[dqfry]

Despite my non existent medical or scientific background I can give this much input...Infection/virus did play a role on Nathan's ALL and there were at least 2 more cases of early diagnosis in our hospital at the same time. One of the nurses (15 years at pediatrics hem/oc) said "they come in clusters". I still don't understand why don't we have a national cancer registry where you could go online and answer a questionarie related specifically to the diagnosed cancer (specially with childhood cancer) Here is a thought...4,000 Leukemia cases a year in USA and there are 4 kids that I've known of in our neighborhood (Redondo Beach, small bay city outside Los Angeles)with the same diagnose. Not exactly a "cluster" but definetely something to be better analyzed.

[iko (OP)]

Welcome back dqfry,

Cluster, cluster...I have been reading those reports for years and counting consecutive cases at work.
In my opinion (!) this wouldn't take us anywhere: difficult to rule out 'coincidence' on one side and to find anything interesting on the other.
Cancer Registries are not public (so far) and their compilation is up to the health care operators.  All over the world epidemiologists analyse them and report increase-decrease and clustering in a short while.  Over the years this type of study is more and more accurate, but results are poor.  Actually it is frustrating, if you think of the bulk of work involved.
In multifactor phenomena like these, time required for developing a disease may be quite different in different patients.
Even seasonal-effects, bound to vitamin D deficiency, may be masked by other factors.
Persistent infections are invisible and may last weeks and months after the contact (epidemics) before switching on the now famous 'overridden' immune response.
I understand your point: we should concentrate on the cause first.
Engineers, physicists, even biologists would insist on searching a cause.
Unfortunately, most people in this field seem to have given up on that, after years and years of 'no result'.
It is commonly accepted that once the disease started, knowing its origin wouldn't affect treatment results.  It was like this in the case of gastroduodenal ulcers.
And this is wrong.

ikod

P.S.
Searching for specific infectious agents by the current sophisticated technologies (PCR, etc.) is one way to look for the etiology, the cause.  It should be done extensively for a long list of 'germs', as many as possible, in every single patient.
Unfortunately, so far only single agents have been studied by single groups.  An interesting report is about parvovirus B19 and leukemia, followed by many others: we still cannot say if B19 might be one of the 'wanted' agents bastards!
Br J Haematol. 2003 Jan;120(1):168-9
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12492595&query_hl=54&itool=pubmed_docsum

[Zoey]

HI dqfy,
Welcome back! I have no "scientific" background either, just a bad case of terminal curiosity and easy access to the internet. There may be a pattern if  more cases of leukemia turn up where there is also a greater number of some infection, influenza being one that's been studied.
   It isn't a scientific study, but have you spoken to the parents in Redondo Beach whose kids developed leukemia? Maybe if you all look at each child's medical history you will see a possible common thread, to study further.
  My current searching is turning up some older studies done on seasonal patterns in development of leukemia and am trying to get a full copy of one article now. They go back about to the sixties, before the value of vitamin D was so well understood. But if the studies show that more cases are reported in some areas during winter months [when vitamin D deificiency is more common] it may point to a pattern involving vitamin D. We could then check and see what studies have been done on Vitamin D deficiency in those areas to see if there may be a correspondence.
Quote from Iko:
...wait, but the chain of events:

1) epidemic - immune response - normal response - neutralizing antibody - healing
2) epidemic - immune response - overridden reaction - CLONE expansion - organ invasion

leave plenty of space to environmental AND nutritional factors
don't you think?
-------------
  Is there anything you have noticed that suggests any kind of pattern to you on what may have led to your child developing the disorder?

   

[Zoey]

Hi Zoey,

I should re-check piles of papers, but I am afraid that a proper seasonality as never been reported for leukemias.
In the past, spots of lymphoma and leukemia cases called 'clusters' had been reported now and then to propose an infectious etiology for these diseases: nothing scientifically 'heavy' I must say.
ikod
[/quote]

Greetings ,
 The search on seasonal variations in development of leukemia is bearing fruit-- perhaps for vitamin D deficiency and infection  as predisposing factors?  Some studies were done long before vitamin D's importance was recognized. One name keeps turning up, FR Fekety, but I've not succeeded yet in finding who or where this person may be, if still around. A lot of this person's publications are in the Maryland Medical Journal so maybe this is where to find out more about this researcher.

1: Md State Med J. 1969 Nov;18(11):73-7 passim. Links
Season and the onset of acute childhood leukemia.Fekety FR Jr, Carey JJ.
PMID: 5352399 [PubMed - indexed for MEDLINE]{I am getting a copy of this article}
-----------

                         
The Niavaran branch of the National Library of Iran offers a pleasant environment for its users.


The population of Iran is about 68,000,000. I couldn't tell from the more recent article below how signifigant the numbers of cases of childhood leukemia are in relation to other counties. I didn't find how many cases are diagnosed yearly countrywide.

2.Review Article

Seasonal variations in the onset of childhood leukemia/lymphoma: April 1996 to March 2000, Shiraz, Iran
Mehran Karimi, Hooman Yarmohammadi *
Hematolgy Research Center, Department of Pediatrics, Shiraz University of Medical Sciences, Shiraz, Iran
 
email: Hooman Yarmohammadi (yarmohml@sums.ac.ir)

*Correspondence to Hooman Yarmohammadi, Hematology Research Center, Nemazee Hospital, PO Box 71935-1311, Shiraz, Iran.

Keywords
seasonal variations • leukemia and lymphoma in childhood • infection


Abstract
Infection has long been suspected as a possible factor in the aetiology of leukemia and lymphoma, one of the most common malignancies in children. Since most viral infections have seasonal variations of onset, if seasonal trends in 1 month of diagnosis of leukemia and lymphoma could be proved, this would be supportive evidence for an infectious aetiology. A total of 367 cases in the Hospitals of Shiraz University of Medical Sciences, from April 1996 through March 2000, who were diagnosed as having acute lymphocytic leukemia (ALL), acute myeloblastic leukemia (AML), Burkitt's lymphoma (BL) chronic myeloblastic lymphoma (CML), Hodgkin's disease (HD) or non-Burkitt's type non-Hodgkin's lymphoma (NBNHL) were analysed. The month of appearance of the first symptom and the date of diagnosis were recorded. ALL demonstrated statistically significant monthly variation in the date of appearance of the first symptom (p < 0.05; peak in October) and the date of diagnosis (p < 0.05; peak in November). Seasonal variation was demonstrated in the date of the first appearance of symptoms in BL (p < 0.042), and in the date of diagnosis in AML (p < 0.049). There was no statistically significant seasonal variation in the month of diagnosis for other groups. Analysis based on the date of the first symptoms and the date of diagnosis for ALL patients, using summer-winter ratios, also showed a significant winter excess (p < 0.001). Our data provide modest support for an autumn-winter peak in the diagnosis of childhood ALL, underlying mechanisms that account for these patterns are likely to be complex and need more definitive studies. Copyright © 2003 John Wiley & Sons, Ltd.


------------

Do the cases of rickets described below not suggest a problem with vitamin D deficiency in this same region?

