Herbal Remedies For Leukemia - How Can They Help?

Leukemia is a blood disorder that affects a surprisingly large number of people. The death rate of this disease is alarming and it causes people to turn to other treatments that science can provide. Herbal remedies for leukemia has been given consideration as an alternative treatment.
What is leukemia?
Leukemia is another type of cancer that begins in the blood cells. For people suffering from leukemia, their bone marrows generate abnormal white blood cells. These are called the leukemia cells.
During the first stage of this disease, the leukemia cells may look like they are functioning normally. But after some time, they begin to out populate the normal white blood cells and also the red blood cells of our body. This is the reason why the blood cannot function correctly.
Cause of Leukemia
The exact cause of leukemia still remains a mystery. Experts cannot explain why this disease sprouts in random people. However, due to intensive studies, they have found some factors that may put you at risk of leukemia. Here are some of them:
1. Exposure to high level radiation
Those people who are regularly exposed to a high level of radiation have a high chance of developing leukemia.
2. Exposure to certain chemicals
Exposure to chemicals, such as Benzene can put you at a risk of developing leukemia. Another chemical that may cause considerable damage to your cells is formaldehyde.
3. Chemotherapy
This might seem crazy since chemotherapy is used to treat cancer patients. However, there are some studies conducted that people fighting from a different type of cancer can later develop leukemia because of their frequent chemotherapy sessions.
4. Down Syndrome
People with Down syndrome have a higher risk of developing leukemia because of their abnormal chromosomes.
Treatment
The first line of treatment that people with Leukemia would most likely utilize is chemotherapy. However, chemotherapy can also assault your immune system and can leave you defenseless against other viral infections and other complications.
Patients undergoing chemotherapy are all physically spent after every session. Chemotherapy also causes these patients to lose hair. This is why many have also turned to herbal remedies for leukemia.
These herbal remedies for leukemia have helped many a number of leukemia sufferers:
1. The nutrients found in garlic can protect our body from infections. Since chemotherapy can lower your immune system, Garlic can aid that problem.
2. You can also concoct an herbal tea out of stinging nettle, elder blossoms, brooklime herb and dandelion to help your body gain back its strength and normalize its primary functions.
It is also important for a leukemia sufferer to have a balanced diet and regular exercise to support their body in the fight against cancer cells.
Along with these, they can also take an herbal remedy that can help promote healthier cells. A product called Bio-Oxidate Defense can help a lot.
This product can support healthy cells in our body and can help the body fight the effects of bad cells. Bio-Oxidate Defense can also up your immune system so you will not be defenseless against other diseases.
This product is 100% safe to use because it uses natural herbal ingredients such as Green Tea, Rooibos and Grape seed extract which are a very helpful combination in supporting the body and help healthy cell growth.
When it comes to the battle against Leukemia, every help is needed. Herbal remedies for leukemia and a product like Bio-Oxidate Defense is just what you need to help you in this fight.

