cancer could develop. The team of investigators aims to find a new protein complex which is needed in order to keep the benefic telomere hat on the chromosomes and they hope that this would lead the way for innovative studied associated with the illnesses affecting human beings.

The common weed, Arabidopsis, is present all over the Globe and is part of the cabbage, radish and mustard plant family of plants. Due to its genetic architecture, the Arabidopsis has been long studied as a standard “lab plant” in researches related to the cells and molecules coming from plants with flowers.

The multi-organizational investigation group states that their discoveries pave the way for new researches, which could end up with an innovative finding regarding the telomeres.

As one of the leading authors explains, future study in this matter would bring more knowledge regarding the telomeres` composition and their functionality. This, in turn, would provide scientists with a chance in finding the precise roles of the telomeres as guardians of the human beings` DNA. In addition, the future research could present the big picture of the manner in which damages to the telomeres inhibit the division process of the cells. Having discovered that the proteins act as essential actors in the DNA replication in the end of the chromosomes, the investigators suggest that new investigations should be undergone in order to gain more knowledge about just how the guardian hats function during the cellular division. As a conclusion, one of the leading investigators states that all these issues have to lead to answers in order to gather a complete understanding of the telomeres` roles in human beings.

The COX-2 (Cyclooxgenase-2) represents an enzyme which synthesizes prostaglandin. An evolved expression of Cyclooxgenase-2 is found in a great variety of malignant tumors affecting human beings which also comprise the gastric cancer. Experiments done on animals revealed that a long-term treatment with medication that inhibits the gastric carcinogenesis related to Cyclooxgenase-2. However, using such inhibiting drugs on humans is still not done due to the fact that the medication can trigger harmful and even fatal cardiovascular side-effects. This is why it is of great importance to discover the best and harmless therapy comprising Cyclooxgenase-2 inhibiting medications that also inhibit the Helicobacter pylori linked to gastric carcinogenesis.

A recent study regarding this matter was released in the World Journal of Gastroenterology in the October edition. Professor Wu coming from the Department of Gastroenterology within the Kaohsiung Medical University Hospital was the leader of the investigation. He utilized the Mongolian gerbil model in order to observe the best point of Cyclooxgenase-2 inhibiting medication for inhibiting gastric carcinogenesis produced by Helicobacter pylori. This new research also takes a closer look at the chemotherapy use for preventing this condition and also at the adverse effects the Cyclooxgenase-2 inhibiting medication may produce to the human body.

Earlier investigations utilized chemotherapies on a long-run basis for preventing the gastric carcinogenesis. Nonetheless, the Cyclooxgenase-2 inhibiting drugs did not come in placebo format and affected the patients. This group of medications must not be utilized on a long-run basis in the chemoprevention of the gastric malignant tumors.

As the investigation pointed, Celecoxib is a drug which might trigger anti-oncogenic effects. It can also inhibit the angiogenesis and the spreading of malignant tumors in the whole body. Moreover, this medication proved to be efficient in obtaining these effects either if it was used on a short- or a long- term basis. Celecoxib acted as a guardian who connotes an early oncogenic stage and not an inflammatory one. In addition, the utilization on short-term of Celecoxib proved to bring harmless inflammations and also stopped the spreading of gastric malignant cells in the organism.

If we were to listen to what the investigation has to say, the short- and long-term use of Celecoxib for counteracting Helicobacter pylori` infection pathway in a medical case is the best thing to do. This finding has been never present in earlier researches. Thus, the new discovery is essential in diminishing the adverse effects produced by Cyclooxgenase-2 inhibiting drugs.

The team of investigators state that Cyclooxgenase-2 inhibiting medication might be utilized as a chemoprevention treatment for patients that are 40 years or older. This approach may prove to play an essential part in the life of patients who suffer from extended metaplastic gastritis with an enhanced predisposition of developing gastric malignant tumors. Moreover, the therapy is essential also for people who suffer from refractory Helicobacter pylori infections with an increased predisposition for gastric malignant tumors.

As a gastroenterological specialist stated the research outcome provides new insights into a customized treatment against gastric malignant tumors starting with the prevention phase and also it may bring advantages for medical therapy in the near future.
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Their discoveries are released in The Proceedings of the National Academy of Sciences. The recent study presents the way the cells of the naked mole rats generate a gene entitled p16 which triggers a claustrophobic characteristic. In turn this phobic state brings to a stop the multiplication of the cells in the case a big number of them becomes crowded. This means that the process impedes the abnormal growth even before it could commence. The effects of the p16 gene are so strong that at the time the scientists triggered mutations in the cell in order to develop a tumor, the growth of the cells did not transform very much. This is a very important discovery due to the fact that when applied on normal mice cells, the mutations would lead to malignant tumors creation.