Evaluation of patients with different types of rickets in Fars Province

 H. Karamifar

 Department of Pediatrics, Division of Pediatric Endocrinology, Shiraz University of Medical Sciences, Shiraz-IRAN

 There are different causes for rickets. Vitamin D deficiency, disorder in vitamin D metabolism and action, familial X-linked

hypophosphatemia, renal failure, hepatic disease & oncogenous rickets are some of the major causes of rickets. In this research we had the opportunity to study 50 cases of rickets during one year period in Shiraz University of Medical Sciences hospitals. The diagnosis of rickets was besed on clinical, biochemical and radiological evidence. The results showed that vitamin D deficiency was the most common form of rickets. 36 cases (72%) had vitamin D deficiency rickets, 3 cases (6%) had vitamin dependent rickets and 11 cases (22%) had vitamin D resistant rickets. The sex distribution was 26 (52%) females and 24 (48%) males. There was not a significant difference in female to male ratio in this study. We found that 71.4% of patients had used breast milk during infancy and they had not used vitamin D supplement. Almost all of them were from cold climate regions of Fars Province. Sixteen (32%) of vitamin D dificiency cases were under one year age and they were cared at home. Radiological finding in wrist X-Ray was present in all patients. The most important symptoms of patients that were comming to hospital or office were convulsion and infections especially pneumonia, respectively. These results indicate that although several factors are concerned in the development of rickets, the main cause is lack of vit D in Fars Province. There is less sun in the winter months when it is cold, children are kept indoors for most of the first year of life and when they go out in the winter they are well wrapped up. This suggests that lack of sun light in the absence of adequate dietary intake of Vit D is the main causal factor.

http://erc.ac.ir/iced/5/oral/Evaluation%20of%20patients%20with%20different%20types%20of%20rickets%20in%20Fars%20Province.htm

There is a problem with vitamin D deficiency in Iran as this excerpt describes:

Vitamin D status in mothers and their newborns in Iran
Zhila Maghbooli,1 Arash Hossein-Nezhad,1 Ali Reza Shafaei,1 Farzaneh Karimi,1 Farzaneh Sadat Madani,1 and Bagher Larijani1
1Endocrinology and Metabolism Research Center, Tehran University of Medical Sciences, 5th Floor, Shariati Hospital, North Kargar Avenue, Tehran 14114, Iran
Corresponding author.
Zhila Maghbooli: zhilayas@yahoo.com ; Arash Hossein-Nezhad: ahosseinnezhad@sina.tums.ac.ir ; Ali Reza Shafaei: emrc@sina.tums.ac.ir ; Farzaneh Karimi: emrc@sina.tums.ac.ir ; Farzaneh Sadat Madani: emrc@sina.tums.ac.ir ; Bagher Larijani: emrc@sina.tums.ac.ir
Received July 13, 2006; Accepted February 12, 2007.

Discussion:

Our findings reveal a high prevalence of vitamin D deficiency among pregnant women and newborns. Almost two in three mothers had vitamin D deficiency (VDD), while one in ten newborns had normal vitamin D. Vitamin D deficiency in pregnant women and newborns has been reported in several studies [18,26-28]. This prevalence is reported based on an old definition of vitamin D deficiency, and many investigators now define deficiency as <80 nM (32 ng/mL) circulating 25(OH)D/L [29,30]. Based on this cut-off, only 4% of pregnancies in our study had normal serum vitamin D concentrations. It seems most studies define the cut-off point for vitamin D and calcium intake based on serum vitamin D and calcium concentrations. Thus new cut off point definition based on outcomes may be more suitable [12,23,31-34]
------

The full article is available online:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1808477

[iko (OP)]

http://geronimoplugins.com/images/puzzle-cropped.jpg

Thank you Zoey,

other pieces in the vitamin D puzzle.
I printed that paper from Iran...it's really neat.
Wow, we started from 1988 Shanghai, went through Finland to Egypt!
Paradoxycally Norwegian people have the highest levels of vitamin D all over the year (thanks to their diet + cod liver oil) compared to the rest of Europe and countries with a lot of sunshine like Iran.
Human societies with their traditions and religion can really make the difference.

I would not expect a significant difference in leukemia incidence based ONLY on the difference in vitamin D levels between different countries:

- incidence figure for leukemia is 4 to 5 new cases a year per 100,000 people,
  truly tiny, regardless of where you live in relation to sun exposure.
- vitamin D deficiency may be only one of the environmental causes, bound to diet (cod)
  and individual 'solar' attitudes ("drink your milk and GO PLAY OUTSIDE!").
- The supposed 'protective effect' given by cod liver oil supplement should take time to
  work (3-12 months?) -over 1 year in the 1988 report- and vitamin D levels are quite
  different in seasons.

Everything gets trickier and more confusing, as you see.

Nevertheless we do need these pieces for the puzzle.
I personally discovered so many fascinating things I totally ignored before exploring this vitamin D issue, mostly thanks to http://www.vitamindcouncil.com/ by Dr.J.J.Cannell from Atascadero State Hospital in California.

You may have read one of Michael Holick's basic papers, I think you mentioned it many weeks ago and I had just received a preprint copy of it. Now it is free full-text on the web: what a treat!
http://www.jci.org/cgi/reprint/116/8/2062.pdf
Every time I read it and check its references I find something new that deserves to be reported in this topic.

We all know that malnutrition in a pregnant woman and/or in a breast-feeding mother later, can heavily affect the future health of the foetus-newborn-infant in terms of brain development mostly, but even growth and immune strenght.
Surprisingly, just one cofactor deficiency (vitamin D) might increase the risk of specific diseases years, even decades later in the previously malnourished or sun-deprived child.
I hope prof. Holick won't mind if I report his conclusion in full-text, from:
"Resurrection of vitamin D deficiency and rickets" published in 2006.
These things should 'invade' the media instead of being confined in the narrow scientific circuit of information.

Conclusion

Vitamin D–deficiency rickets is a sunlight deficiency disease. The inability to appreciate the beneficial effect of sunlight for health had devastating consequences for both children and adults for more than 300 years. When it was finally realized that exposure to sunlight could prevent and treat rickets, this led to the recommendation that all children be exposed to sensible sunlight to maximize bone health. The fortification of milk with vitamin D eradicated rickets as a major health problem, and, therefore, it was thought to have been conquered.

Rickets has, however, made an unfortunate comeback (120). The major cause of rickets in the United States is a lack of appreciation that human milk contains very little if any vitamin D to satisfy the infant’s requirement. African American women are often vitamin D deficient, and women who always wear sun protection and only take a prenatal multivitamin are also at a high risk of vitamin D insufficiency. If they provide breast milk to their infant as the sole source of nutrition, the infant will become vitamin D deficient. If the infant is not exposed to sunlight or does not receive a vitamin D supplement, the infant will inevitably develop rickets.
However, the skeletal manifestations of rickets represent only the tip of the vitamin D deficiency iceberg. Vitamin D deficiency in utero and during the first year of life has devastating consequences and may imprint on the child’s life chronic diseases that will shorten his/her life span (24, 57). In utero, vitamin D deficiency results in reduced intrauterine long bone growth and slightly shorter gestation (121). This has been linked to increased risk of osteoporosis and fractures later in life (24, 60, 61, 82, 122). Children born and raised at latitudes below 35° for the first 10 years have a 50% reduced risk of developing multiple sclerosis later in life (103, 104). Neonates who are vitamin D deficient during the first year of life are 2.4-fold more likely to develop type 1 diabetes compared with children who received 2,000 IU of vitamin D3/day (105). It has been suggested that the increased risk of developing schizophrenia may be initiated in utero and during childhood due to vitamin D deficiency (102). Muscle function, innate immunity, cellular growth and maturation, immunomodulation, insulin secretion, as well as regulation of calcium, phosphorus, and bone metabolism are all affected or controlled by vitamin D. Thus, ensuring that women during pregnancy are vitamin D sufficient and that newborns either be immediately evaluated for their vitamin D status by measuring 25(OH)D levels in cord blood or given vitamin D prophylactically should be a high priority. Vitamin D deficiency should be immediately treated with at least 1,000 IU of vitamin D2 or vitamin D3/day for the first week of life. Alternatively, a single dose of 200,000 IU of vitamin D should suffice for the first few months of life.