The Chronic and Acute Myelogenous Leukemia

Acute myelogenous leukemia (AML), as well called acute nonlymphocytic leukemia (ANLL), is a rapidly progressive neoplasm resulting from hematopoietic precursors, or myeloid stem tissue, that give rise to granulocytes, monocytes, erythrocytes, and platelets. There's growing evidence that genetic events occurring early in stem mobile maturation can lead to leukemia. Very first, there's a lag time of 5-10 years towards the development of leukemia after coverage to known causative agents such as chemotherapy, radiation, and particular solvents.
2nd, many instances of secondary leukemia evolve out of a prolonged "preleukemic phase" manifested like a myelodysplastic syndrome of hypoproduction with abnormal maturation without having precise malignant behavior. Finally, examination of precursor cells at a stage earlier than the malignant expanded clone in a provided kind of leukemia can reveal genetic abnormalities such as monosomy or trisomy of various chromosomes. In maintaining using the general molecular theme of neoplasia, extra genetic modifications are witnessed in the malignant clone compared with the morphologically normal stem cell that developmentally precedes it.
Acute myelocytic leukemias are classified by morphology and cytochemical staining. Auer rods are crystalline cytoplasmic inclusion bodies characteristic of, though not uniformly witnessed in, all myeloid leukemias. In contrast to mature myeloid tissue, leukemic cells have large immature nuclei with open chromatin and prominent nucleoli. The look from the individual kinds of AML mirrors the cell kind from which they derive. M1 leukemias originate from early myeloid precursors with no apparent maturation toward any terminal myeloid mobile type. This really is apparent within the lack of granules or other features that mark more mature myeloid cells. M3 leukemias are a neoplasm of promyelocytes, precursors of granulocytes, and M3 cells exhibit abundant azurophilic granules which are common of normal promyelocytes.
M4 leukemias arise from myeloid precursors that may differentiate into granulocytes or monocytes, whereas M5 leukemias derive from precursors currently committed towards the monocyte lineage. Therefore, M4 and M5 cells both include the feature folded nucleus and gray cytoplasm of monocytes, whereas M4 cells include also granules of the granulocytic cytochemical staining pattern. M6 and M7 leukemias can't be readily identified on morphologic grounds, but immunostaining for erythrocytic proteins is positive in M6 tissue, and staining for platelet glycoproteins is apparent in M7 tissue.
Chromosomal deletions, duplications, and well balanced translocations had been noted about the leukemic tissue of some patients prior to the introduction of molecular genetic techniques. Cloning from the regions exactly where well balanced translocations occur has, in some cases, revealed a preserved translocation website that reproducibly fuses a single gene with an additional, producing in the manufacturing of a brand new blend protein. M3 leukemias show a really higher frequency of the t(15;17) translocation that juxtaposes the PML gene with the RAR- gene. RAR- encodes a retinoic acid steroid hormone receptor, and PML encodes a transcription factor whose target genes are unknown. The blend protein possesses novel biologic action that presumably results in improved proliferation and a obstruct of differentiation.
Interestingly, retinoic acid can induce a short-term remission of M3 leukemia, supporting the importance of the RAR--PML blend protein. Monosomy of chromosome seven can be observed in leukemias arising out from the preleukemic syndrome of myelodysplasia or in de novo leukemias, and in both instances this finding is associated with a worse clinical prognosis. This monosomy as well as other serial cytogenetic modifications may also be seen right after relapse of treated leukemia, a scenario characterized by a a lot more aggressive program and resistance to therapy.
As hematopoietic neoplasms, acute leukemias involve the bone marrow and usually manifest abnormal circulating leukemic (blast) cells. Occasionally, extramedullary leukemic infiltrates recognized as chloromas can be observed in other organs and mucosal surfaces. A marked improve within the number of circulating blasts can sometimes trigger vascular obstruction associated with hemorrhage and infarction within the cerebral and pulmonary vascular beds. This leukostasis results in symptoms such as strokes, retinal vein occlusion, and pulmonary infarction.
In most instances of AML along with other leukemias, peripheral blood counts of mature granulocytes, erythrocytes, and platelets are decreased. This is probably because of crowding from the bone marrow by blast tissue as nicely as the elaboration of inhibitory substances by leukemic cells or alteration of the bone marrow stromal microenvironment and cytokine milieu required for normal hematopoiesis. Susceptibility to infections consequently of depressed granulocyte amount and function and abnormal bleeding as a result of reduced platelet counts are common problems in sufferers initially presenting with leukemia.
Chronic myelogenous leukemia (CML) is an indolent leukemia manifested by an increased quantity of immature granulocytes in the marrow and peripheral circulation. One of the hallmarks of CML may be the Philadelphia chromosome, a cytogenetic function that is due to balanced translocation of chromosomes 9 and 22, producing in a fusion gene, bcr-abl, that encodes a kinase that phosphorylates a number of key proteins included in cell development and apoptosis. The fusion gene can recreate a CML-like syndrome when released into mice.
CML eventually transforms into acute leukemia (blast crisis), which is associated with further cytogenetic changes and a clinical course similar to that of acute leukemia. New courses of medicines that block the bcr-abl kinase by competing with the ATP-binding site, induce remissions in most patients in chronic phases of CML. Moreover, resistance to these bcr-abl inhibitors can include amplification from the bcr-abl breakpoint as nicely as the development (or clonal expansion) of mutations in the ATP-binding pocket of bcr-abl, which no longer allows binding of inhibitors.

