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There is no single known cause for any of the different types of leukemias.

Common leukemia signs and symptoms include:

• Fever or chills
• Persistent fatigue, weakness
• Frequent or severe infections
• Losing weight without trying
• Swollen lymph nodes, enlarged liver or spleen
• Easy bleeding or bruising
• Recurrent nosebleeds
• Tiny red spots in your skin (petechiae)

The few known causes, which are not generally factors within the control of the average person, account for relatively few cases. The cause for most cases of leukemia is unknown. The different leukemias likely have different causes.

• Every four minutes, someone is diagnosed with blood cancer – more than 201,870 new cases are expected this year in the United States.
• More than 327,520 Americans are living with leukemia
• Nearly 761,659 Americans are living with Hodgkin’s or non-Hodgkin’s lymphoma.
• An estimated 35,000 to 55,000 people are living with myelodysplastic syndromes in the United States
• An estimated 95,874 people are living with myeloma in the United States
• An estimated 67,870 deaths will result from blood cancer this year.
• Leukemia causes more deaths than any other cancer among children and young adults under the age of 20; however, leukemia is diagnosed 10 times more often in adults than children.
• Non-Hodgkin’s lymphoma is the 6th most common cancer in the U.S.
• Every day 148 Americans are diagnosed with leukemia and 67 lose the fight.
• Every day 221 Americans are diagnosed with lymphoma and 57 lose the fight.
• Leukemia strikes males and females of all ages and all races. It does not discriminate.
• The five-year relative survival rate for non-Hodgkin’s lymphoma and leukemia is about 8% lower for African-Americans than that of whites.
• Leukemia is the most common cancer in Hispanic children and adolescents; five-year relative survival rate is slightly lower for Hispanics than that of non-Hispanic whites.

Leukemia, like other cancers, results from mutations in the DNA. Certain mutations can trigger leukemia by activating oncogenes or deactivating tumor suppressor genes, and thereby disrupting the regulation of cell death, differentiation or division. These mutations may occur spontaneously or as a result of exposure to radiation or carcinogenic substances.

Among adults, the known causes are natural and artificial ionizing radiation, a few viruses such as human T-lymphotropic virus, and some chemicals, notably benzene and alkylating chemotherapy agents for previous malignancies. Use of tobacco is associated with a small increase in the risk of developing acute myeloid leukemia in adults. Cohort and case-control studies have linked exposure to some petrochemicals and hair dyes to the development of some forms of leukemia. Diet has very limited or no effect, although eating more vegetables may confer a small protective benefit.

Viruses have also been linked to some forms of leukemia. For example, human T-lymphotropic virus (HTLV-1) causes adult T-cell leukemia.

Some people have a genetic predisposition towards developing leukemia. This predisposition is demonstrated by family histories and twin studies. The affected people may have a single gene or multiple genes in common. In some cases, families tend to develop the same kinds of leukemia as other members; in other families, affected people may develop different forms of leukemia or related blood cancers.

In addition to these genetic issues, people with chromosomal abnormalities or certain other genetic conditions have a greater risk of leukemia. For example, people with Down syndrome have a significantly increased risk of developing forms of acute leukemia (especially acute myeloid leukemia), and Fanconi anemia is a risk factor for developing acute myeloid leukemia. Mutation in SPRED1 gene has been associated with a predisposition to childhood leukemia.

Whether or not non-ionizing radiation causes leukemia has been studied for several decades. The International Agency for Research on Cancer expert working group undertook a detailed review of all data on static and extremely low frequency electromagnetic energy, which occurs naturally and in association with the generation, transmission, and use of electrical power.They concluded that there is limited evidence that high levels of ELF magnetic (but not electric) fields might cause some cases of childhood leukemia. No evidence for a relationship to leukemia or another form of malignancy in adults has been demonstrated. Since exposure to such levels of ELFs is relatively uncommon, the World Health Organization concludes that ELF exposure, if later proven to be causative, would account for just 100 to 2400 cases worldwide each year, representing 0.2 to 4.9% of the total incidence of childhood leukemia for that year (about 0.03 to 0.9% of all leukemias).