There has been a great fear about causing vitamin D intoxication in neonates. This resulted from the poorly described outbreak of neonatal hypercalcemia in the 1950s in Great Britain (123), which led to the enactment of laws in Europe forbidding the fortification of dairy products as well as all other products with vitamin D. In 1997 the Institute of Medicine recommended that the AI for infants and children of all ages be 200 IU/d. The same recommendation was made for pregnant and lactating women. The safe upper limit for infants ages 0–12 months was 1,000 IU/d and for children older than 1 year of age, 2,000 IU/d. However, it is now obvious based on the historical literature (14–16) as well as the recent literature (23, 24, 30, 36, 81, 86, 87) that these recommendations are inadequate without sensible sun exposure. It is well documented that neonates and children can tolerate a single dose of 200,000 IU of vitamin D2 or vitamin D3 or doses of vitamin D up to 3,000 IU/d without any untoward side effects. Indeed 400–1,000 IU/d to maintain serum 25(OH)D levels between 30–50 ng/ml should be the goal, just as it is in adults. Infants and children have routinely received 400–2,000 IU vitamin D2 or vitamin D3/day for the first years of life without any reports of toxicity (23, 80, 105, 107). Typically, doses of more than 50,000 IU/d of vitamin D2 were found to cause toxicity (12–14).

In Canada, it is recommended that all infants receive 400 IU/d from birth. This recommendation has been successfully implemented and has not resulted in any reported cases of vitamin D intoxication or hypercalcemia. I believe that the 200 IU of vitamin D that is recommended by the American Academy of Pediatrics is suboptimal (124). This dose may prevent overt rickets but will not prevent vitamin D deficiency.

Hopefully, history will not repeat itself. The widespread concern about any direct sun exposure increasing the risk of the relatively benign and nonlethal squamous and basal cell cancers needs to be put into perspective. It is chronic excessive exposure to sunlight and sunburning experiences during childhood that increases risk of nonmelanoma skin cancer (125). Melanoma, one of the most feared cancers because of its ability to rapidly metastasize before it is obvious to either the patient or physician, has been branded as a sun-induced skin cancer. However, most melanomas occur on the least sun-exposed areas, and it has been reported that occupational exposure to sunlight decreases risk of melanoma (125).

The 30-year campaign to recommend abstinence from sun exposure has not stemmed the increase in skin cancer incidence (125). It is curious that in the 1930s and 1940s, when children were encouraged to be exposed to sunlight and artificial UV radiation to treat rickets, the incidence of skin cancer did not increase. Thus, there needs to be a reevaluation of the beneficial effect of sensible exposure to sunlight as noted by the Australian College of Dermatologists and the Cancer Council Australia, which recommend a balance between avoiding an increase risk of skin cancer and achieving enough UV radiation to maintain adequate vitamin D levels. 

Holick MF.
Resurrection of vitamin D deficiency and rickets
J Clin Invest. 2006 Aug;116(:2062-72.

 

[iko (OP)]

Von Jacksch-Luzet syndrome.

Another piece of the puzzle?  Maybe.
Perhaps it will only increase the level of confusion and number of things that we should know by now, but we don't.  Complexity is actually the rule in this area: imagine that it is now recognized that activated vitamin D3 helps control the expression of more than 200 genes.

http://www.bulkgraphicmedia.com/images/flip-puzzle-pieces.jpg

Von Jacksch-Luzet syndrome may be another piece, certainly not the 'missing link'.
It is an hematologic disorder observed in common rickets, somehow similar to acute myeloid leukemia or its precursor, a severe form of anemia called myelofibrosis.
Bone metabolism is heavily compromised in severe vitamin D deficiency, so even hematopoietic cells hosted there are affected, cannot proliferate properly and go to other organs like spleen, liver and lymphnodes.
It is not true leukemia, but it seems very similar. Cured by vitamin D treatment in weeks, it practically disappeared in developed countries together with rickets.
So there might be a correlation between these phenomena, difficult enough to understand.  Giving vitamin D3 to patients with only myelofibrosis but no rickets seems to improve their anemia in some cases; it has been done since 1980, without extraordinary results, I'm afraid.
Vitamin D3 works in myeloid leukemic cells 'in vitro', but the dose would be too toxic for patients, so vitamin D3 analogues are under study.  A researcher from Israel is studying the synergistic effect of carnosic acid (rosemary) that would allow positive effects with non-toxic dosages of vitamin D3 in leukemic patients.

The effect of vitamin D3 on CD34 progenitor cells in vitamin D deficiency rickets

Sevgi Yetgin, S Songül Yalçın
Vitamin D metabolites have multiple functions not only in calcium homeostasis, but also in hematopoiesis. To detect the effect of vitamin D on hematopoiesis with a surface glycoprotein marker, the proportions of the CD34+ cells were measured in bone marrow, peripheral blood and spleen prior to and after vitamin D3 treatment in an infant with severe rickets, myelofibrosis and myeloid metaplasia. CD34+ cells measured 0.4% in bone marrow, 8.0% in peripheral blood and 8.7% in splenic aspirate. The detection of a high and comparable level of CD34+ cells in both peripheral blood and splenic aspirate on admission and the decline in the level of CD34+ cells (2%) following treatment support that CD34+ cells were from extramedullary hematopoiesis in spleen. The improvement of rickets and hematological findings with treatment at the same time raises the possibility of vitamin D3 acting directly upon the same target or upon different targets at the same time or of the presence of interaction between two targets. Our findings may also show a relation between vitamin D3 and its metabolites to bone marrow stem cells.

Turk.J.Ped. 2004 46(2),164-166.

[iko (OP)]

Tahini (Sesame butter) recent findings

You probably remember the note about sesame seeds butter and childhood leukemia a few posts ago: a scam, commercial crap, pure quackery?  I leave it open for the discussion, reporting the new text-string -just found 'fishing' on Google- together with the already posted recent article about sesame and leukemia.
Now we even know the name of the mysterious doctor: he was one of Dr. Lee's colleagues!  Neat uh?
We just emphasized the need to stick to just one subject (cod liver oil), but I made this exception before with tahini in a discussion with GBSB that actually could summarize the whole childhood leukemia topic.
Hope that dear Zoey won't mind too much, we'll go back to 'cod' in a minute.