Vitamin D - A New Protective Mechanism Against Colon Cancer

According to Ministry of Health and Consumption, colon cancer is the deadliest malignancy in Spain, causing over 25,000 deaths annually. Although progress is made continually in research and treatment, survival of patients with colorectal cancer are diagnosed in advanced stage of the disease has not improved significantly since many years. While it is accepted that the most effective against cancer in general and in particular colorectal cancer is prevention, campaigns in this regard have failed so far the desired results.
Vitamin D has been traditionally associated with the regulation of bone biology and the prevention of rickets. However, numerous recent studies support a protective effect of vitamin D against various cancers, particularly colon and prostate, breast and others. As Bert Vogelstein, a professor at the Faculty of Medicine, Johns Hopkins researcher Universitad the Howard Hughes Medical Institute of Maryland (USA) and Prince of Asturias Prize said: "Studies on the relationship between vitamin D3 (active of vitamin D found in the body), bile acids and colorectal cancer have significant implications for the prevention of colorectal cancer in the future "
Most epidemiological studies suggest that reduced concentrations of vitamin D in blood is associated with an increased risk for colorectal cancer, whereas those with concentrations in the highest rank have lower risk. These results have motivated a great interest in studying the action of vitamin D as a preventive agent against colorectal cancers.
The team of Prof. Alberto Munoz at the Institute for Biomedical Research "Alberto Sols" located on the campus of the Faculty of Medicine of the Universidad Autonoma de Madrid, joint center of this University and the National Research Council investigates the action of calcitriol (vitamin D3) in human cells of colon cancer. In collaboration with the group led by Dr. Felix Bonilla at the Hospital Universitario Puerta de Hierro move to human samples, taken from tumors taken from cancer patients, noting the current ethics rules, results in vitro in cell cultures and in experimental animals in order to elucidate the mechanisms and possibilities for use of calcitriol and vitamin D in preventing and perhaps treating this malignancy.
Today it is accepted that one of the initial and fundamental alterations in the vast majority of colorectal cancers is abnormal activation of a molecular signaling pathway called Wnt / beta-catenin. This occurs because the mutation of one of three genes: APC, or Axin CTTNB1/beta-catenina. The latest finding made by the group led by Alberto Muñoz published in the journal Carcinogenesis shows that calcitriol increases the expression of a gene called Dickkopf-1 (DKK-1). This gene is a natural inhibitor of the Wnt pathway / beta-catenin, and since this acts as an engine that initiates and promotes tumor progression, induction of DKK-1 may be relevant to its antitumor action. The authors have also shown a relationship between the expression of DKK-1 receptor and vitamin D in human colorectal tumors, and further, that DKK-1 has tumor suppressor activities in addition to inhibition via Wnt / beta-catenin.
These findings help explain the molecular mechanisms of action of vitamin D, and support its role in the prevention of human colon cancer and therefore the importance of maintaining adequate levels of vitamin multifunctional body.

Colonoscopy - What to Expect and How to Prepare For It

What is Colonoscopy?
Colonoscopy is the internal examination of the colon and rectum by a colonoscope (a long, flexible tube about half an inch in diameter with a camera attached to the end), to evaluate symptoms of the colon (eg. Rectal bleeding, change in bowel habits and persistent abdominal pain), or to screen asymptomatic individuals who are at risk of colon cancer.
It can detect ulcers, inflammed tissue and abnormal growths in the walls of the colon.
Preparing for a Colonoscopy
For successful visualization of the colon and rectum, the bowel must be clean and free of accumulated faeces. It is thus very important that you follow the instructions for preparing your bowel, given by your doctor. Without proper preparation, the colonoscopy may not be successful and may have to be repeated.
The Colonoscopy
You will be given a pain reliever and some sedation, so that you will be relaxed and comfortable. You may be asleep during the colonoscopy or be unable to remember it following the procedure. You will be made to lie on your side with your knees drawn up towards your chest, and your doctor will pass the well lubricated colonoscope into your anus, gently guiding it through the rectum and into the colon. Small amounts of air will be pumped in to expand the colon for proper visualization of the colon walls.
Your doctor can remove growths, called polyps during the colonoscopy, and later send it to the laboratory to test for signs of cancer. Polyps are common and usually benign, however, most colorectal cancers begin as polyps, so they should always be tested.
Biopsies can also be taken from abnormal looking tissues in the walls of the colon. If bleeding occurs following biopsy or removal of polyps, it can be stopped via diathermy (an electrical probe) passed through the colonscope.
The entire procedure lasts about 30 minutes to an hour.
Following The Colonoscopy
You may be required to remain at the clinic for 1 to 2 hours after the procedure to allow time for the sedative to wear off. Cramping, bloating and passing of flatus (gas) is common following a colonoscope due to the air pumped in during the procedure.
You should contact your doctor if you have any of the following rare side effects:

• Fever
• Severe abdominal pain
• Blood in your stools

Dr Ang C.D. is has been in medical practice for over 12 years. He graduated with an M.B.B.S. degree from the National University of Singapore in 1997 and subsequently completed his post-graduate diploma in Family Medicine.
He has had training in Emergency Medicine, Internal Medicine, Geriatric Medicine, Orthopaedic Surgery, Obstetrics & Gynaecology, Neurosurgery, General Surgery, Colorectal Surgery and Urology.
Dr Ang currently practices in a family clinic in Singapore, seeing a good mix of paediatric, adult and geriatric patients.
With the goal of providing local and international patients with a resource for specialist care in Singapore, Dr Ang has founded SingaporeDoc.com, a Web Directory of Specialists in Private Practice in Singapore.

Microscopes and Hodgkin's Lymphoma - Understanding the Pathophysiology of a Common Cancer

First off What is Lymphoma?
We have to first define what lymphoma is before discussing Hodgkin's disease. Lymphoma is a cancer that develops from cells in the body known as "lymphocytes." Lympocytes are a subcategory of white blood cells. There are two different types of lymphocytes: B-cells and T-cells. Almost all lymphomas, including Hodgkin's disease, stem from B-cells.
In Hodgkin's lymphoma a B-cell, for unknown reasons, becomes cancerous. The cell then makes many many clones of itself. These cells bundle together to form a solid tumor known as a lymphoma. There are several hypotheses for why these cells become cancerous in Hodgkin's. One belief is that infection with Epstein-Barr virus (EBV, the same virus that causes infectious mononucleosis) can cause the cells to turn malignant in genetically susceptible people. Other theories are that certain genetic translocations may be the underlying factor. As of yet, no particular theory has significant supporting data to call it the "cause." In fact, there may be multiple unrelated causes.
Types
There are different subcategories of Hodgkin's lymphoma. They are based on several microscopic characteristics, and are important in determining prognosis. The features the pathologist is looking for are the number of Reed-Sternberg cells, as well as the number of lymphocytes present in the biospy specimen. A Reed-Sternberg cell is a funny shaped cell with two nuclei that looks like owl's eyes.
The first subcategory, and most common type, is nodular sclerosing Hodgkin's lymphoma. In this type there are very few Reed-Sternberg cells with a moderate number of lymphocytes. It commonly occurs in younger individuals, and with treatment, the prognosis is excellent.
The second subcategory is mixed cellularity Hodgkin's lymphoma. This type has many Reed-Sternberg cells and a moderate number of lymphocytes when viewed under the microscope. It has an intermediate prognosis.
The third subcategory is lymphocyte predominant Hodgkin's. It has very few Reed-Sternberg cells and many lymphocytes. It occurs most commonly in males less than 35 years of age. It is also one of the few types that is not associated with Epstein-Barr virus infection.
The last subcategory is lymphocyte depleted. It is the rarest form of Hodgkin's lymphoma. It typically affects older males. Unfortunately it has the worst prognosis of the four types.

Colon Cancer Prevention - What You Need to Know

More than 100,000 Americans are diagnosed with colon cancer every year. According to the American Cancer Society most colon cancers occur in folks over the age of 35.
The good news is this cancer is very easy to prevent. Just remember if you experience any blood in your stools or any unusual changes in your bowel habits for more than a few weeks you should get it checked out. In addition, if you experience symptoms like unusual weight loss, fatigue, nausea, anemia or jaundice for more than a few days you need to see a doctor right away.
The simple fact is the key to beating colon cancer is early detection. Current colon cancer treatments are over 85% successful when diagnosed early. So this is important.
But I'm sure you'd agree, the best thing to do is prevent getting it all together. To do this all you'll need to do is make a few lifestyle and dietary changes.
* Eat a high fiber diet to keep your colon healthy and free of carcinogens. Think beans, whole grains, fruits and veggies.
* Drink more water. You know you're getting enough if you need to urinate about 5 times a day.
* Ease up on the alcohol. Studies show the more you drink, the more likely it is you'll get colon cancer.
* Avoid too much red meat. Limit your intake of beef, pork and lamb to once or twice a week.
* Make sure you're getting enough calcium and magnesium. These minerals help protect the colon from carcinogens. The best thing to do here is take a good high-quality supplement.
Also, it's good idea to do a colon cleanse a few times a year. This removes toxins and rejuvenates your colon. In addition it helps your body absorb nutrients more efficiently. To make this easier consider getting a high-quality colon cleansing product that contains bentonite clay.
The take-away here is to remember that a healthy person will not suffer from constipation and will have at least one bowel movement every day. Just following the simple guidelines listed here is not too difficult, will increase your energy, and most importantly, prevent colon cancer.