A few cases of maternal-fetal transmission (a baby acquires leukemia because its mother had leukemia during the pregnancy) have been reported.

According to a study conducted at the Center for Research in Epidemiology and Population Health in France, children born to mothers who use fertility drugs to induce ovulation are more than twice as likely to develop leukemia during their childhoods than other children.

Leukemia is a cancer of the tissues that produce blood cells, resulting in abnormal blood cells.  Leukemia appears to be related to damage to chromosomes or genes.  The damage disrupts the process by which blood cells achieve their final and functional form.

Leukemia is the most common kind of cancer in children

Leukemia also causes more deaths than any other form of cancer in children.  Fortunately, improved treatment methods have greatly reduced deaths from leukemia.

Leukemia rates are higher for white children than black children.

There are several forms of leukemia, two of which are particularly important in children.  These are usually known as ALL and AML.

Acute lymphoblastic leukemia (ALL) is the most common form in children and represents 78% of cases of leukemia.   (ALL is also called acute lymphocytic leukemia.)  From 1991 to 1994, the incidence rate was 59 cases per million children under five.   ALL reaches its greatest frequency in children between 2 and 6, with a peak of more than 80 cases per million children per year at ages 3 to 4.  Rates then decline to age 20.  Scientists believe that this pattern means that two genetic changes are needed to cause the disease and that one occurs before a child is born.

ALL increased about 1% per year between 1977 and 1995, though some of this change may result from changes in the groups that are tracked for cancer . However, many scientists believe that this change represents a genuine increase in the frequency of the disease that could be caused by environmental factors.

Acute non-lymphocytic leukemia is the second most common form of leukemia in children and represents 19% of cases.  It is also called acute myelogenous leukemia (AML).  It is the form of leukemia most commonly diagnosed in children less than one year old.   Rates are higher at ages 1-3 and in late adolescence .

Unlike ALL, the rates for AML do not appear to have increased since 1975 .

Known and Suspected Causes of Leukemia

Both pre-natal and post-natal exposure to ionizing radiation (particularly X rays) can cause leukemia in children.  Pre-natal exposure to X rays has been greatly reduced with the adoption of ultrasound for screening in pregnant women.

Several studies link pesticide exposure by both parents and children to leukemia.  The pattern of disease suggests that some damage to chromosomes may occur before the child is born (3).  Children born to parents employed in certain occupations that have chemical exposures are more likely to have leukemia . Chemicals, specifically including benzene, have been shown to cause leukemia in adults.

A recent review of 48 epidemiological studies concluded that the strongest evidence for a relationship between a parent’s exposure to chemicals other than pesticides and childhood leukemia was for solvents, paints, and employment in motor vehicle-related occupations .

These studies tend to look at the occupation of fathers more often than those of mothers, despite the fact that exposures of mothers are likely to be at least as important.  For occupations of the mothers, the review concluded that the most significant were employment in personal services industries, in metal processing, and in textiles.   All three categories had significantly elevated risks.  For occupations of fathers, employment in painting led to increased risk of leukemia in a child..

Some studies show that exposure to electric and magnetic fields (EMFs) is associated with increased risk of leukemia.

There has been some evidence for an association between leukemia and smoking by parents, though the largest study performed to date did not find that smoking by parents, either before birth or afterwards, increased risk of ALL or AML in children .

IONIZING RADIATION

Ionizing radiation is considered a “known” cause of childhood leukemia.  Follow-up studies of people who survived the detonation of atomic bombs at Hiroshima and Nagasaki found that the risk of leukemia was higher for those exposed to radiation.  The risk is also higher for those exposed at an earlier age .  Radiation from nuclear power plants is a known cause for both kinds of leukemia .  A recent study found that exposure to X rays after birth also increased the risk of leukemia.  Infants receiving diagnostic X rays had 60% more leukemia than other children .