"...Sesame seeds are rich in a substance Lee called "vitamin T." (The other major sources of this nutrient are termites and mealworms. :p ) Among other things, vitamin T helps to build red blood cells. Lee personally knew a doctor who had helped several children to recover from leukemia, just by having their parents feed them lots of tahini and sesame oil. Another excellent feature of sesame is that the oil is very resistant to oxidation. Lee was very concerned about the health hazards of rancid oils, and believed that nut butters needed to be made fresh each day, as they spoiled very quickly, even in the fridge. In his opinion, tahini was the only such product that was okay to buy in a jar."

http://209.85.129.104/search?q=cache:Ef6aex9vo0IJ:www.mothering.com/discussions/archive/index.php/t-529959.html+%22tahini%22+leukemia&hl=it&ct=clnk&cd=2&gl=it

...From an unspecified topic in "General Science" NSforum:
Sesame seeds
sesame butter
sesaminol
sesamolin

http://www.grainfieldsaustralia.com/US/ingredients/graphics/sesame-seeds.gif

Sesaminol from sesame seed induces apoptosis in human lymphoid leukemia Molt 4B cells.

Miyahara Y, Hibasami H, Katsuzaki H, et al.

The exposure of human lymphoid leukemia Molt 4B cells to sesaminol, a component of sesame oil led to both growth inhibition and the induction of apoptosis. Morphological change showing apoptotic bodies was observed in the cells treated with sesaminol. The fragmentation of DNA by sesaminol to oligonucleosomal-sized fragments that are characteristics of apoptosis was observed to be concentration- and time-dependent. These findings suggest that growth inhibition of Molt 4B cells by sesaminol results from the induction of apoptosis in the cells.

Int J Mol Med. 2001 May;7(5):485-8.




Now then, if in your frantic 'surfing' on the Web you found something like this:
...According to medical authorities nothing is supposed to be effective in treating leukemia -- that's cancer of the blood. We know a doctor in the Midwest who had three children who got over leukemia just by eating sesame butter. He gave them six tablespoonfuls of sesame butter a day. Brown sesame seed butter (Tahini). That's not a very glamorous treatment for a serious illness but it worked.

http://209.85.129.104/search?q=cache:GztTWKxLt78J:www.usaplaza.com/scripts/wcom_producttree.asp%3FStoreID%3D1340%26ProductID%3D48398+%22sesame+butter%22+leukemia&hl=it&gl=it&ct=clnk&cd=1
...given the initial statement that "nothing is supposed to be effective", as a medical doctor you would correctly think that's a scam, a totally unproven commercial crap, just quackery.

Nevertheless, as a parent of a leukemia 'survivor' you would easily consider giving her/him at least some sesame-seed bread (traditional Sicilian bread) and grissini (sesame bread sticks), so tasty and good for you.  They make them fresh at the bakery just across the street, so it doesn't cost much to buy some once a week.  They disappear quite quickly from the kitchen counter (beside the cod caps container).
 

ikod

   

http://img.alibaba.com/photo/11081131/Sesame_Bread_Stick.jpg
http://www.pccnaturalmarkets.com/health/Food_Guide/Sesame_Seed_Butter.jpg

Hi Luka.
thanks for appreciating my efforts and for the discussion.
It helps me to explain better the point in this topic.
I'll reply shortly to your post, step by step:

quote
I’d read every your post on this forum. I find most of your posts interesting; some of them are mind opening.
But, I was disappointed that you posted this link. http://209.85.129.104/search?q=cache:GztTWKxLt78J:www.usaplaza.com/scripts/wcom_producttree.asp%3FStoreID%3D1340%26ProductID%3D48398+%22sesame+butter%22+leukemia&hl=it&gl=it&ct=clnk&cd=1

Sorry if the sesame butter story comes out from a commercial link, I had to report it anyway...you cannot find it anywhere else.  A scam? A real story? I leave it open.
I do not even remember how, but I found it years ago.  It was easy to check on PubMed and find a "scoop", one recent positive 'in vitro' result for sesaminol against a leukemic lymphoblastic cell-line.
It may be a promising result, believe me.
In 1980, like other groups years before, we worked on retinoic acid versus a promyelocytic cell-line (HL-60): the bad cells stopped dividing and became mature white cells within 5days.  That miracle took 10-15 years to reach the 'real' patients.  These days a vitamin A derivative (retinoid) is in the standard treatment for promyelocytic leukemia (AML-M3).
So the story of the doctor in the Midwest may be just fantasy, but the japanese report (actually there are two papers) is real and scientifically correct.A parent usually needs more hope, and tends to take into account even those 'fantasies'...

quote
How significantly is it, we can’t see from this report (the “Shanghai report”).
How we do know, that if children take tablespoon of honey every day, that incidence of leukemia will be lower than if they take cod liver oil.

I gave instructions to check that abstract: did you reach it? We'll do it together later on.
Sorry Luka, no honey, no ascorbic acid, no aloe whatsoever.  They may work, I don't know.
I certainly know that the only scientific report on a positive effect of a nutrient, or nutritional supplement if you like, capable of reducing incidence of childhood leukemia to half or 1/3 is the 1988 paper from Shanghai published in Cancer.  I've searched around, believe me...and I am not a scientist, but I've been in this field for a long time.
Distinguished journal, well-done study, statistically sound.

We really have to 'codcentrate' on one thing.

quote
I think that diet approach in understanding cause of illnesses has reached own limit long time ago.
It is necessary to find “missing link” between nutrition and physical activity on one side and health and illnesses on the other side.

To speculate about the possible causes of leukemia is not the aim of this topic: I suggested to read Mel Greaves's hypothesis (there are several papers about it). Vitamin D deficiency may represent one of the many  "missing links" (personal opinion), but still we are not in a position to do much about it.

This is no chat or fantasy.
I am concerned as a parent.
I am serious and I feel I carry a sort of responsability about it.

A bit of help (cod liver oil) together with standard treatments could improve,
starting tomorrow, the quality of life and may be (fingers crossed) even survival...

...one percent? 5 percent? I do not care much:
just one kid who feels a bit stronger and
grows up properly in spite of chemo would do.

I do not want to be alone in reminding one of the kids to take his 'cod'.

The discussion here should be on how to let those parents know what nobody told them before.
asap.

ikod

Post Scriptum:

  Actually I don't exactly think I am the only parent reminding 'cod': the Shanghai report has been cited around, even in the "Cod liver oil - number one superfood" commercial website.
Knowing the amount of adrenaline you get in the endless months following a diagnosis of childhood leukemia,
I'm pretty sure that some other parent has snagged this information and is probably doing the same thing.

  Let's be a bit more positive about medical progress:

maybe a few open-minded consultant hematologists around the world are recommending every day 'cod' to parents of leukemic children. Following the 'Shanghai report' indications or who knows what other mysterious path or fascinating suggestion.  Adopting the old fashioned "ex-adjuvantibus" criteria.
Maybe.

          
http://www.flyanglersonline.com/lighterside/dennisdickson.jpg
http://www.immunizenc.com/images/ped_andchild.jpg
http://allconsortium.dfci.harvard.edu/public/images/lewis.jpg

Yes. Better keep 'tahini' recipe in our minds. A last resort, like a parachute.
Sort of a dream, maybe just fantasy: we need these things, we're humans.
When parachute doesn't work you just die in a second,
but in the end of a wonderful, happy jump in the sky.
Good night,

ikod   [^]

 

http://www.dc-skydivers.com/SunsetTandem.jpg

[iko (OP)]

Addendum from Myke's Weblog, February 28, 2005 in Food and Drink, Health, Science | Permalink:

Sesame: Consider the Source
I received a comment from John Grey about my post on Eat More Sesame. Based on the link he provided, I'll be eating less tahini and more freshly ground sesame seeds. The information below is from RawVeg.info.