How to Start a Colon Cancer Diet

When we reach the age of 50, one out of four individuals that we know or might be acquainted with will develop colorectal cancer. This figure is high enough to get us alarmed to prepare for our uncertain future. No one would like to suffer such an unbearable disease when we reach our golden years, where possibly, eating can be the only one of our lives' greatest highlights.
A proper diet has always been a man's greatest preventative measure against developing serious or fatal diseases. Coupled with our knowledge of the benefits of a healthy diet and proper nutrition, how are we to start a colon cancer diet? Can this diet actually guarantee a life free from colorectal cancer? We will find out! Before we start, we have to understand that dieting has always been a misnomer for the diets that Hollywood actresses practice in order for them to look extremely bony or extremely sexy thin. We have to take note that dieting is comprised of a balance between the major food groups (go, grow, glow) to attain good health.
To begin starting and formulating our own diet, we must know the food that we are supposed to eat that shall aid our efforts in preventing colorectal cancer.
• It remains true that a high-fiber diet helps in colon cleansing, hence decreasing one's risk of developing colon polyps that may result in colorectal cancer in a matter of 10 years. This is the main reason why high-fiber diets will indirectly help us prevent the development colon cancer. Foods that have helpful high-fibers are fruits and vegetables, barley, bran, brown rice, whole-grain bread and whole-wheat pasta.
• Food high in folic acid will aid in reducing the risk of developing colon cancer as well as breast cancer. This finding was supported by the fact that incidents are associated with the polymorphism of a gene for methylene tetrahydrofolate reductase, an enzyme involved in folic acid metabolism. The kinds of food that are high in folic acid include spinach, asparagus, broccoli and beets among many.
• Low-fat food should be taken more than red meats or charred meat since it increases the risk to colorectal cancer. These low-fat foods include fish such as tuna, lobster and other crustaceans, skimmed milk, cornflakes etc.
• Vitamin D and Calcium has also been found to reduce the risk of colorectal cancer by reducing the formation of colorectal adenoma polyps. Vitamin D can be supplemented by taking vitamins while calcium can be found in dairy.
So as we start on our colon cancer diet, will we be assured that this diet can prevent colon cancer development? The answer still is, "No". Even if a person followed a strict regimen to prevent colon cancer, he may not be guaranteed that colon cancer development will cease to exist. This is due to the fact that diet is just one of many risk factors in the development of colon cancer. Other factors include heredity, age, environment, behavior, and pre-existing conditions such as Diabetes.
But in the end, we have to put this colon cancer diet in good light. Mainly because dieting and eating healthy can provide you a generally healthy body and the benefits of a colon cancer diet still outweighs the weak effect it produces as preventive measure against colorectal cancer. So, let's start our colon cancer diet now.