PESTICIDES

Several studies have linked leukemia to pesticides.  Two recent reviews concluded that pesticide exposure may be a cause of leukemia (10)(11). These reviews report that most, though not all, studies find leukemia was more likely in children whose fathers were exposed to pesticides at work than other children.   Risks for children are often reported to be greater than risks for adults (12).

• One large recent study of 491 children with ALL found that risk was increased by home use of some kinds of pesticides and by use of multiple different pesticides. Herbicide use during pregnancy was associated with a 50% increase in risk.  Use of insecticides in the home was associated with increased risk of ALL, and frequent use was associated with higher risk.  Use of some garden products also seemed to increase risk.  The heightened risk was associated with use of multiple products (13).
• A study of childhood leukemia cases in Shanghai found a more than threefold increase in risk for children whose mothers were exposed to pesticides at work (14).
• A study of children under 15 in the Denver area reported that use of pest strips was associated with higher risks of leukemia (15).
• A study of children in the US found that AML risk was increased when either parent was exposed to pesticides or when the child was exposed to pesticides after birth (16).
• In 1989, the Children’s Cancer Study Group reported that, among families of 204 children with AML, children whose fathers worked with pesticides for more than 1000 days had nearly three times the risk of other children. The risk was greater for children under the age of 6.    Children regularly exposed to pesticides in the household had 3.5 times greater risk of leukemia than those not exposed (17).
• In a 1987 National Cancer Institute study, the risk of childhood leukemia increased nearly four times when pesticides were used within the house at least once per week. The risk increased more than six times when garden pesticides were used at least once per month (18).
• Children of fathers with jobs including pesticide exposure had a 2.7 times higher risk of leukemia when compared to controls (17).
• A small study in the Netherlands reported increased risk of leukemia in children who were exposed to pesticides directly or whose fathers were exposed at work (19).
• An increased risk was found for children whose parents used pesticides in the home (OR = 3.8, P = .004) or garden (OR = 6.5, P = .007) or who burned incense in the home (OR = 2.7, P = .007). The risk was greater for frequent use (18).

SOLVENTS

• A 1998 review concluded that the evidence for an association between childhood leukemia and paternal exposure to solvents is “quite strong.” Chemicals where risks are elevated include solvents in general, chlorinated solvents, benzene, carbon tetrachloride, and trichloroethylene (TCE) .
• A study of nearly 2,000 children found that the risk of acute lymphoblastic leukemia (ALL) was increased if the children’s mothers were exposed to solvents, paints, or thinners before conception or during pregnancy or to plastics after birth. The father’s exposure to plastics before conception was associated with greater risk.  This study reported that the timing of exposure was an important factor (20).
• A study of children in the US found that the father’s exposure to petroleum products increased the risk of AML (16). Petroleum products usually contain benzene.
• An earlier study had found that children born to fathers with exposure to solvents, petroleum products, plastics or lead were more likely to have AML than other children (17). For solvents, the excess risk was substantial. The same study found that children born to mothers with exposure to metal dusts, pigments and paints at work were more likely to have AML.
• A case-control study of 123 children 10 and under in Los Angeles County looked at specific occupational and home exposures and found an increased risk of leukemia for children whose fathers were exposed at work after the birth of the child to chlorinated solvents {odds ratio (OR) = 3.5, p = .01}. Risk of leukemia was related to mothers’ employment in personal service industries (OR = 2.7, p = .04) but not to specified occupational exposures (18).
• A Scottish study found greatly increased risk of leukemia for children born to fathers who had exposure to benzene (21).
• A study of children in Shanghai reported increased ALL in children whose mothers were employed in the chemical industry during pregnancy, increased AML in children whose mothers were exposed to benzene and increased AML and ALL to children whose mothers were exposed to gasoline (14). Also children born to women employed in metal processing were more likely to have AML.
• A study in the Netherlands found that mothers who were exposed to hydrocarbons at work or certain other chemicals in the year before the birth of their child were more likely to have a child with ALL (22).
• A study in New York found that children born to fathers who worked in motor vehicle-related jobs were more than twice as likely to have leukemia (23).