Tahini is a refined food, don't use it. It's made from ground peeled sesame seeds, the bran is missing. Sesame butter is made from ground whole brown sesame seeds. It's a whole food, but not freshly made. Make your own sesame spread, fresh, by blending whole raw sesame seeds with water. If you do use sesame butter, be sure not to get the toasted kind. Sesame oil is a refined food, don't use it. Beneficial substances are lost when oil is made: fiber, minerals, IP-6, etc. Chinese sesame oil is a refined food made from toasted sesame seeds, don't use it. Use uncooked fresh whole foods.

Buying sesame seeds.
There are three types of sesame seeds: Brown, black and white.
White sesame seed is a refined food, similar to white rice. It starts out as whole brown sesame, then the outer bran layer is removed. Don't use it.
Brown sesame seed has a milder flavor and less antioxidants than the black seeds.
Black sesame seed has more antioxidants and a richer flavor. Black sesame has a reputation in both the Ayurveda and Chinese traditions as an anti-aging food.

Find a natural food store or co-op that sells black or brown sesame seeds in bulk. Buying from the bulk bins saves you money, and reduces consumption of throwaway plastic packaging. The black seeds are best, brown is next best.

Using sesame seeds.
Grind the seeds fresh shortly before using them. You can dry grind them in a blender, on the 'Pulse' setting. It only takes a few seconds. If you hold the 'Pulse' button down for too long, the ground seeds will cake together. If you put too many seeds in at once, they may cake together.
You can use a coffee grinder (but not one that's been used for coffee, the taste will get in the food).
Hand-operated spice grinders are similar to a pepper grinder, but with a small glass jar on top.
Mortar and pestle is a traditional low-tech tool for grinding and blending.
Sprinkle the ground seeds over cereals, vegetable dishes, or fruit.

http://www.mykesweblog.com/2005/02/sesame_consider.html#more

12. Tahini and sesame butter (just like peanut butter but from sesame) and sesame seeds. Sesame products are eaten in some cultures in place of dairy products because of their high calcium content (calcium from sesame seeds is more easily used by our bodies than calcium from milk and a higher percentage of the calcium contained actually works for us). Eaten for thousands of years, sesame seeds were believed to possess magical properties, and they contain sesamol, which fights rancidity. Another quick easy breakfast is apple slices dipped into tahini or tahini with banana or tahini on toast. Use tahini to replace peanut butter in cookies.


DEBRA STARK
Concord

http://debrastark.com/portfolio_twelve.html

As the magic words, “Open, sesame!” indicate, many excellent
properties are hidden in the tiny sesame seed and these have
become clear by the studies described above. Sesame seed will
contribute much to the health and prosperity of people throughout
the entire world.


from:  Nutraceutical Functions of Sesame: A Review
MITSUO NAMIKI   Nagoya University, Nagoya, Japan
Critical Reviews in Food Science and Nutrition, 47:651–673 (2007)

http://www.informaworld.com/smpp/content~db=all?content=10.1080/10408390600919114

[Zoey]

 One of the CLL groups did post a long newsletter, much like you, Iko, suggesting the use of CLO in leukemia. They asked it not be reproduced so am trying to contact them about it. As per your recent posts, the focus will shift back to how to alert parents of ALL children.
Zoey

[dqfry]

Hi Zoey and Iko, just a quick 'hello' and a note of appreciation for all the posts.  It's definitely fascinating how many people (parents) and doctors disregard any kind of supportive or alternative treatment to ALL. We continue doing our daily CLO (the whole family) and hoping that it's making a difference on my son's treatment outcome. On a side note, I was raised on CLO on its most fishy taste and that was not pleasant at all (lots of tears with each spoon)...my son, in the other hand, will not drink his orange juice unless I add his "yummy lemon taste CLO" to it.

Cheers,

DQ 

[iko (OP)]

One of the CLL groups did post a long newsletter, much like you, Iko, suggesting the use of CLO in leukemia. They asked it not be reproduced so am trying to contact them about it. As per your recent posts, the focus will shift back to how to alert parents of ALL children.
Zoey

Hi Zoey,

Thanks for the good news. I hope the CLL group is claiming a 'little help' from CLO, instead of an alternative, miracle cure and all that bla bla bla!
We have to be careful not to give any opportunity of criticism by the skeptical party.
They seem to be too many.
In this context, if anything improved 5 years survival of 5% it would be a great achievement indeed, but you would't even notice it, because -fortunately- survival rate is already high (>65%).  It would only come out much later, analyzing all the data again and again. How boring.
Take care

ikod

[iko (OP)]

It's definitely fascinating how many people (parents) and doctors disregard any kind of supportive or alternative treatment to ALL.

Hi Dqfry!

Well, for doctors it is correct: they should be busy on what they know for sure, with no distraction, without 'improvising' anything, yes, like robots.  It is much better to concentrate on proper dosages of chemo all the time, and prevent/treat side effects. You have specific protocols to follow strictly and carefully: guidelines that have been discussed and shared with thousands of specialists, nationwide and worldwide.
No time for jokes.
It is really hard to go from a BMsampling to a couple of SPs in small kids plus all the rest. I personally couldn't make it (I tried many years ago).  It is a sort of combat, a war against the invisible enemy.
Tough, really hard.

Dieticians might be more inclined to go for 'anti-oxidants', following a sort of present fashion.

Parents should be more interested: diet is one of their duties, and they might feel guilty for not having given the "right things".  May be some 'remove' these thoughts.  And that's much better.
You take care of orange juice and cod liver oil because it's "your" family tradition, education, and for many other reasons; other people don't.
That's all right anyway.
Cheers,

ikod

[Zoey]

Below is the newsletter from the CLL group. I wasn't able to get a response about posting, but think it is ok to do so.
---------------

Thttp://www.clltopics.org/Alert/direct_display_alert.php?reqnum=47

 

Topics Alert Archive

Alert Number 47

Those Pesky Aches and Pains
Date: October 5, 2004

One of the common mistakes we (and our doctors!) make is attributing everything that goes wrong to CLL. If you are tired, you hurt all over, your muscles ache, heck you can feel the pain in your very bones, and nothing works, not even fistfulls of NSAIDs, why, it must be the dreaded CLL acting up, right?

Not so fast, you could be dead wrong laying this at the door of the 'dragon'. You could be suffering from something that can be very easily corrected, a real cheap fix. Not only does it not cost a lot, it is not even toxic (isn't that a welcome change from the usual caveats with chemo drugs?), and it might even help you fight the CLL. What is this drug? It is called vitamin D3. I have discussed this topic before on Topics (Vitamin D3 Essential for Health) but I think it bears repeating. Below are direct quotes from a very recent paper in the prestigious Mayo Proceedings, December of 2003. You can read the whole article for free, as well as the editorial that accompanied it. I have provided the links below.