Acute Lymphoblastic Leukaemia in Children

This information is about acute lymphoblastic leukaemia in children. It is helpful to read general information on children's cancer, which contains more information about cancers in children, their diagnosis and treatment and the support services available.
* Leukaemia
* ALL
* Causes of ALL
* Signs and symptoms
* How it is diagnosed
* Treatment
* Side effects of treatment
* Clinical trials
* Follow-up
* Your feelings
* References
Leukaemia
One third of all childhood cancers are leukaemia, with approximately 400 new cases occurring each year in the UK. Approximately three quarters (75%) of these are acute lymphoblastic leukaemia. ALL can affect children at any age but is more common between the ages of 1 and 4. ALL is more common in boys than girls.
ALL
Leukaemia is a cancer of the white blood cells. All blood cells are produced in the bone marrow. Bone marrow is the spongy substance at the core of some of the bones in the body. Bone marrow contains:
* red blood cells that carry oxygen around the body
* white blood cells that help fight infection
* platelets that help the blood to clot and control bleeding.
There are two different types of white cell: lymphocytes or myeloid cells. These white blood cells work together to fight infection. Normally white blood cells repair and reproduce themselves in an orderly and controlled way. In leukaemia, however, the process gets out of control and the cells continue to divide, but do not mature.
These immature dividing cells fill up the bone marrow and stop it from making healthy blood cells. As the leukaemic cells are not mature, they cannot work properly. This leads to an increased risk of infection. Because the bone marrow cannot make enough healthy red blood cells and platelets, symptoms such as anaemia and bruising can occur.
There are four main types of leukaemia: acute lymphoblastic (ALL), acute myeloid (AML), chronic lymphocytic (CLL) and chronic myeloid (CML). Chronic leukaemias usually affect adults and are extremely rare in children and young people. Each type of leukaemia has its own characteristics and treatment. Acute lymphoblastic leukaemia is a cancer of immature lymphocytes, called lymphoblasts or blast cells.
There are two different types of lymphocytes: T-cells and B-cells. Often the leukaemia occurs at a very early stage in the immature lymphocytes, before they have developed as far as becoming either T-cells or B-cells. However, if the cells have developed this far before becoming leukaemic, the type of leukaemia may be known as T-cell or B-cell leukaemia.
Causes of ALL
The exact cause of ALL is unknown. Research is going on all the time into possible causes of this disease. Children with certain genetic disorders, such as Down's syndrome, are known to have a higher risk of developing leukaemia. Brothers and sisters of a child with ALL have a slightly increased risk of developing ALL themselves, although this risk is still small.
In recent years there has been publicity about leukaemia occurring more often in children living close to nuclear power plants or high-voltage power lines. Research is still under way to see if there is any definite link between these factors but as yet there is no evidence of this. ALL, like other types of cancer, is not infectious and cannot be passed on to other people.
Signs and symptoms
As the leukaemia cells multiply in the bone marrow, the production of normal blood cells is reduced. Children may therefore become tired and lethargic due to anaemia, which is caused by a lack of red blood cells. They may develop bruises, and bleeding may take longer to stop due to low numbers of platelets. Sometimes children may suffer from infections because of low numbers of normal white blood cells.
A child is likely to feel generally unwell and may complain of aches and pains in the limbs, or may have swollen lymph glands. At first the symptoms are just like those of a viral infection, but when they continue for more than a week or two the diagnosis usually becomes clear.
How it is diagnosed
A blood test usually shows low numbers of normal white blood cells and the presence of the abnormal leukaemic cells. A sample of bone marrow is needed to confirm the diagnosis. A lumbar puncture is done to see if the spinal fluid contains any leukaemia cells. A chest x-ray is also done, which will show if there are any enlarged glands in the chest. Other tests may be necessary, depending on the child's symptoms.
These tests will help to identify the precise type of leukaemia involved.
Treatment