Vera Gorbunova from the University of Rochester is the leading researcher of this investigation. The associate professor states that her team believes that they have discovered the reason for which the naked mole rats do not develop malignant tumors and it came as a shock to them. The implications of their discovery are many and important, but the speculations of stimulating the p16 gene in the case of human beings are just a matter of time and research. It this process could be accomplished in the case of people, this would represent the means to stop cancer evolution even before it can be triggered by various factors.

This species of rodents look rather strange; they have an unpleasant appearance because they have no hair covering their body and they live underground forming naked mole rats communities. In comparison to other mammals, the naked mole rats gatherings comprise queens and workers which is an odd feature due to the fact that this hierarchy is commonly found in bees. The rodents have a life span of approximately thirty years, a figure which is very big compared to the normal lifespan of tiny rats.

Even during the investigation a high number of naked mole rates were observed, the team of scientists did not manage to induce or find any animal presenting cancer tumors. A curiosity which also arises on these mammals` behalf is the fact that they grow older at a faster pace in the near end of their lives, whereas they age just a bit during their normal lifespan.

Vera Gorbunova, accompanied by a fellow researcher Andrei Seluanov who is a professor of biology within the University of Rochester, underwent an investigation which lasted for three years. During their research, the two scientists strived to study naked mole rats from all over the world in order to better understand the similarities of the species and what differentiated each group coming from different regions from one another. Moreover, the researchers wanted to acquire more information on how these differences and similarities were related to the naked mole rats ability to not develop cancer.

In the year 2006, Vera Gorbunova found out that an enzyme which can trigger a longer lifespan of the cells which is entitled telomerase has an enhanced activity in the case of small rats but not in larger ones. The telomerase enzyme is also a factor which can enhance malignant tumors` rate.

Prior to the investigation of Gorbunova and Seluanov, the existing idea was that any animal which had a lifetime span similar to the human beings` one had to stop or diminish the activity of the cells` telomerase in order to prevent malignant tumors from developing. This enzyme aids the cells in their reproducing stage and being well-known that cancer is the abnormal growth and multiplication of cells, any animal that could live for seventy years presented a high predisposition for developing cancer. The life span of a mouse is decreased due to natural agents like, for example, predators. This is why past wisdom stated that mice could manage a small risk for developing malignant tumors in order to enable the telomerase`s action and heal in at a faster pace.

Even though these beliefs were shattered by this new investigation, a new vagueness appeared. What is the case of animals that live for more than 24 years, like the well-known grey squirrel, for example? Considering the amplitude of the telomerase expression in these mammals due to a long time span, why do not they develop malignant tumors?

Vera Gorbunova strived to provide answers to these questions and in the year 2008 she discovered that the small rodents which enjoyed a longer lifetime span had evolved so much that their organism developed a method of counteracting cancer. This interesting mechanism differs a lot from other large animals and human beings` way to fight naturally against cancer.

At that specific moment, the assistant professor did not manage to discover which the cancer prevention mechanism in the naked mole rates was. As she explains past research was not able to identify this anti-malignant tumors mechanism due to the fact that scientists used only common mice and human beings` samples in their clinical and laboratory tests. The mouse is a mammal that has a short life span and people have large bodies. This is why the investigators found out that the anti-cancer mechanism is present only in the case of mammals that have a long life span and are very small.

By conducting this new investigation, Vera Gorbunova thinks she has discovered the first and main reason for which the naked mole rodents do not develop malignant tumors. It seems that this anti-cancer mechanism comprises a gene with a sort of early signal of attention that the mammal expresses in its body cells.

In the moment the team of researchers started to observe the cells coming from naked mole rats, they were shocked to discover just how hard it was for them to grow cells in the laboratory. The in vitro cells just stopped multiplying at the moment when they reached a specific number in a certain location. Human cells, for example, refused to replicate when they grew great in number, but in the case of the naked mole rodents this stopping of cell multiplication was triggered in an earlier stage compared to human beings and large mammals.

