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19.01.2015

Cancer cures that work, how to get rid of herpes in the mouth - Test Out

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There were an estimated 12.7 million cancer cases around the world in 2008 (latest year available).
Proton radiation beams are generated from a particle accelerator, similar to what physicists use to study the properties of matter, and a series of electromagnets steer the beams to a rotating nozzle that moves around a patient’s bed. The beam energy has to be such that the protons stop at the correct location and depth in the patient's body. The goal is to complete these treatment planning calculations in the time it takes to move a cancer patient from an MRI or CT scan into the radiation therapy treatment room – mere minutes.
A few weeks or months ago you may not have known much about prostate cancer – or only heard anecdotal stories from friends or family. Microscopic capsule penetration is one of the most important concepts to understand about prostate cancer and has been extensively studied at Johns Hopkins University.29 Prior to surgery (radical prostatectomy), between the years 2000 and 2005, a group of 5,730 men had a prostate biopsy, PSA and were staged either T1 or T2 based on DRE (digital rectal exam). To be cured of prostate cancer, any treatment must destroy all the prostate cancer cells, which is possible if your cancer is located only inside the prostate contained by the capsule (Step 1) or if you have microscopic capsule penetration through the capsule (Step 2).
OICR is an innovative translational research institute dedicated to research on the prevention, early detection, diagnosis and treatment of cancer. Cancer stem cells (CSCs) are a small group of cells within a tumour, which have the exclusive potential to generate a new tumour with all of the same diversity of cells in the original tumour. Since CSCs are inherently more resistant to the most common cancer therapies, effectively treating tumours that include cancer stem cells will likely require changing our therapeutic goals – from one aimed at eliminating rapidly dividing, fully differentiated tumour cells, to one targeting this distinct sub-population of cells located at the top of the cell lineage hierarchy. The technologies required for genomic sequencing are becoming increasingly available, putting personalized cancer medicine within the reach of the clinical setting. To understand the relationship between genes and cancer, we must first define the term gene. Campbell Family Institute for Breast Cancer Research at the Princess Margaret Cancer Centre and Dr.
Most vaccines have been developed to generate immune responses to pathogens that the body has never seen. Identifying a cancer at an early stage on medical images can be challenging, even for an experienced radiologist. To illustrate how this works, imagine some honey (representing the cancer) spilled on a wooden cutting board (representing a patient’s body).
Targeted imaging probes are designed to accumulate in cancerous tissue by taking advantage of our knowledge about what makes some cancers different from normal tissue. Early in the development of a cancer, the changes in appearance of the cancer compared to the normal cell may be very subtle, making detection from a medical image even more challenging. TTargeted cancer therapies are tailored to take advantage of cellular properties that distinguish cancer cells from normal cells.
Other targeted cancer therapies exploit the properties of viruses to kill cancer cells but leave healthy cells alone. As the study of cancer genomes continues to expand, new genomic driven cancer therapies will be developed and patient outcomes will continue to improve.
Anderson Medical Cancer Center in Houston, are working to reduce the cost of identifying and treating cancer patients with proton radiation therapy by shortening the time required for treatment planning from several days to a few minutes.
And so far, scientists at IBM Research - Austin have simulated the automatic creation of treatment plans that cut the entire planning process down to about 15 minutes. We do know, however, that the chance of developing prostate cancer increases as a man ages and that it is rare in men younger than 40 years old.
Surgical removal of the prostate was performed on these men, and the entire prostate was given to the pathologist for microscopic examination to determine, among other things, if cancer cells had leaked through the capsule and were outside the prostate, which means that men were really stage T3.
The first way is through development of cancer adjacent to the capsule with the cancer simply destroying the capsule (eating a hole in the capsule) and leaking out.
We also want to destroy all the normal prostate cells to prevent you from getting another cancer. Let’s assume you have 100 prostate cancer cells, all 100 are contained by the capsule inside the prostate and you have no microscopic capsule penetration (this is Step 1 in cancer cell growth).
To illustrate this point, let’s assume you have 100 prostate cancer cells and were stage T1c before radical prostatectomy, which means, as far as we know, all your 100 prostate cancer cells were contained inside the prostate by the capsule prior to your surgery. Cancer stem cells are named for their similarities to organ stem cells – both types of stem cells have the ability to self-renew and to differentiate. The first model argues that CSCs are derived from organ stem cells, which possess properties of self-renewal, but acquire genetic and epigenetic changes that render them capable of causing tumours. Personalized cancer medicine would allow us to sequence an individual’s tumour and determine the underlying mechanisms controlling its growth, while guiding therapies directed at that specific tumour so they are more precise, with fewer side effects for patients. The nanotechnology concept is still new, and current products have yet to achieve the full spectrum of safety and anti-cancer effect suspected possible. Sometimes a gene contains an error, so the instruction for producing that protein is incorrect.
Some cancers are associated with viruses that the immune system recognizes as foreign and can eliminate. Some cancer cells consume more glucose than healthy cells and could be targeted by creating imaging probes similar to glucose that show up clearly in positron emission tomography.