There are two reason for my visiting the issue of vitamin D3 deficiency again. First, it is all too easy to dismiss the symptoms of vitamin D3 deficiency, especially when we are dealing with a bunch of cancer patients. Doctors expect us to complain of aches and pains, what else is new? If they take us seriously at all, they may consider something like fibromyalgia, in addition to the catch-all of CLL. Most often, you are expected to grin and bear it, with the not-so-subtle sub-text: stop whining. The other reason is that I still see "miraculous" claims made for "coral" calcium, with no understanding of calcium homeostasis and how calcium is used in our bodies. Calcium absorption needs adequate vitamin D3, otherwise it just goes for the ride, in one end and out the other. Trust me, your toilet does not need any more calcium. "Coral" calcium is no better than regular calcium you get at the drug store, or even antacids like Tums, it just costs more. It is also significantly worse in one important respect, the presence of high levels of very toxic heavy metals such as mercury. Coral has had a long time to accumulate the heavy metal toxins we have been putting out into the oceans. You worry about eating fish that have lived for a few years, about the level of heavy metals they may have accumulated over that time. Folks, coral has been around a lot longer, and was busy accumulating all the mercury and other heavy metals we were pumping into the oceans in the bad old days, before environmentalism became 'cool'.

Here is what the Mayo Clinic had to say on the subject of vitamin D3, calcium, mysterious aches and pains. They specifically talk about potential misdiagnosis of fibromyalgia, when the problem could well be vitamin D3 deficiency - something that can be easily tested for, and fixed. The quotes are from Mayo, but I did the highlighting to identify points of interest.

Overall, 93% of the 150 children and adults in the study, which included 6 broad categories of ethnic groups, were vitamin D-deficient. Is this unexpected? No. Is this newsworthy? Yes.
(The authors) evaluated both children and adults who reported persistent musculoskeletal pain that did not meet the strict criteria for fibromyalgia defined by the American College of Rheumatology. The association between nonspecific musculoskeletal pain and vitamin D deficiency was suspected because of a higher prevalence of these symptoms during winter than summer.
Vitamin D is essential for the efficient utilization of dietary calcium. In a vitamin D-deficient state, the amount of calcium absorbed is inadequate to satisfy the body's calcium requirement, This results in osteopenia and osteoporosis. This is the likely explanation of why patients with osteomalacia often experience a dull unrelenting aching sensation in their bones. These symptoms are either dismissed or misdiagnosed as fibromyalgia by many physicians.
Vitamin D deficiency causes muscle weakness and muscle aches and pains in both children and adults.
It has been estimated that 90% or more of our required vitamin D comes from exposure to sunlight. Anything that interferes with the penetration of solar ultraviolet radiation into the skin, such as increased melanin pigmentation and sunscreen use, will diminish the cutaneous production of vitamin D3.
People who live at higher latitudes and who are more prone to vitamin D deficiency are at increased risk of developing prostate, colon, breast, and other solid tumors; autoimmune diseases including multiple sclerosis and type 1 diabetes; hypertension; and cardiovascular heart disease.
When patients with nonspecific skeletomuscular pain are evaluated, their serum 25-hydroxyvitamin D levels should be obtained. Physicians should disregard the laboratory-reported lower limit of the normal range. A serum 25-hydroxyvitamin D level of at least 20 ng/mL is necessary to minimally satisfy the body's vitamin D requirement. Maintenance of a serum 25-hydroxyvitamin D level of 30 to 50 ng/mL is preferred.
Patients should have their vitamin D status, ie, serum 25-hydroxyvitamin D levels, tested once a year, preferably at the end of the fall season, to ensure that they do not become vitamin D-deficient before winter.
http://www.mayo.edu/proceedings/2003/dec/7812e1.pdf

http://www.mayo.edu/proceedings/2003/dec/7812a1.pdf

I thought you folks might also like to see the two abstracts below. The first one talks about calcitriol (another name for Vitamin D), in clinical trials at Roswell Park Cancer Institute for its anti-cancer activity. The second one talks about a vitamin D3 analog that seems to be effective in CLL. Why the vitamin D3 analog? Why not just use the cheap and available vitamin D3? That is an important question. If you overdose on vitamin D3, it can lead to something very dangerous, called hypercalcemia, which means too much calcium in your blood. Hypercalcemia can be fatal, if it is not immediately detected and treated. The reason for developing the vitamin D3 analog is to see if we can keep the anti-cancer effects, while avoiding the problems with hypercalcemia. Good concept: we need to keep an eye on this initiative, see how far it goes.

In the meantime, please do discuss your vitamin D3 status with your doctor. You may want to revisit our review article "Vitamin D3: Essential for your health" on our website, to get your arms around the arguments you may need to make, to bring your doctor on board. In my opinion, it surely pays to be pro-active on this front. Do remember, unlike the general Joe Shmoe basking on the beach, as CLL patients you have significantly higher (ten times higher!) risk of skin cancer, so getting all the vitamin D3 you need from sun-bathing is not a really good option for you (Do read the article Dying to Get a Tan?. Stay in the shade, pop your doctor's recommended dose of vitamin D3 supplement with a nice cup of freshly brewed green tea (or a good glass of pinot noir!) - that should do it right by you. And get yourself some over-the-counter calcium tablets. Stop wasting good money and destroying coral reefs, while you poison yourself with mercury and other heavy metals.

Be well,

Chaya
__________

Abstracts:

J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):519-26.

Anti-tumor activity of calcitriol: pre-clinical and clinical studies.

Trump DL, Hershberger PA, Bernardi RJ, Ahmed S, Muindi J, Fakih M, Yu WD, Johnson CS.

Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

1,25-Dihydroxycholecalciferol (calcitriol) is recognized widely for its effects on bone and mineral metabolism. Epidemiological data suggest that low Vitamin D levels may play a role in the genesis of prostate cancer and perhaps other tumors. Calcitriol is a potent anti-proliferative agent in a wide variety of malignant cell types. In prostate, breast, colorectal, head/neck and lung cancer as well as lymphoma, leukemia and myeloma model systems calcitriol has significant anti-tumor activity in vitro and in vivo. Calcitriol effects are associated with an increase in G0/G1 arrest, induction of apoptosis and differentiation, modulation of expression of growth factor receptors. Glucocorticoids potentiate the anti-tumor effect of calcitriol and decrease calcitriol-induced hypercalcemia. Calcitriol potentiates the antitumor effects of many cytotoxic agents and inhibits motility and invasiveness of tumor cells and formation of new blood vessels. Phase I and II trials of calcitriol either alone or in combination with carboplatin, taxanes or dexamethasone have been initiated in patients with androgen dependent and independent prostate cancer and advanced cancer. Data indicate that high-dose calcitriol is feasible on an intermittent schedule, no dose-limiting toxicity has been encountered and optimal dose and schedule are being delineated. Clinical responses have been seen with the combination of high dose calcitriol+dexamethasone in androgen independent prostate cancer (AIPC) and apparent potentiation of the antitumor effects of docetaxel have been seen in AIPC. These results demonstrate that high intermittent doses of calcitriol can be administered to patients without toxicity, that the MTD is yet to be determined and that calcitriol has potential as an anti-cancer agent.

PMID: 15225831
_____________

http://www.bloodjournal.org/cgi/content/full/bloodjournal;101/7/2454

Blood. 2003 Apr 1;101(7):2454-60. Epub 2002 Nov 21.

The vitamin D3 analog EB1089 induces apoptosis via a p53-independent mechanism involving p38 MAP kinase activation and suppression of ERK activity in B-cell chronic lymphocytic leukemia cells in vitro.