As the leading investigator explains cancer represents an abnormal multiplication of the body`s cells. But her team discovered that the process which triggered cancer development was also the factor which prevented the malignant tumors` formation in the naked mole rats.

Similar to human beings and a great number of animals, the naked mole rats comprise a gene entitled p27 which has the role to stop the dense growth of cells. However, the latter also utilize the p16 gene as an early warning signal. It has been shown that cells find ways to avoid the activity of the p27 gene, but the tiny hairless rodents enjoy double means of stalling and stopping the abnormal cellular growth.

As the leading author of the study states the team thinks that another protection layer produced by the action of these two genes (p16 and p27) triggers the ability of the naked mole rats to prevent malignant tumor appearance in their organism.

The two investigators plan to investigate more this issue and take a closer look at the genetic features of the naked hairless rodents in order to observe if their resistance to malignant tumors` development could be used in the case of human beings.

The investigation was released in the Alcoholism: Clinical and Experimental Research edition. The study comprises the researchers` findings regarding how alcohol triggers the epithelial-to-mesenchymal transition. During this transition, the mild cancerous cells transform in aggressive one and start invading the whole body in a process entitled metastasis.

As assistant professor Christopher Forsyth from the medicine and biochemistry division within the Rush University Medical Center explains the information provided by the team of investigators led by him is the first of its kind. This is due to the fact that their data presents the pathway in which alcohol stimulates specific triggers within a cell which are implicated in the metamorphosis into an aggressive form of the cells.

The notion of epithelial-to-mesenchymal transition is a highly researched matter nowadays due to the fact that it represents one of the processes involved in the mechanism of cancer spreading in the whole organism. An amalgam of laboratory investigations and clinical trials shows that this epithelial-to-mesenchymal transition is a prime factor in triggering the aggressiveness of the cancerous cells.

Professor Christopher Forsyth stated that the malign cells acquire a dangerous characteristic in the moment when they start spreading in the whole body. The operations can resection a malign tumor, but the aggressive cells have the ability to spread out in the whole human organism and conquer it. If medical doctors could stop this process, they would be able to limit the spreading of the malignant tumors.

The team of investigators put alcohol in cellular lines coming from colon and breast cancers and observed them in order to find the biochemical distinct signs of the epithelial-to-mesenchymal transition also including the presence of both Snail which is a transcription agent and the receptor concerned with the growth agent of the epidermis. The Snail represents the epithelial-to-mesenchymal transition`s control factor. On experiments undergone on mice, it was observed that if there is an over-expression of this factor, multi tumors are prone to develop. The second agent, the epidermal growth one is just like a drug for the cancer cells, they require large quantities of it.

The testing undergone in laboratories proves that alcohol triggered both factors and also other biochemicals agents related to the epithelial-to-mesenchymal transition. The trials also proved that the cells which were put in alcohol lost their strong links to adjacent cells, a characteristic which resembles the metastasizing process of the malign tumors.

Furthermore, professor Christopher Forsyth`s team of researchers discovered that the similar group of biomarkers was triggered in healthy intestinal cells which were put in alcohol. In addition to the aggressive metamorphosis alcohol triggers in cancer cells, this finding could mean that alcohol may also trigger the development of cancer.

The results of the research are based on a case-control investigation of people from New Hampshire. The outcomes and discoveries of the investigation were released in the British Journal of Cancer`s September edition. The leading author of the investigation is Karl Dietrich who is a student within Dartmouth Medical School. Accompanying him are professors: Alan Schned, John Heaney and Margaret Karagas who is also a professor in the Dartmouth Medical School in the family and community medicine department.

The research investigates the utilization of glucocorticoids on a long-term basis. The studied sample comprised 786 people suffering from bladder-cancer and 1,083 people who represented the control group. The amalgam of cytotoxic and glucocorticoids medications is recommended and prescribed by physicians in immunosuppressive treatments in order to aid ill people who underwent organ transplants to counteract the body`s rejection of the foreign organ. In addition, the glucocorticoids are also prescribed to people who suffer from asthma, rheumatoid arthritis and various other diseases.

Earlier investigations, some of which included Margaret Karagas as fellow researcher, reported links between these types of medication treatments and an increased predisposition to lymphoma and skin cancers.

As the new investigation presents the predisposition of developing bladder malignant tumors associated with the above mentioned therapies may be an indicator for the need of taking a closer look at patients who constantly take glucocorticoids as part of their treatments.