The aim of treatment for ALL is to destroy the leukaemia cells and allow the bone marrow to work normally again. Chemotherapy is the main treatment for ALL. Usually a combination of chemotherapy drugs are given according to a treatment plan (often called a protocol or regimen). The treatment is given in several phases, or 'blocks', which are outlined below.
Induction This phase involves intensive treatment aimed at destroying as many leukaemia cells as possible. The induction phase lasts for 4-6 weeks. A bone-marrow test is taken at the end of induction treatment to check if the child is in remission. Remission is where there is no evidence of leukaemia.
Consolidation and central nervous system (CNS) treatment The next phase of treatment is aimed at maintaining the remission and also at preventing the spread of leukaemia cells into the brain and spinal cord (the central nervous system). CNS treatment involves injecting a drug, usually methotrexate, directly into the spinal fluid (intrathecally) during a lumbar puncture. Occasionally radiotherapy to the brain is also necessary.
Further doses of chemotherapy treatment (somtimes called 'intensification blocks') are given in order to kill off any remaining leukaemia cells. Between 2 and 4 blocks of treatment may be needed, depending on your child's particular treatment plan.
Maintenance treatment This phase of treatment lasts for up to 2 years for girls and up to 3 years for boys, from diagnosis. It involves daily tablets and monthly injections of chemotherapy.
Children will be able to take part in their normal daily activities as soon as they feel able to. Some children return to school before maintenance treatment.
Bone-marrow transplantation Bone-marrow transplantation is only used for children with ALL that is likely to come back following standard chemotherapy, or for children whose leukaemia has come back (recurred) following standard treatment.
Testicular radiotherapy In some situations it may be necessary for boys to have radiotherapy to their testicles. This is because leukaemia cells can survive in the testicles despite chemotherapy.
Side effects of treatment
Many cancer treatments will cause side effects. This is because while the treatments are killing the cancer cells they can also damage some normal cells. Some of the main side effects are:
* hair loss
* reduction in the number of blood cells produced by the bone marrow, which can cause anemia, an increased risk of bruising, bleeding and infection
* loss of appetite and weight
* nausea (feeling sick) and vomiting
Most side effects are temporary and there are ways of reducing them and supporting your child through them. Your child's doctor or nurse will talk to you about any possible side effects.
Late side effects
A small number of children may develop late side effects, sometimes many years later. These include possible problems with puberty and fertility, a change in the way the heart works and a small increase in the risk of developing another cancer in later life. Your child's doctor or nurse will explain about any possible late side effects.
Clinical trials
Many children have their treatment as part of a clinical research trial. Trials aim to improve our understanding of the best way to treat an illness (usually by comparing the standard treatment with a new or modified version of the standard treatment). Specialist doctors carry out trials for ALL. Your child's medical team will talk to you about taking part in a clinical trial (if appropriate) and will answer any questions you may have. Written information is often provided to help explain things. Taking part in a research trial is completely voluntary and you'll be given plenty of time to decide if it is right for your child. At present the main trial for ALL is called 'UKALL 2003'.
Most children with ALL are cured. If the leukaemia comes back, it normally does so within the first three years after stopping treatment. Further treatment can then be given. Long-term side effects are uncommon and most children with ALL grow and develop normally.
If you have specific concerns about your child's condition and treatment, it is best to discuss them with your child's doctor, who knows the situation in detail.
Your feelings
As a parent, the fact that your child has cancer is one of the worst situations to face. You may have many different emotions, such as fear, guilt, sadness, anger and uncertainty. These are all normal reactions and are part of the process that many parents go through at such a difficult time. There is not enough space here to address all of the feelings you may have. However, general information on children's cancer talks about the emotional impact of caring for a child with cancer and suggests sources of help and support.