EMFs – Electric and Magnetic Fields

Evidence about whether Electric and Magnetic Fields (EMFs)contribute to leukemia in children is contradictory, with some studies finding an effect and others not finding an effect.  However, there are many ways to measure these fields (24), and the various approaches do not correlate in all cases (25).    Some of the contradictory results could be due to differences in methods of measuring the EMFs.  Also, as is true with other possible causes, there may be a specific time period when children are most susceptible, studies do not necessarily identify the relevant time period.

• More positive results are found when EMFs are measured according to “wire codes,” which are classifications based on how wiring is configured (26) than when EMFs are measured directly (27).
• Several studies have found that exposure to EMFs increases risk of leukemia for children (28). One study found that children living near high voltage power installations were more likely to be found to have leukemia than other children.  However, other studies have failed to find any link.
• A 1995 review of several studies reported a link between EMF exposure and increased leukemia that cannot be readily explained by errors in the studies.
• One recent study found that risk of leukemia was elevated when exposure to EMFs was consistent over the term of the pregnancy and in cases where the design of the water system in the home led to “ground currents” from connections between plumbing pipes and the grounding for the electricity.
• A large study in Britain found no association between exposure to EMFs and leukemia in 3,838 children. A study in Los Angeles that looked at combined measures of EMF found increased risk of leukemia to be associated with increased EMF exposure.
• A first study of exposures of parents to EMFs at work before their children were born found that fathers with high exposures were more likely to have children who got leukemia. This study had several good design elements that avoided problems with recall of exposures by parents.

Radon

Radon is a naturally occurring radioactive gas that gets into homes from materials underneath houses, such as soil or rocks, or from water piped into the houses.  Two studies have investigated whether radon exposure is related to ALL but have not found any relationship.  Both of these studies were limited in the conclusions that they could draw because participation rates were low.  One earlier study reported an association between levels of radon in geographic areas and increased risk of childhood leukemia.

http://www.envirohealthpolicy.net/kidstest/Cancer%20Pages/Individual%20Cancers/Leukemia.htm

PTEN is one of the most commonly lost tumor suppressors in human cancer; in fact, up to 70% of men with prostate cancer are estimated to have lost a copy of thePTEN gene at the time of diagnosis. D…

Source: PTEN gene and cancer

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PTEN is one of the most commonly lost tumor suppressors in human cancer; in fact, up to 70% of men with prostate cancer are estimated to have lost a copy of thePTEN gene at the time of diagnosis.

During tumor development, mutations and deletions of PTEN occur that inactivate its enzymatic activity leading to increased cell proliferation and reduced cell death. Frequent genetic inactivation of PTEN occurs in glioblastoma, endometrial cancer, and prostate cancer; and reduced expression is found in many other tumor types such as lung and breast cancer. Furthermore, PTEN mutation also causes a variety of inherited predispositions to cancer.

Non-cancerous neoplasia

Researchers have identified more than 70 mutations in the PTEN gene in people with Cowden syndrome.^{[citation needed]} These mutations can be changes in a small number of base pairs or, in some cases, deletions of a large number of base pairs.^{[citation needed]} Most of these mutations cause the PTEN gene to make a protein that does not function properly or does not work at all. The defective protein is unable to stop cell division or signal abnormal cells to die, which can lead to tumor growth, particularly in the breast, thyroid, or uterus.^[20]

Mutations in the PTEN gene cause several other disorders that, like Cowden syndrome, are characterized by the development of non-cancerous tumors calledhamartomas. These disorders include Bannayan-Riley-Ruvalcaba syndrome and Proteus-like syndrome. Together, the disorders caused by PTEN mutations are calledPTEN hamartoma tumor syndromes, or PHTS. Mutations responsible for these syndromes cause the resulting protein to be non-functional or absent. The defective protein allows the cell to divide in an uncontrolled way and prevents damaged cells from dying, which can lead to the growth of tumors.^[20]