Pepper C, Thomas A, Hoy T, Milligan D, Bentley P, Fegan C.

Department of Haematology, Llandough Hospital, Penarth, Vale of Glamorgan, United Kingdom.

EB1089, a novel vitamin D3 analog, has been shown to have cytotoxic and antiproliferative properties in a variety of malignant cells. However, its potential as a treatment for B-cell chronic lymphocytic leukemia (B-CLL) has not been evaluated. EB1089 induced apoptosis in all of the 102 B-CLL samples tested with a mean LD(50) (the concentration of EB1089 required to kill 50% of cells) value (+/- SD) of 2.1 x 10(-8) M (+/- 1.4 x 10(-8) M). Furthermore, no significant difference was found in the cytotoxicity of EB1089 in B-CLL samples from previously treated and untreated patients (P =.1637). Induction of apoptosis was associated with a reduction in Bcl-2 and Mcl-1 protein expression, but this was evident only in the apoptotic cells. In contrast, the expression of Bax, p21, and p53 was not altered in the viable or apoptotic cells from either B- or T-lymphocyte lineages. EB1089-induced apoptosis was preceded by activation of p38 mitogen-activated protein (MAP) kinase and suppression of extracellular signal-regulated kinase (ERK) activity, and this was associated with downstream activation of caspase-3. The pancaspase inhibitor (Z-VAD-FMK) and the caspase-9 inhibitor (Z-LEHD-FMK) were able to partially abrogate the apoptotic effects of EB1089 but did not affect the phosphorylation of p38 MAP kinase or the suppression of ERK. The B-CLL cells in the study were shown to highly express vitamin D receptor, but an additional receptor-independent mechanism of cell killing cannot be ruled out at this stage. These findings show that EB1089 is a potent apoptosis-inducing agent in B-CLL cells and may be useful in the treatment of B-CLL patients, particularly those with p53 mutations or drug-resistant disease.

PMID: 12446453
_____________

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[iko (OP)]

Topics Alert Archive
Alert Number 47

Those Pesky Aches and Pains
Date: October 5, 2004
One of the common mistakes we (and our doctors!) make is attributing everything that goes wrong to CLL. If you are tired, you hurt all over, your muscles ache, heck you can feel the pain in your very bones, and nothing works, not even fistfulls of NSAIDs, why, it must be the dreaded CLL acting up, right?
Not so fast, you could be dead wrong laying this at the door of the 'dragon'. You could be suffering from something that can be very easily corrected, a real cheap fix. Not only does it not cost a lot, it is not even toxic (isn't that a welcome change from the usual caveats with chemo drugs?), and it might even help you fight the CLL. What is this drug? It is called vitamin D3. I have discussed this topic before on Topics (Vitamin D3 Essential for Health) but I think it bears repeating. Below are direct quotes from a very recent paper in the prestigious Mayo Proceedings, December of 2003. You can read the whole article for free, as well as the editorial that accompanied it. I have provided the links below.
...
In the meantime, please do discuss your vitamin D3 status with your doctor. You may want to revisit our review article "Vitamin D3: Essential for your health" on our website, to get your arms around the arguments you may need to make, to bring your doctor on board. In my opinion, it surely pays to be pro-active on this front. Do remember, unlike the general Joe Shmoe basking on the beach, as CLL patients you have significantly higher (ten times higher!) risk of skin cancer, so getting all the vitamin D3 you need from sun-bathing is not a really good option for you (Do read the article Dying to Get a Tan?. Stay in the shade, pop your doctor's recommended dose of vitamin D3 supplement with a nice cup of freshly brewed green tea (or a good glass of pinot noir!) - that should do it right by you. And get yourself some over-the-counter calcium tablets. Stop wasting good money and destroying coral reefs, while you poison yourself with mercury and other heavy metals.

Be well,

Chaya

http://www.clltopics.org/Alert/direct_display_alert.php?reqnum=47

Thanks for your contribution Zoey!

I'll copy it somewhere in the cod liver oil topic.
Vitamin D3 'tsunami' was starting in 2004 and you see its consequences right here.
Green tea for CLL still is a question mark: research is in progress at Mayo (1) and may be somewhere else.
I hope we'll have a nice surprise in the next few years!
Take care

ikod

1)  http://www.clltopics.org/Phyto/LatestonGreenTea.htm

[iko (OP)]

There are rare observations that seem to suggest an external cause for leukemia.
Not just an expanding bad clone of genetically abnormal lymphoid or myeloid cells...
In some rare cases, leukemia has been reported coming back (relapse) after bone marrow transplantation in the very same hematopoietic cells derived from a normal donor... []

Recurrence of acute leukemia in donor cells after bone marrow transplantation:
documentation by in situ DNA hybridization.

Mouratidou M, Sotiropoulos D, Deremitzaki K, Spathas DH, Hoffbrand AV, Prentice HG, Papanastasiou K, Tsakanikas S, Tsaftaridis P, Stamatelou M, et al.
Hematology Division, Greek Anticancer Institute Athens.

Donor cell leukemia after BMT has been documented in a small number of cases mainly by cytogenetic studies. We describe a case of leukemia relapse in a 16-year-old girl 1 year after BMT from her histocompatible brother. Relapse in donor cells was initially suspected on the basis of cytogenetic analysis and confirmed by DNA in situ hybridization in blast cells using a Y chromosome-specific probe.

Bone Marrow Transplant. 1993 Jul;12(1):77-80.

[iko (OP)]

- Parents of leukemic children will consider to give their kid some cod liver oil, instead of getting confused between hundreds of alternative and unproven nutritional supplements.
...and they (the parents) will immediately start feeling better...and less terrified.

Why are these parents so scared?

Just because they are told that their child's disease will be effectively cured in a certain percentage of cases after a series of cycles of highly toxic drugs. But in a consistent number of cases (25-30%) the disease will come back, resistent to further treatment.
When this happens, more toxic cycles of chemo will be required, and may be RADIATION TREATMENT and a bone marrow transplantation.  In some patients the disease comes back even after a graft, in one case out of two...

After chemo and during maintenance therapy there is no official recommendation for parents:
going down to the seaside or up to the mountains, to the pool or living sealed at home, staying in the shade or in the sunshine, eating this food and avoiding that...nothing.
There is no confirmed evidence about these factors (are we sure?).
So do what you want, but please follow your regular checkups every two weeks and then every month.

In the meantime...we all wait and see if and when IT strikes again.

When IT strikes again it's a real tragedy for patients and parents.
They suddenly realize why doctors were never totally relaxed during their regular checkups, even  months and years from stop-therapy.  The invisible enemy is back and nobody seems to know why, as it was at the very beginning of their illness.  Girls and boys have grown up and forgotten about those awful days, such a long time has past, wasted without anything specific to do or even try, to avoid all this mess coming back again.
Something should be done for these people.  Quick.

[dqfry]

IT strikes back? What's IT?

As I try to understand the "leukemia monster", from cytogenitics to possible causes, I always come to the same conclusion. Chemotherapy treatment is only treating the disease. It doesn't fix a possible gene lesion or DNA. So, if a certain gene translocation is present within the Leukemia cells and it's known as a pre-leukemic event (predisposition) and a second or even third event starts the Leukemia, It's possible that even after treatment the same sequence of "hits"  could start the Leukemia again since the cytogenetic event/predisposition is still present.

