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 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.

The apoptosis represents the process of killing cells in a predetermined manner. This programmed cellular death is very important for the human body because it defends the organisms against the cancer tumors evolution and counteracts various illnesses which comprise the harmful activity of the human immune system in the case things go wrong and the latter starts attacking its own cells or organs. Examples of such immune system diseases are lupus and insulin-dependent diabetes.

The activation of the apoptosis process is achieved by some proteins that are located on the cellular surface. One of these notorious proteins is the Fas ligand which can be found in two forms, either linked to the cellular membrane or as a secretion of the cell. This protein located on the cellular surface ties to the Fas which is a receptor located also on the cell`s surface.

Professor Andreas Strasser is co-head of the Walter and Eliza Hall Institute`s department of Molecular Genetics of Cancer. His counterpart is Professor Jerry Adams. The first has been striving over the period of ten years to reach a conclusion regarding the notorious medical debate. Professor Strasser underwent a research in order to observe if either the Fas ligand protein that was tied to the cellular membrane or the form that was secreted or both of these variants provoked cellular killing.

As the co-head of the Molecular Genetics of Cancer department states the research community found itself at the core of a decade long debate contesting which variant of the Fas ligand protein is the one that kills cells and which of the versions could produce inflammations. His investigation group managed to discover that the actor who played the greatest role in cellular death was the form of Fas ligand which was connected to the cell`s membrane. Thus, they established that this version of the protein acts as a protector against the inflammation of the lymph nodes entitled lymphadenopathy, autoimmunity illnesses and cancer, as well.

This investigation regarding the notorious research debate was published in the Nature journal. The research was accomplished with the aid of doctor Lorraine O’Reilly, Lin Tai and doctor Lorraine Robb. All these three researchers come from the Walter and Eliza Hall Institute, but the first two work in the department of Molecular Genetics of Cancer and the latter works in the Cancer and Haematology division.

This recent investigation proved at the same time that even though the secreted form of the Fas ligand protein does not play any part in causing cellular death; if it exists in large quantities it can favor the cancer tumors` growth and autoimmune illnesses` evolution.

As the leading investigator of the study states his team observed that in specific autoimmune diseases and some variants of leukemia or lymphoma, the secreted form of the Fas ligand protein is found in excessive amounts in the human body. Hence their investigation proved that this form of the cell surface protein could cause inflammations and is harmful in excessive quantities and the autoimmune conditions and some types of leukemia or lymphoma cause swelling in the tissues, medics would be able to counteract or mitigate some of the symptoms of these illnesses by counteracting the secreted form of the protein with the help of antibodies or substance receptors.

The group of investigators from the Walter and Eliza Hall Institute managed to draw a conclusion for the debate which lasted for ten years. They managed to accurately state the roles both forms of the Fas ligand protein. Nowadays, the team of researchers underwent a new study in order to observe the effects over the molecules in case the secreted form of the Fas ligand is found in excessive quantities in the human body and these pathways` part regarding autoimmune illnesses and leukemia or lymphomas.

For those who do not know, the B-cell lymphomas represent those types of cancer that affect most commonly the human being immune system. Some of the triggering causes for this type of tumors are the epigenetic transformations like for example the hyper-methylation of the DNA. Due to these changes, the B-cell lymphomas start appearing mainly because the epigenetic transformation affect the cancer suppressor receptors that are, in this way, unable to stop the development of the mutating tissues.

The SPAK protein has as main role in the human body to supervise and fix the response of the cells to the stress they encounter during their life span. The study from the University of California observed that during the tumor development, the levels of the SPAK protein are significantly diminished.

The team of scientists experimented on samples comprising human and mice tissues affected by the B-cell lymphomas. Balatoni and his team state that part of the B-cell cancers comprise lower expression levels of SPAK mainly due to the DNA hyper-methylation. In addition, the diminished levels of the SPAK protein act as defenders of the B-cell lymphomas and this affected by the human body`s stressors that would trigger the healthy cells` death instead of that of cancer cells. Due to this, the tumors are kept alive and unthreatened, free to spread in the whole body, leading to metastasis.

Doctor Teitell`s team concluded that the fact that the levels of SPAK protein were lowered in the patients suffering from B-cell lymphomas would aid the tumor cells in growing and getting to advanced stages of cancer. The team of researchers explained that the role of the SPAK protein is to prevent the evolution of the B-cell lymphomas by damaging the activation genes of the sick cells. It appears that the findings of the scientists from the University of California are valid in general also for other types of cancer such as breast, prostate and maybe other tumors ahead of the B-cell lymphomas. Furthermore, the investigators stated that the protection offered by the SPAK proteins diminishes and the organism cannot attack the genetic material of the cancer cells in order to counteract their deadly effects. In addition, it appears that the role of protection from the SPAK`s behalf is somehow deactivated in the stages in which the tumor cell evolve.

