I've already highlighted this in misc.health.aids.

The theory here seems to be that the negative affect of having cancer
is outweighed by the positive affect selling AZT has on drug company
profits.

Something many people don't know is that AZT isn't a new drug created
to combat 'HIV.'  AZT is an old drug, developed in the 1960s, as a
treatment for cancer.  Unfortunately it's extremely toxic and failed.
In the 1980s it was taken down from the shelf, dusted off, and hailed
as a new wonder drug to fight HIV.  Unfortunately it once again failed
in trials because more in the sample groups who took it died than
those who didn't.  So the dosage was simply lowered so patients were
poisoned and died over a longer period of time.

[ Message was illegally cancelled/censored by the criminal organization AIPAC at $$5lqnjainkc7o5.news.x-privat.org via x-privat.org on 23 Apr 2007 05:55:07 +0200 --> see headers

http://www.sciencedaily.com/releases/2007/04/070406140932.ht

Drug Used To Prevent HIV Transmission From Mother To Child Damages DN

Science Daily - Studies demonstrate that AZT causes genetic damage that may increase future cance
risk

HIV transmission from mother to child can occur in utero, during labo
or from breastfeeding. If left untreated, approximately 25 percent o
newborns exposed to the virus from their infected mothers will becom
infected themselves and potentially develop AIDS. Fortunately
antiretroviral drug combinations, which typically include AZT (zidovudine)
a nucleoside reverse transcriptase inhibitor (NRTI), have reduced th
rate of transmission from mother to child to less than 2 percent in infant
who are not breast fed

NRTIs work by inhibiting the viral reverse transcriptase and by incorporatin
into the viral DNA and terminating nascent strands, thus preventing the viru
from duplicating. However, previous research has shown that NRTIs als
incorporate into the DNA of host cells, causing damage that could hav
long-term health consequences for those exposed to the drugs

Two new animal studies have examined the cancer-causing effects o
transplacental exposure to AZT in mice and rats and found increase
rates of tumors and tumors with gene changes that frequently occur i
human cancer. In addition, two human studies are the first to observ
the induction of mutations and large scale chromosomal damage in re
blood cells of newborns exposed to NRTIs in utero

These, and other, studies were published in April 2007 in a special issu
of Environmental and Molecular Mutagenesis that examines the lates
research on DNA damage and potential health risks related to the us
of NRTIs. Besides the effects of NRTIs on nuclear DNA and cance
risk, the issue also contains recent findings on the toxicity of thes
drugs toward mitochondrial DNA

Researchers led by Dale M. Walker of Experimental Patholog
Laboratories in Herndon, VA, administered AZT in varying dose
to female mice and rats during the last 7 days of gestation an
examined the tissue of their offspring two years later. They foun
clear evidence of an AZT-induced increase in the incidence o
hemangiosarcoma (cancer originating in cells that line the bloo
vessels) in male mice and mononuclear cell leukemia in femal
rats

There was also some evidence of increased liver cancer an
reproductive tumors. "Although the implications of these finding
for the long-term health of human children exposed tranplacentall
to AZT are uncertain, the possibility of increased cancer risk fo
a subset of these children in mid and late adulthood appears highl
plausible," the authors state

The carcinogenic effects of AZT were further demonstrated by
study on mice led by Hue-Hua Hong of the National Institute o
Environmental Health Sciences in Research Triangle Park, NC
This study found mutations in the K-ras and p53 cancer genes tha
are often mutated in human lung tumors. The development of lun
cancer in these mice suggests that the incorporation of AZT or it
metabolites into DNA, oxidative stress, and genomic instabilit
may be the contributing factors to the pattern of mutations observe
in the study, according to the authors. They conclude, "Th
cumulative mutagenesis data suggest that infants expose
transplacentally to AZT may be at increased risk for cancer as they age.

