5 replies to this topic

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NON-HODGKIN'S LYMPHOMA SECONDARY TO AMPHETAMINE USE
1) Nelson RA, Levine AM, Marks G, Bernstein L. Alcohol, tobacco and recreational drug use and the risk of non-Hodgkin's lymphoma. British Journal of Cancer 1997;76(11):1532-7
From Department of Preventive Medicine, School of Medicine, University of Southern California


A population based case-control study was conducted to determine whether risk of non-Hodgkin's lymphoma is related to previous tobacco, alcohol or recreational drugs. Amphetamines were associated with a significantly increased risk of non-Hodgkin's lymphoma (Odds ratio OR = 2.44, 95% CI = 1.13-5.31). In regards to dose-response relationships, there was a statistically significant trend observed with increasing use of amphetamines (P = 0.03) (i.e. the risk was greater among those with more frequent amphetamine use.)

2) Doody MM, Linet MS, Glass AG, Curtis RE, Pottern LM, Rush BB, Boice JD Jr, Fraumeni JF Jr, and Friedman GD. Risk of non-Hodgkin's lymphoma, multiple myeloma, and leukemia associated with common medications. Epidemiology 1996;7:131-139
From Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD

Data from two Kaiser Permanente medical care programs were used to
evaluate risks of hematopoietic and lymphoproliferative malignancies after use of 14 common medications. Included in the study were 510 patients with hematological and lymphoproliferative malignancies and 695 controls. In contrast to data from interview studies, medical record data are not subject to possible bias in the form of differential recall between case and control subjects. Using a minimum 5-year exposure lag between first notation and malignancy diagnosis the risk of non-Hodgkin's lymphoma was greater among plan members who were prescribed amphetamines (Odds ratio OR = 2.2; 95% CI = 1.1-4.8). The risk of non-Hodgkin's lymphoma rose with increasing number of medical record notations for amphetamines (P = 0.01). The OR for greater than or equal to 3 notations for amphetamines was: OR = 9.5; 95% CI 2.0-44.0).

Note: The OR for greater than or equal to 3 notations for amphetamines was: OR = 9.5; 95% CI 2.0-44.0).

The study by Nelson RA et al above (Department of Preventive Medicine, School of Medicine, University of Southern California) and the study by Doody MM et al above (Epidemiology Branch, National Cancer Institute) – both show:

1) A significant relationship between amphetamine use and the development of non-Hodgkin's lymphoma.

2) A dose response relationship. In the National Cancer Institute study, if there was three notations or more in the chart for amphetamine use the OR = 9.5; 95% CI 2.0-44.0).

A prospective case-control study of the aetiologic factors involved in the production of lymphoid malignancies was conducted within a defined geographic area covering six health districts in Yorkshire Region. Included in the study were 285 patients with lymphoid malignancies and an equal number of controls. Amphetamine use was associated with an increased risk ratio but this did not reach statistical significance in this study (Risk ratio = 3.04; 95% Confidence limits 0.66-14.09)

A case-control study of patients with Hodgkins disease from the Los Angeles County was performed. Included in the study were 218 patients with Hodgkin's disease and 218 controls. An assessment and determination of risk ratios for various risk factors was performed. The authors state quite clearly that one of the prestudy objectives was to assess the association between amphetamines and Hodgkin's disease. This study was performed to confirm a previous study by these authors that showed a significant relationship between amphetamine use and Hodgkin's disease. The authors again found a strong statistically significant association between Hodgkin's disease and amphetamine use (Risk ratio = 3.0, P = 0.01). A dose-effect relationship was suggested as the risk ratio for using amphetamines for at least 1 year was markedly increased (Risk ratio = 11.0, P = 0.003)

A case-control study of patients with Hodgkin's disease was undertaken
seeking clues to disease etiology. The above two manuscripts reported Hodgkin's disease patients had a sixfold increase in prior history of Dexedrine use when compared to matched nonrelated controls (relative risk = 6.3, P = < 0.01).