Taking a closer look at the expression of SPAK in the human body, one can examine this protein`s levels and see whether they are diminished. This process is a key element in counteracting the cancer cells due to the fact that a thorough research may show those people suffering from cancer that must or not receive genotoxic treatments. This is a milestone in the process of the individualizing treatments and alongside them, the medicine in its whole, in order to develop better therapies and encounter success in counteracting cancer.

The investigators state that a closer observation of the malign disease in dogs should be thoroughly studied in order to create and implement new treatments, gadgets and scanning methods for people that are affected with cancer.

Statistics claim that nearly one million fresh cancer illnesses are diagnosed in dogs all over the territory of the United States yearly. The suffering animals are taken care of in a similar way human beings are. Their therapy includes operations, irradiation and even chemo treatments. Furthermore, the owners of the quadrupeds show significant interest in trying brand new treatments and drugs in order to heal or at least diminish their pets` sufferings.

Doctor Chand Khanna is the leading author of this study which took place at the Centre for Cancer Research at the National Cancer Institute. His opinion is that by examining the cancers` evolution in our quadruped friends, the medical world will be able to get a better understanding of this matter and come up with new strategies for dealing with human beings` cancers. Thus, he proposes clinical trials on dogs to acquire this knowledge. The reason for experimenting on dogs is the fact that the malign sufferings they have are very similar to the tumors affecting people.

The investigation group state that the decision of a person owning a dog to try alternative and novel treatments with the view to cure their animals is linked to a series of factors. These main decision agents are represented by the risks and success a novel treatment comprises and also the fact that the price of the therapy is lower in a clinical trial than in an ordinary veterinary office.

Another important issue in the clinical trials for cancer suffering dogs is the fact that their owners see these experiments as a chance to improve the evolution of therapies counteracting human beings` cancer and also discovering new ways to fight against dog cancer as well.

Studying the animal cancer`s features and corresponding therapies is entitled comparative oncology. This strategy dates back over 30 or 40 years ago and many researchers made use of the comparative oncology in order to acquire more knowledge about how to counteract and understand the cancer affecting people. Some examples of the types of cancers studied in the comparative oncology are: osteosarcoma or bone cancer, melanoma and lymphoma.

Noticing this absence, scientists have shown that the replacement of a single microRNA in mice with an extremely aggressive form of liver cancer can be enough to halt their disease and have published the results in Cell, June 12.

Josh Mendell, M.D., Ph.D., an associate professor in the McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine says “This work suggests that microRNA replacement may be a highly effective and nontoxic treatment strategy for some cancers or even other diseases,” and “We set out to learn whether tumors in a mouse model of liver cancer had reduced levels of specific microRNAs and to determine the effects of restoring normal levels of these microRNAs to these cancer cells. We were very excited to see that the tumors were, in fact, very vulnerable to microRNA replacement”

Mendell and his team discovered that the tumor cells in the mouse were indeed sensitive to the restoration of the microRNA. “This concept of replacing microRNAs that are expressed in high levels in normal tissues but lost in diseases hasn’t been explored before,” Mendell says.

The Hopkins team showed that in a Petri dish, replacing microRNAs in lymphoma cells stopped the formation of tumors, Mendell stating that “Our work raises the possibility of a more general therapeutic approach that is based on restoring microRNAs to diseased tissues.”

The scientist chose liver because of its large function in detoxification and because it is a relatively accessible target for the delivery of small molecules. They injected a virus containing microRNA in a group of mice and a virus containing no microRNA in another group of mice.

Six of eight injected with the virus without microRNa experienced in three weeks time an aggressive disease progression. In contrast, eight of ten mice treated with microRNA exhibited only small tumors or complete absence of tumors.

As a conclusion to this experiment, Mendell said “The livers of the mice that received the microRNA virus glowed fluorescent green, showing that the microRNA ended up where it was supposed to go, and the cancer was largely suppressed.”

He also reported that “The tumor cells that received the microRNA were rapidly dying while the normal liver cells were completely spared. These findings, as well as the results of specific tests for liver damage, demonstrated that the microRNA selectively kills the cancer cells without causing any detectable toxic effects on the normal liver or other tissues.”

The study concludes by saying that the sensitivity of tumor cells to this microRNA suggests that its absence is a cause in the transformation of normal cells in cancer cells and that this discovery will help the development of strategies to ease patients diagnosed with liver cancer.