The increase in contrast achieved by using targeted imaging probes may enable cancers to be seen earlier than would otherwise be possible.
Unlike standard chemotherapeutic agents, which affect the whole body, targeted cancer therapies are able to recognize and attack cancer cells with little to no harm to healthy tissues. This promising targeted cancer therapy is currently in clinical trials and uses oncolytic viruses (OVs) to infect and destroy cancer cells without causing harm to normal tissues.
The survival of tumour cells and tumour progression rely on mutations in genes that lead to uncontrolled cell growth. Personalized cancer medicine will become a reality when a patient can be profiled for the mutations driving their cancer and a therapeutic decision is made based on this profile. By creating advanced algorithms running on IBM POWER7 systems and utilizing IBM ILOG optimization software, they can simulate how far the proton beams travel in a body 1,000 times faster than conventional methods; and can solve the complex optimization problem of treatment planning 500 times faster than current practice.
This additional quality assurance process still takes quite a bit of time and wastes radiation machine time that could be used for treating patients. Continued work with partners such as MD Anderson will soon make this a reality in the fight against cancer. For reasons we do not understand, one or more normal prostate cells transform into prostate cancer cells and begin to grow.
The chance of cancer cell leakage was then correlated with Gleason score, stage and PSA in the Partin tables.29 The chance of microscopic capsule penetration ranged from 7% to 89%.
A second way is through perineural invasion, which means cancer cells travel along branches of the sex nerve and “tunnel” through the capsule to escape the prostate (see Question 22). Cure, both destruction of all your prostate cancer cells and normal prostate cells, is determined by using the PSA test.
However, since microscopic capsule penetration CANNOT be detected before any treatment, including surgery, let’s realistically assume that of your 100 prostate cancer cells, 95 are actually inside the prostate and five cancer cells penetrated the capsule and leaked into the area surrounding the prostate, which includes the rectum, bladder, sex nerves and muscles that control urination. Your cancer is regrowing because the only other cells that make PSA are normal prostate cells, but they were all removed during surgery.
From a practical standpoint, almost all prostate cancer that is going to grow back will do so within 10 years of treatment.
Since a CSC has the potential to regenerate the original tumour, cancer stem cells must be eliminated in order to find a permanent cure to the cancer. The second model argues that CSCs represent proliferative founder or progenitor cells that have dedifferentiated and are able to both self-renew, and give rise to further proliferative progenitors. Cancer immunotherapy takes this power and directs it towards cancer because the immune system also has the ability to seek out and destroy cancer cells. The main type of immune cell that can kill tumour cells are white blood cells known as T-cells. Most cancers arise from our own normal cells and thus express mostly normal proteins to which the immune system has been trained not to respond.
Other cancer cells have a much higher density of marker proteins, called antigens, than healthy cells, and could be targeted by designing compounds that attach to these specific proteins and are visible in MRI.
This technique is routinely used in cancer research to compare cancer cells with their healthy counterparts. To achieve this, targeted therapies exploit the differences between cancer cells and healthy cells.
This works because OVs, like drug-based targeted therapies, exploit cancer-specific cellular properties, such as the inability to activate an immune response against virus infection. The sequencing of tumour genomes will allow us to learn which mutations in which genes are important in causing cancer, and which can be targeted with therapies. This decision may be to give a drug that will specifically target the patient’s tumour, or to rule out a drug with severe side effects because that patient will likely not benefit from the treatment. Protons can penetrate deep into a body without disrupting healthy cells – and only impact the cancer cells as they slow down at the end of their path.
For example, men from Western industrialized countries have a higher incidence of prostate cancer than men from Asia.
The hallmark of any cancer is cancer cell growth – reproduction, or making more cancer cells.
Microscopic capsule penetration is important to understand because it will determine your chance of cure.
The third method of microscopic capsule penetration occurs at the bottom (apex) of the prostate because the prostate capsule thins out and does not exist in this location, which makes it easy for cancer cells to escape the prostate in this area. Consequently, all your normal prostate cells, as well as the 100 prostate cancer cells, would be removed. With a radical prostatectomy, your prostate would be removed along with all normal prostate cells and the 95 cancer cells inside the prostate.
Unlike normal progenitor cells however, CSCs are inherently more resistant to the most common cancer therapies, which are aimed at eliminating rapidly dividing and differentiated tumour cells. It is a formidable challenge to awaken the immune system to respond to self-antigens expressed on cancer cells. Targeted imaging probes are compounds given to patients designed to ease this challenge by enhancing the differences in appearance between a target, such as cancerous tissue, and the surrounding tissue.