The Colon Cancer

The design of stepwise genetic modifiation in cancer is best highlighted by observations made in colonic lesions representing various phases of development to malignancy. Particular anatomical alterations are discovered commonly in early-stage adenomas, whereas others have a tendency to occur with substantial frequency only after the development of wide spread neoplasia. These modifications are in maintaining with the idea that serial phenotypic modifications must happen in the mobile for it to exhibit full malignant (wide spread and metastatic) properties. Two principal lines of proof assistance the model of stepwise genetic modifiation in intestinal tract cancer.
1. The uncommon familial syndromes associated with predisposition to colon most cancers at an early age are now recognized to result from germline mutations. Familial adenomatous polyposis is the end result of a mutation within the APC gene, which encodes a cell adhesion protein which has also been implicated within the control of -catenin, a potent transcriptional activator. Within the tumors that subsequently produce, the remaining allele have been lost. Similarly, hereditary nonpolyposis colorectal most cancers is linked with germline mutations in DNA repair genes such as hMSH2 and hMLH1. These genes can also be affected in sporadic cancers.
2. The carcinogenic effects of factors known to be linked to an elevated risk of colon most cancers constitute the second line of evidence for the anatomical basis for colon most cancers. Substances derived from bacterial colonic flora, ingested meals, or endogenous metabolites such as fecapentaenes, 3-ketosteroids, and benzo[]pyrenes are mutagenic. Amounts of those ingredients can be reduced by low-fat and high-fiber diets, and several epidemiologic studies confirm that this kind of diets decrease the risk of intestinal tract cancer. Furthermore, because the chance of sporadic intestinal tract cancer in older individuals is mildly elevated in the presence of a good family background, there might be other inherited anatomical abnormalities that interact with environmental elements to trigger colon most cancers.
The sequence of genetic changes might not require to become exact to result in the improvement of an wide spread cancer, although there is mounting evidence that some genetic lesions tend to produce earlier, whereas other people may develop late in the course of the natural disease. All phenotypic changes can't be explained by a known anatomical abnormality, nor do all identified anatomical modifiation have a known phenotypic result. Nevertheless, the stepwise dynamics of genotypic and phenotypic irregularities is well set up.
The earliest molecular defect within the pathogenesis of intestinal tract cancer is the acquisition of somatic mutations in the APC gene within the normal colonic mucosa. This defect brings about abnormal regulation of -catenin, which leads to abnormal cell proliferation and the initial actions in tumor formation. Subsequent defects in the TGF- signaling pathway inactivate this important growth inhibitory pathway and lead to more tumor mucosal proliferation and the introduction of little adenomas. Mutational activation of the K-ras gene leads to constitutive activation of the essential proliferative signaling pathway, is common at these stages, and further boosts the proliferative potential of the adenomatous tumor cells. Deletion or reduction of expression from the DCC gene is common in the progression to wide spread intestinal tract cancers.
The DCC protein is a transmembrane protein from the immunoglobulin superfamily and might be a receptor for certain extracellular molecules that guide mobile development and or apoptosis. Mutational inactivation of p53 can also be a frequently observed step in the development of wide spread intestinal tract cancer, observed in late adenomas and earlier wide spread cancers, and prospects to loss of an essential mobile cycle checkpoint and inability to activate the p53-dependent apoptotic pathways. Identification of genetic irregularities within the development of colon cancer to metastatic disease is presently under investigation.
In parallel to these sequential irregularities in the regulation of mobile proliferation, colon cancers also acquire defects in mechanisms that guard genomic stability. These generally include mutations in mismatch restore genes or genes that prevent chromosomal instability. Mismatch restore genes are a family of genes which are involved in proofreading DNA throughout replication and consist of MSH2,MLH1,PMS1, and PMS2. Germline mutations in these genes cause the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome. Nonhereditary colon cancers develop genomic instability via defects within the chromosomal instability (CIN) genes. Defects in these genes result in the gain or reduction of large segments or whole chromosomes throughout replication primary to aneuploidy.
The stepwise acquisition of genetic irregularities described previously is associated with modifiation in the phenotypic behavior of the colonic mucosa. The earliest change in the development to colon most cancers may be the improve in cell number (hyperplasia) on the epithelial (luminal) surface. This creates an adenoma, which can be characterized by gland-forming cells exhibiting increases in sizing and cell number but no invasion of surrounding structures. Presumably, these changes are due to improved proliferation and loss of mobile cycle manage but prior to acquisition of the capacity to invade ECM. Additional dysplastic modifications such as reduction of mucin production and altered mobile polarity may be present to some variable degree.
Some adenomas may improvement to carcinoma in situ and ultimately to invasive carcinoma. An early function linked with disrupted architecture even prior to invasion occurs is the development of fragile new vessels or destruction of existing vessels that may trigger microscopic bleeding. This could be examined for clinically like a fecal occult blood determination employed for screening and earlier diagnosis of preinvasive and invasive intestinal tract cancer. It isn't known regardless of whether all wide spread colon cancers pass via a hyperplastic or preinvasive stage, and there is no information available for epithelial malignancies generally.
Additional functional modifications in the cell and surrounding tissue are also manifested in the preinvasive and wide spread stages. Once the basement membrane is penetrated by invasive malignant tissue, entry could be gained towards the regional lymphatics, and spread to regional pericolic lymph nodes can occur. Entry of cells into the bloodstream can result in distant distribute in the pattern that reflects venous drainage. Consequently, hematogenous spread from primary colon tumors towards the liver is common, whereas rectal tumors usually disseminate to liver, lung, and bone. Additionally to anatomic considerations, there may exist specific tropism of malignant cells mediated by surface proteins that cause the cells to preferentially home in on certain organs or sites.
Colonic epithelium is specialized to secrete mucus proteins and to get water and electrolytes. The upkeep of a tight luminal barrier, intracellular charge distinctions, and the capability to exclude toxins are additional specialized features. Some of these features are maintained within the progression to neoplasia and may lead to some specific phenotype of the malignant cell. One instance is the expression of a transporter membrane protein, MDR-1, present on a number of types of epithelium, such as the colon.
MDR-1 is recognized to trigger efflux of several compounds out from the tissue, presumably like a protective system to exclude poisons. In sophisticated colon cancer, this protein might lead to the relative resistance of this along with other tumor types to some variety of chemotherapeutic agents which are transported by MDR-1. In some instances, the activation of a latent gene encoding carcinoembryonic antigen (CEA) can result in measurable levels from the CEA protein in the serum of sufferers with localized or metastatic colon cancer as well as other adenocarcinomas.