National Institutes of Health, the Sol Goldman Center for Pancreatic Cancer Research and the Research Institute at Nationwide Children’s Hospital supported the research.

Colon cancer usually takes birth from benign but abnormal growths in the intestinal lining called polyps, which are called adenomas when they become cancerous. When developing advanced adenomas, people undergo repeated invasive surveillance tests, such as colonoscopy, in order to remove recurrent polyps which can aggravate the patients’ situation.

Advanced adenomas and cancers produce in excess an altered version of the MUC1 cell protein. While known vaccines work by blocking infection with viruses that are linked with cancer- for example, Gardasil protects against human papilloma virus associated with cervical cancer and hepatitis B vaccine protects against liver cancer, the research team used MUC1 as a target, as lead investigator Robert E. Schoen, M.D., M.P.H., professor of medicine and epidemiology at the University of Pittsburgh explains:
“By stimulating an immune response against the MUC1 protein in these precancerous growths, we may be able to draw the immune system’s fire to attack and destroy the abnormal cells. That might not only prevent progression to cancer, but even polyp recurrence.”

In order to establish the vaccine’s safety and immunogenicity, first tests were conducted on patients suffering of late-stage colon cancer and pancreatic cancer. Despite their cancer-weakened immune systems, they were able to generate an immune response. This led to the conclusion that patients with advanced adenomas who are otherwise healthy could produce a stronger response which could stop precancerous lesions from transforming into malignant tumors.

Researchers are currently looking to expand the study group and are looking for about 50 new participants in addition to dozen that already received this treatment. The participants must be between 40 and 70 years old, with a history of developing adenomas that are greater than or equal to 1 centimeter in size, typed as villous or tubulovillous, or contain severely dysplastic or abnormal cells. They’ll receive three inoculations with the vaccine, an initial one and another shot after two and 10 weeks followed by blood tests at those time points as well as 12 weeks, 28 weeks and one year later, in order to measure the immune response.

“Immunotherapy might be a good alternative to colonoscopy because it is noninvasive and nontoxic and it could provide long-term protection” said Dr. Schoen.

The molecule in question is in fact a type of microRNA, which are abundant in the cell and regulate the quantity of proteins produced by RNA strands, proteins that determine the unique characteristics of every cell type.

MicroRNA-125b, as the researcher found out after tests conducted on zebrafish, keeps the level of p53 low to avoid excessive cell death during embryonic development; the molecule’s level is reduced to allow an increase in p53, which eliminates damaged cells and thus preventing tumor formation if the DNA is damaged. Combined with the fact that high levels of this microRNA are found many types of human cancers, these findings could lead to the conclusion that it may contribute to the formation of tumors by suppressing the p53 protein.

The researchers, a joint team of Singapore and U.S. scientists, are excited about these findings, stating that the understatement of how exactly this molecule works could lead to the development of new drugs that could treat diseases for which no effective treatment exists right now, primarily cancers.

The research reports that a certain region of chromosome 9 could acquire mutations but only in individuals with a particular makeup. The zone includes the JAK2 gene and said individuals are more than three times likely to develop an MPD, such as polycythaemia vera (PV). The leader of the research team, Professor Nick Cross, from the University of Southampton stated that: “This research provides strong evidence that at least half of the cases of PV diagnosed each year are linked to an inherited genetic variant on chromosome 9. Whilst this risk is still very small it nonetheless confirms that individual susceptibility to acquiring cancer-causing mutations is linked to genetic inheritance. Now that we have this evidence we can carry out studies to determine exactly how the variant contributes to this risk.”

Whilst in the UK, 40% of the population carries the chromosome 9 variant, only 1 in 20,000 people develop an MPD each year, but the research shows that the inheritance of this variant increases the risk of developing the disease.

The importance of the study lays in the future understanding of the ways in which predisposition to genetic mutations can lead to cancers.

One of the known factors that regulate Src is reactive oxygen species (ROS), produced when the cell is under growth stimulation. A new study concerning the way Src responds to this regulation could bring real benefits for the development of new drugs targeting specific cancers.

The research, conducted by Doctoral student David J. Kemble and Professor Gongqin Sun in the University of Rhode Island Department of Cell and Molecular Biology, was able to identify the sensor that enables Src to respond to ROS regulation trough a systematic approach which involved the study of all the potential mechanisms and lead to finding the same sensor present in a other similar enzymes, such as the Fibroblast Growth Factor Receptor (FGFR) family.

Regarding further investigation on Src function in the cell, Dr. Sun stated that “Src function is under the control of several different mechanisms; each one needs to fit in with the others to form a seamless regulatory system.”