Brain function and autism

Defects of the PTEN gene have been cited to be a potential cause of autism spectrum disorders.^[21] When defective, PTEN protein interacts with the protein of a second gene known as Tp53 to dampen energy production in neurons. This severe stress leads to a spike in harmful mitochondrial DNA changes and abnormal levels of energy production in the cerebellum and hippocampus, brain regions critical for social behavior and cognition. When PTEN protein is insufficient, its interaction withp53 triggers deficiencies and defects in other proteins that also have been found in patients with learning disabilities including autism.^[21]

Patients with defective PTEN can develop cerebellar mass lesions called dysplastic gangliocytomas or Lhermitte–Duclos disease.^[20]

Cell regeneration

PTEN’s strong link to cell growth inhibition is being studied as a possible therapeutic target in tissues that do not traditionally regenerate in mature animals, such as central neurons. PTEN deletion mutants have recently^[22] been shown to allow nerve regeneration in mice.^[23]

Cell lines

Cell lines with known PTEN mutations include:

• prostate: LNCaP, PC-3
• kidney: 786-O
• glioblastoma: U87MG^[26]
• breast : MB-MDA-468, BT549^[26]
• bladder: J82, UMUC-3

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Cowden syndrome, tumor syndrome

Cowden syndrome (CS) is part of the PTEN hamartoma tumor syndrome. Hamartomas are benign, meaning noncancerous, tumor-like growths. Other clinical syndromes that are part of the PTEN hamartoma tumor syndrome are Bannayan-Riley-Ruvalcaba syndrome (BRR; diagnosed in children), Proteus syndrome, and Proteus-like syndrome. CS is characterized by a high risk of both benign and cancerous tumors of the breast, thyroid,endometrium (uterus), colorectal, kidney, and skin (melanoma).

Skin Melanoma

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Major and minor criteria as well as the testing criteria for CS:

Major criteria:

• Breast cancer
• Endometrial cancer
• Follicular thyroid cancer
• Multiple gastrointestinal hamartomas or ganglioneuromas
• Macrocephaly
• Macular pigmentation of glans penis, meaning a discolored area on the skin
• Mucocutaneous lesions
• One biopsy-proven trichilemmoma
• Multiple palmoplantar keratosis, meaning abnormal thickening of the hands and feet
• Multifocal or extensive oral mucosal papillomatosis
• Multiple cutaneous facial papules that are often verrucous, meaning wartlike projections

Minor Criteria:

• Colon cancer
• Esophageal glycogenic acanthosis
• Autism-spectrum disorder
• Mental retardation
• Papillary or follicular variant of papillary thyroid cancer
• Thyroid structural lesions, such as adenoma, nodule(s), goiter
• Renal cell (kidney) carcinoma
• Vascular anomalies, including multiple intracranial developmental venous anomalies
• Lipomas, meaning benign soft tissue tumor
• Single gastrointestinal hamartoma or ganglioneuroma
• Testicular lipomatosis

Cowden Syndrome PTEN Gene Testing Criteria

• People with a personal history of:
• A family with a known PTEN gene mutation
• Meeting clinical diagnostic criteria for CS
• Bannayan-Riley-Ruvalcaba syndrome (BRR)
• Adult Lhermitte-Duclos disease (cerebellar tumors)
• Autism spectrum disorder and macrocephaly
• Two or more biopsy-proben trichilemmomas
• Two or more major criteria (one must be macrocephaly)

Source: Eng C. Will the real Cowden syndrome please stand up: revised diagnostic criteria. Med Genet 2000;37:828-830.

CS is suspected if a person has either three major criteria without macrocephaly, one major and three minor criteria, four minor criteria, or a relative with a clinical diagnosis of CS or BRR.

Research is ongoing to better understand CS. Approximately 80% of the people who meet the current clinical diagnosis of CS have a mutation in the PTEN gene. A blood test can determine if someone has a mutation in thePTEN gene.