In the first of the two human studies, researchers led by Patrici
A. Escobar of the University of Pittsburgh, in Pittsburgh, PA
measured DNA damage caused by AZT in the blood of newborns
They found increased frequencies of glycophorin A mutations i
the red blood cells of newborns who had been exposed to AZ
plus lamivudine (another type of NRTI) in utero, and these change
persisted for the most part through one year of age. The researcher
note that although the combination of the two NRTIs is more effectiv
at preventing transmission of HIV from mother to fetus, it is also more
genotoxic than AZT alone. They conclude that "there is a need for
careful monitoring of the future health of children who received
peripartum AZT-based therapies, the development of new safer
NRTIs, and the identification of antimutagenic drugs that will mitigate
the side effects of NRTI-based highly active antiretroviral therapy."

In the second study involving humans, researchers led by Kristine L.
Witt of the National Institute of Environmental Health Sciences in
Research Triangle Park, NC measured the frequency of immature
red blood cells (reticulocytes; RET) containing micronuclei (MN),
indicators of chromosomal damage, in blood samples of HIV-infected
women and their infants exposed to antiretroviral drugs during pregnancy.
Most, but not all, of the prenatal treatment regimens in this study
included AZT. At birth, the researchers observed ten-fold increases
in the frequencies of micronucleated reticulocytes (MN-RET) in the
women and infants whose prenatal drug regimen included AZT.

No increases were detected in the women and infants who did not
receive prenatal AZT. The frequency of MN-RET in the AZT-exposed
newborns decreased over the first 6 months of life to levels seen in
nonexposed infants. These findings imply a strong potential for
AZT-induced genetic damage in the developing fetus. The authors
state "We are concerned about the long-term health implications for
these infants because the MN increases noted in this study add to the
growing body of evidence that ZDV [AZT] readily induces genetic
damage," The authors conclude by emphas
izing that they do not
advocate eliminating the use of AZT in the treatment of HIV because
it is highly effective in preventing mother to child transmission of the
virus. However they recommend long-term monitoring of AZT-exposed
infants who are HIV uninfected.

Articles:

"Genotoxicity Assessed by the Comet and GPA Assays Following In
Vitro Exposure of Human Lymphoblastoid Cells (H9) or Perinatal
Exposure of Mother-Child Pairs to AZT or AZT-3TC,"
Patricia A. Escobar, Ofelia A. Olivero, Nancy A. Wade, Elaine J. Abrams,
Carol J. Nesel, Roberta B. Ness, Richard D. Day, Billy W. Day, Quanxin Meng, J.
Patrick OfNeill, Dale M. Walker, Miriam C. Poirier,
Vernon E. Walker, William L. Bigbee, Environmental and
Molecular Mutagenesis, April 2007, 48:330-343.

"Genetic Alterations in K-ras and p53 Cancer Genes in
Lung Neoplasms From Swiss (CD-1) Male Mice Exposed Transplacentally
to AZT," Hue-Hua L. Hong, June Dunnick, Ronald Herbert,
Theodora R. Devereux, Yongbaek Kim, Robert C. Sills,
Environmental and Molecular Mutagenesis, April 2007, 48:299-306.

"Transplacental Carcinogenicity of 3O-Azido-3O-Deoxythymidine in
B6C3F1 Mice and F344 Rats," Dale M. Walker, David E. Malarkey,
Steven K. Seilkop, Frederick A. Ruecker, Kathleen A. Funk, Marilyn J. Wolfe,
Christopher P. Treanor, Julie F. Foley, Fletcher F. Hahn, Jerry F. Hardisty,
Vernon E. Walker, Environmental and Molecular Mutagenesis, April 2007, 48:283-298.

"Elevated Frequencies of Micronucleated Erthrocytes in Infants Exposed
to Zidovudine In Utero and Postpartum to Prevent Mother-to-Child
Transmission of HIV," Kristine L. Witt, Coleen K. Cunningham, Kristine B. Patterson,
Grace E. Kissling, Stephen D. Dertinger, Elizabeth Livingston, Jack B. Bishop,
Environmental and Molecular Mutagenesis, April 2007, 48:322-329.

Note: This story has been adapted from a news release issued by John Wiley & Sons, Inc..