For many cancers, we do not yet have targeted imaging probes that can reliably detect them. For example, cancer cells have numerous genetic mutations that either increase or decrease the abundance of cellular proteins, some of which act as good targets for therapy. When a normal cell turns into a cancer cell (by a process called carcinogenesis), it gains the ability to grow perpetually but loses the ability to protect itself from infection.
Many targeted therapies are already available commercially or are currently in clinical development.
African-American men have a higher incidence of more aggressive prostate cancer than Caucasian men. For a long period of time, prostate cancer grows only inside the prostate and is contained by the capsule that surrounds the prostate. Check your pathology report to see if you have cancer at the apex because this is the most common place for positive surgical margins, meaning cancer cells cut across and left behind after radical prostatectomy. An equally important use of the PSA test is to find out if men are cured of prostate cancer.
Some of the five cancer cells that leaked out of the prostate would also be removed, but typically not all of these cancer cells can be cut out since they are around your normal adjacent organs. By sequencing the genomes of tumours and determining which changes have occurred compared to the normal genome, we are able to gain insight into the underlying mechanisms that lead to cancer. This specificity is one key difference between immunotherapy and other types of cancer therapy such as chemotherapy or radiation therapy. This honey example is a simplified version of how targeted imaging probes help distinguish cancer cells from the rest of the human body (although the human situation is much more complex). As our knowledge of the biology and chemistry of different cancers expands, the potential for targeted imaging probes expands with it. We say that a gene is "expressed" in a cell at a certain time, under a certain condition, if the protein it encodes is being manufactured by the cell at that time under that condition.
Ideally, it will yield, relatively quickly and inexpensively, a short list of genes that have abnormal expression levels in cancer.
Drug-based targeted therapies are thus often designed to correct a particular genetic abnormality in cancer, such as inhibiting the action of certain oncoproteins that trigger unregulated cell growth.
For example, imatinib (Gleevec®) is a targeted therapy used to treat a type of chronic myelogenous leukemia (CML) that contains a specific genetic translocation known as the Philadelphia chromosome. Additionally, the incidence of prostate cancer is significantly increased in men who have a family history of this disease, meaning their father, brother, uncles or grandfather had prostate cancer.
Eventually, the second step occurs – cancer cell leakage through the capsule outside the prostate, which is officially called microscopic capsule penetration. Cancer cell leakage through the capsule cannot be detected before treatment because the DRE, prostate biopsies, CAT scans or MRI scans cannot detect cancer that can ONLY be found with a microscope. To be cured of prostate cancer, your PSA must fall to an undetectable level after treatment and remain there forever. Doctors are not going to cut out your rectum or bladder, nor do they want to cut out the muscles that control urination or the sex nerves (where microscopic cancer cells can leak through the perineural space). Nanomedicine uses the EPR effect for two practical reasons: (1) improved tumour treatment, and (2) improved cancer detection.
In these other types of therapies, healthy cells are often destroyed in addition to cancer cells. It will then be followed up with much more labour intensive laboratory work to determine which of these short-listed genes contribute to cancer, and how exactly they do so. Moreover, OVs can be re-engineered to express proteins that trigger apoptosis or recruit cancer-destroying immune cells to the tumour site. Another example is cetuximab (Erbitux®), which is effective in the treatment of certain colorectal cancers that do not harbour mutations in the KRAS oncogene.
About two-thirds of the prostate are normal prostate cells, and the remaining part is the urethra, muscles that act like valves to prevent leakage of urination, fibrous tissue that holds the prostate together, blood vessels and the ejaculatory ducts. Depending upon the treatment method, prostate cancer can still be cured in either Step 1 or Step 2.
Let’s assume that four of the five cancer cells that leaked out of the prostate are removed at surgery, but one cancer cell was left behind. In cancer research, one of the main goals is to learn how and which mutations in which genes cause cancer. Given their ability to leave healthy cells alone, drug-based and OV-based targeted cancer therapies are a primary focus of cancer research today. The third step is the spread of prostate cancer (metastasis) beyond the area of the prostate such as lymph nodes, bones, lungs or any other place in the body.



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