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Connie’s comments: Monitor your body for chronic pain or head ache, skin disorders, digestive issues and family genetic history.

With regards to a cancer treatment, every food that we eat or drink can be categorized into several different categories: Foods that feed and strengthen the cancer cells and/or the microbes …

Source: Cancer fighting diet

Not So Specialized After All: Genes Carry Out Different Repairs — A Finding That Helps Clarify the Development of Cancer In a finding that helps clarify the development of human cancer,scient…

Source: Some genes can detox chemical toxins, prevent cancer

Not So Specialized After All: Genes Carry Out Different Repairs — A Finding That Helps Clarify the Development of Cancer

In a finding that helps clarify the development of human cancer,scientists have demonstrated an additional way in which the samegenes can carry out repairs-or, if mutant, fail to carry themout — to the body’s DNA, the chemical of heredity that directseach cell.

Vera researchers found that the total taxpayer cost of prisons in the 40 states that participated in this study was 13.9 percent higher than the cost reflected in those states’ combined corrections…

Source: Prison costs in the USA

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Vera researchers found that the total taxpayer cost of prisons in the 40 states that participated in this study
was 13.9 percent higher than the cost reflected in those states’ combined corrections budgets. The total
price to taxpayers was $39 billion, $5.4 billion more than the $33.5 billion reflected in corrections budgets
alone. The greatest cost drivers outside corrections departments were as follows:

• underfunded contributions to retiree health care for corrections employees ($1.9 billion);
• states’ contributions to retiree health care on behalf of their corrections departments ($837 million);
• employee benefits, such as health insurance ($613 million);
• states’ contributions to pensions on behalf of their corrections departments ($598 million);
•  capital costs ($485 million);
• hospital and other health care for the prison population ($335 million); and
• underfunded pension contributions for corrections employees ($304 million).
  Among the participating states, costs outside the corrections department ranged from less than 1 percent
  of the total cost of prisons, in Arizona, to as much as 34 percent in Connecticut

Antisocial personality disorder Antisocial personality disorder (ASPD), also known as dissocial personality disorder (DPD) and sociopathy, is apersonality disorder, characterized by a pervasive pat…

Source: Antisocial personality disorder in 70% of prison inmates

Chronic Head ache as the First Symptom of an Undiagnosed Renal Cell Carcinoma Renal cell carcinoma (RCC) is an uncommon tumor that rarely metastasizes primarily to the brain. Brain metastases are c…

Source: Chronic head ache and kidney cancer

Chronic Head ache as the First Symptom of an Undiagnosed Renal Cell Carcinoma

Renal cell carcinoma (RCC) is an uncommon tumor that rarely metastasizes primarily to the brain. Brain metastases are commonly observed in patients with metastatic RCC, with a reported incidence of 2–17%. The prognosis of brain metastatic RCC is poor. In this carcinoma type, the source is commonly evident. We report a case of a patient with undiagnosed incidental RCC, who presented chronic headache as the first manifestation.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251248/

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Connie’s comments: I met a person yesterday who had 10% of his kidney removed due to cancer and the first signs he experienced are headache and gluten intolerance.

So I gave him the following tips as I learned of his eating habits and more:

1. Use whole foods rich in Vit C, magnesium and potassium instead of Gatorade which he uses when ever he has head aches.
2. Limit X-ray but be vigilant after recovering from cancer last year with doctor’s monitoring.
3. Get a genetic test since his dad died of colon cancer.
4. Continue on his gluten-free diet, avoiding molds and fungus like 3-day old rice.
5. Avoid medication, drugs, alcohol and smoking.
6. Continue on his exercise.
7. Be strong in his resolve for wellness and have a stronger immune system with holistic living of massage and wellness.

 

Antisocial personality disorder Antisocial personality disorder (ASPD), also known as dissocial personality disorder (DPD) and sociopathy, is apersonality disorder, characterized by a pervasive pat…

Source: Antisocial personality disorder in 70% of prison inmates