Does a BMTransplant change the individual's DNA? There was a recent discussion on this site about that. Unfortunately,I did not pay much attention to it.

I still believe that viruses (like Epstein Barr and common Flu) play a major role in the Leukemia process (specially ALL) and vaccines will be the way to prevent the disease.

Meanwhile, we keep hoping for a cure or prevention.

Cheers,

[iko (OP)]

IT strikes back? What's IT?

As I try to understand the "leukemia monster", from cytogenitics to possible causes, I always come to the same conclusion. Chemotherapy treatment is only treating the disease. It doesn't fix a possible gene lesion or DNA. So, if a certain gene translocation is present within the Leukemia cells and it's known as a pre-leukemic event (predisposition) and a second or even third event starts the Leukemia, It's possible that even after treatment the same sequence of "hits"  could start the Leukemia again since the cytogenetic event/predisposition is still present.

Does a BMTransplant change the individual's DNA? There was a recent discussion on this site about that. Unfortunately,I did not pay much attention to it.
I still believe that viruses (like Epstein Barr and common Flu) play a major role in the Leukemia process (specially ALL) and vaccines will be the way to prevent the disease.

Meanwhile, we keep hoping for a cure or prevention.

Cheers,

Hi dqfry,

I have my ups and downs like everybody, and what I see at work doesn't help to be positive sometimes.
I apologize for that.   Finding another job is not easy either, I should go back and fix radio and TVsets [].
Trying to fix leukemia is obviously too much for me!
With my limited knowledge of this issue, I'll try to answer your questions shortly.

"Chemotherapy treatment is only treating the disease"...It fortunately does it in the majority of patients, and most of the bad cells die, giving the immune system a chance to control a minimized abnormal clone identical to tiny clones that many of us harbour here and there.

"same sequence of "hits"  could start the Leukemia again since the cytogenetic event/predisposition is still present".
Clever dqfry, you know this stuff as much as I do after years of reading and studying! Yes, it could happen, but we still have to prove it.
We still have to demonstrate the chain of events suggested by Mel Greaves and give a name to the agents and factors responsible for the onset of this disease.
But if we are lucky, the same sequence of events will never combine again in the whole life: a certain germ will find a specific defence that wasn't ready before, macrophages will work properly because of vitamin D3 and other factors previously missing, the whole immune system will 'calm down' after the first decade of life.   It may sound just fantasy but something must happen and change in the body, to justify spontaneous remissions (very rare) on one side, and the presence of tiny genetically abnormal 'clones' in normal people (not so rare, just recently reported), on the other side.

More than EBV, HHV6 (HumanHerpesVirus6) is being investigated by Robert Gallo's research team and others.
Parvovirus B19 has been found 'together' with ALL several times.
Surely it cannot be just one beast. It would have been spotted by now. It could be a series of pathogens, a restricted group, each one giving to different children the same disease.
If a specific virus is bothering a certain patient, incapable of setting up a proper immune response, we have powerful antiviral drugs these days, wonderful agents that were a dream just few years ago.  Same with bacteria and protozoa.
Over twenty years of AIDS research lead to a dramatic improvement in the treatment of persistent infectious diseases.

"Does a BMTransplant change the individual's DNA?"
By BMT most of the marrow blood cells are replaced by donor's cells with their own DNA of course.  In a few weeks, donor's blood type replaces the recipient's old one.
Very few donor's cells had been found around transformed into liver cells, vessels and so on.  Most of them replace the previous bone marrow that has been eliminated by chemo and/or radiotherapy, hoping to kill most of the leukemic cells as well.  But the immune reaction of the donor's T-lymphocytes against a new and different environment (the recipient's body) seems to be of vital importance in keeping residual abnormal cells under control. GVHD is a long story, better to stop here for now.
Take care (how is your little boy doing?)

ikod

[iko (OP)]

I still believe that viruses (like Epstein Barr and common Flu) play a major role in the Leukemia process (specially ALL) and vaccines will be the way to prevent the disease.

Meanwhile, we keep hoping for a cure or prevention.

Cheers,

Sorry, I missed 3 points:

- Vaccines: we couldn't find the beast yet...in cats there is just one virus (FeLV) found over 30 years ago. Now there is a vaccine (I don't know much about it).

- Cure: we, you have the cure dqfry.  Ask your doctors and be positive about it (Low risk!).

- Prevention: no cause, no prevention.   (joke, I know you meant vaccines![] )

seeyousoon,

ikod

[iko (OP)]

I know this is not about cod liver oil.
Allow me a cut&paste from 'Garlic miracle'
topic in Complementary Medicine...
To keep THIS topic alive!

ikod

Iko...would you like me to move the original garlic thread here ?

Thanks me friendos,

I just moved reports and abstracts here,
leaving the entertaining "bagna cauda"
sort of thing down there in Guest Book.
I meant to keep it more scientific here.

ikod

Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy.

Hassan HT.
The reputation of garlic (Allium sativum) as an effective remedy for tumours extends back to the Egyptian Codex Ebers of 1550 b.c. Several garlic compounds including allicin and its corresponding sulfide inhibit the proliferation and induce apoptosis of several human non-leukaemia malignant cells including breast, bladder, colorectal, hepatic, prostate cancer, lymphoma and skin tumour cell lines. Ajoene (4,5,9-trithiadodeca-1,6,11-triene-9-oxide) is a garlic-derived compound produced most efficiently from pure allicin and has the advantage of a greater chemical stability than allicin. Several clinical trials and in vitro studies of ajoene have demonstrated its best-known anti-thrombosis, anti-microbial and cholesterol lowering activities. Recently, topic application of ajoene has produced significant clinical response in patients with skin basal cell carcinoma. Ajoene was shown to inhibit proliferation and induce apoptosis of several human leukaemia CD34-negative cells including HL-60, U937, HEL and OCIM-1. Also, ajoene induces 30% apoptosis in myeloblasts from chronic myeloid leukaemia patient in blast crisis. More significantly, ajoene profoundly enhanced the apoptotic effect of the two chemotherapeutic drugs: cytarabine and fludarabine in human CD34-positive resistant myeloid leukaemia cells through enhancing their bcl-2 inhibitory and caspase-3 activation activities. The two key anti-leukaemia biological actions of ajoene were the inhibition of proliferation and the induction of apoptosis. Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells. The apoptosis inducing activity of ajoene is via the mitochondria-dependent caspase cascade through a significant reduction of the anti-apoptotic bcl-2 that results in release of cytochrome c and the activation of caspase-3. Since acute myeloid leukaemia (AML) is a heterogeneous malignant disease in which disease progression at the level of CD34-positive cells has a major impact on resistance to chemotherapy and relapse and the inability to undergo apoptosis is a crucial mechanism of multi-drug resistance in AML patients. The recent findings of the potent enhancing activity of ajoene on chemotherapy-induced apoptosis in CD34-positive resistant human myeloid leukaemia cells suggest a novel promising role for the treatment of refractory and/or relapsed AML patients as well as elderly AML patients. Further studies are warranted to evaluate similar enhancing effect for ajoene in blast cells from AML patients in primary cultures before its introduction in pilot clinical study.

Leuk Res. 2004 Jul;28(7):667-71.

Here we are dealing with treatment-resistant myelogenous leukemia.
And it's NOT a joke.