CASE REPORT (ACUTE MYELOBLASTIC LEUKEMIA) and AMPHETAMINES
Berry JN. Acute Myeloblastic leukemia in a benzedrine addict. Southern Medical Journal (1966) 59(10):1169-70

This paper reports that a 24 year old benzedrine addict develops acute myeloblastic leukemia after taking massive dosages of the drug benzedrine for more than 2 years. The author reviews briefly some of the hematological effects of amphetamines. The author also raises the question of whether the amphetamines could potentially cause leukemia because it is a synthetic benzene-ring derivative. The author points out that other agents/drugs that are benzene ring derivatives have known toxic hematological effects (e.g. author sites report of acute leukemia associated with phenybutazone therapy).

ACUTE LYMPHOBLASTIC LEUKEMIA AND AMPHETAMINE USE
1) Parental medication use and risk of childhood acute lymphoblastic leukemia. Wen W, Shu XO, Potter JD, Severson RK, Buckley JD, Reaman GH, Robison LL. Cancer 2002 Oct 15;95(8):1786-94

Few studies have examined the risk of childhood acute lymphoblastic leukemia (ALL) associated with parental medication use. As part of a large case-control study conducted by the Children's Cancer Group, we evaluated the association between maternal and paternal medication use and the risk of ALL in offspring. Participants included 1842 children of 14 years or younger with newly diagnosed and immunophenotypically defined ALL and 1986 individually matched controls. Paternal use of amphetamines or diet pills were associated with an increased risk of childhood ALL in the offspring (OR = 2.2, 99% CI: 1.2-3.9). Paternal use of amphetamines or diet pills (during the 1 year before pregnancy) more than doubled the offspring's risk of ALL. When both parents reported using these drugs the risk of childhood ALL rose even further (OR = 2.8). CONCLUSIONS: The findings of this study suggest that amphetamines use immediately before and during the index pregnancy may influence risk of ALL in offspring.

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AMPHETAMINES AND RENAL CELL CARCINOMA
(Human Studies)

RENAL CELL CARCINOMA
1) Yuan JM, Castelao JE, Gago-Dominguez M, Ross RK, Yu MC. Hypertension obesity and their medications in relation to renal cell carcinoma. British Journal of Cancer 1998;77(9):1508-13
From the Department of Preventive Medicine USC/Norris Comprehensive Center, University of Southern California

A population-based, case-control study was conducted in Los Angeles County, California to investigate the inter-relationships of multiple factors including amphetamine use in relation to renal cell carcinoma risk. A total of 1204 patients with renal cell cancer and an equal number of controls were included. Patients received a histological diagnosis of renal cell carcinoma between 1986-1994. Results were as follows: Regular use of amphetamine-containing diet pills was associated with twofold increase in renal cell carcinoma risk(OR= 2.0, 95% CI = 1.4-2.8). In addition the risk of renal cell carcinoma increased with increasing dosages of amphetamines. There was a monotonic increase in risk by increasing maximum weekly dose of amphetamines (P < 0.001, linear trend test) after adjustment for level of education, usual BMI (body mass index) and history of hypertension. The dose-response relationship was observed in both men and women.

A population-based case-control study was conducted to investigate various factors (including pharmacological treatment of obesity) in relation to renal cell carcinoma risk. A total of 379 patients with renal cell carcinoma and 353
controls were included in the study. Patients received a diagnosis of renal cell carcinoma during the period of 1989-1991. The study patients and controls were from Sweden. This study was part of an international collaborative population-based case-controlled study on renal cell cancer. Results were as follows: Regular use of diet pills containing amphetamine was associated with an increased risk of renal cell cancer (OR = 4.06; 95% CI = 1.35-12.22). In women the relative risk for renal cell carcinoma with amphetamine use was particularly elevated (OR = 5.34; 95% CI = 1.52-18.78). Even after adjustment for BMI (body mass index) amphetamine use in women was associated with increased risk of renal cell cancer (OR = 4.57; 95% CI = 1.26-16.57).

A population-based case-controlled study of kidney cancer in patients from New South Wales, Australia was conducted. A total of 489 patients with renal cell carcinoma and 523 controls were included in the study. The diagnosis of renal cell carcinoma was made between 1989-1990. Diet pills (including amphetamines as well as appetite suppressants) even after adjustment for all other significant risk factors, including obesity increased the risk of renal cell cancer (RR = 2.0; 95% CI = 1.2-3.4). (page 329 of study).

D'Amico A, Piacentini I, Righetti R, Curti P, Ficarra V [Article in Italian] [No title given] Arch Ital Urol Androl 2001 Mar;73(1):49-55. Divisione Clinicizzata di Urologia, Universita degli Studi di Verona, Italia. mirsor@tin.it

"The following exposures have been more consistently associated with renal cell carcinoma: tobacco smoking; occupational exposures … ; iatrogenic factors such as analgesics and amphetamines… and hypertension"

Gago-Dominguez M. Yuan JM. Castelao JE. Ross RK. Yu MC. Family history and risk of renal cell carcinoma. Cancer Epidemiology, Biomarkers & Prevention. 10(9):1001-4, 2001 September.

A population-based case-control study involving 550 non-Asian renal cell carcinoma patients 25 to 74 years of age and an equal number of sex-, age-, and race-matched neighborhood controls was conducted in Los Angeles, California. Risk factors for renal cell carcinoma identified in the Los Angeles study include cigarette smoking, chronic obesity, history of hypertension, regular use of analgesics and amphetamines.

1) Freire-Garabal M. Nunez-Iglesias MJ. Rey-Mendez M. Pereiro-Raposo MD. Riveiro P. Fernandez-Rial JC. Losada C. Gandoy M. Mayan JM. Effects of amphetamine on the development of Moloney sarcoma virus-induced tumors in mice. Oncology Reports. 5(2):381-3, 1998 Mar-Apr.

Experiments were conducted to evaluate the effects of amphetamine (0.4 mg/kg) on the development of autochthonous tumors induced by the Moloney sarcoma virus (MSV) in Balb/c female mice. Enhancement of MSV-induced tumor incidence and tumor growth was observed, together with a delay in the usual prompt regression of the tumors, when mice were daily injected with amphetamine for 3 days after MSV-inoculation.

Freire-Garabal M, Nunez-Iglesias MJ, Losada C, Pereiro-Raposo MD, Castro-Bolano C, Heras J, Riveiro P, Mayan JM, Rey-Mendez M. Stimulatory effects of amphetamine on the development of the Walker-256 carcinoma lung metastases in rats. Oncology Reports 3: 201-204, 1996

Experiments were performed in order to evaluate the effects of amphetamine (0.4 mg/kg/day) on the development of lung metastases in rats injected with 104 Walker 256 (W-256) carcinosarcoma cells. The number of metastatic nodules on the surface of the lungs, as well as the percentage-area of metastases in the frontal section through pulmonary hilus were increased in rats injected with amphetamines in comparison with those injected with placebo (P< 0.05). Survival periods were also assessed and amphetamine was found to increase the lethality of rats.

M Rey-Mendez, MJ Nunez Iglesias, JC Fernandez-Rial, L Garcia-Vallejo, M Freire-Garabal. Effects of amphetamine on the development of moloney sarcoma virus (MSV) -induced tumors in mice Neuroimmunology-Univ of Santiago NIMUS, Huerfanas 19, 15703 Santiago de Compostela, SPAIN

Published in Cancer Detection and Prevention 1993; 17(1)

In previous investigations we observed adverse effects of amphetamine on the immune system of mice. Daily injection with 0.4 mg/kg of amphetamine resulted in a reduction of the number and functional capacities of T-cells as well as in a suppression of the activity of phagocytosis. Since it has been pointed out that cell-mediated immunity may regulate the growth of tumors, in the present report we next studied the effects of amphetamine on the development of autochthonous tumors induced by the Moloney sarcoma virus (MSV) in BALB/c female mice. Enhancement of MSV- induced tumor incidence and tumor growth was observed, together with a delay in the usual prompt regression of the tumors, when amphetamine was daily injected at 0.4 mg/kg immediately following MSV i.m. inoculation. These results show adverse effects of amphetamine on tumor development in mice. Paper presented at the International Symposium on Cofactor Interactions and Cancer Prevention; Nice, France; March 17-19, 1993; in the section on Avoidable Risk Factors.

Freire-Garabal M, Nunez MJ, Balboa JL, Suarez JA, Gallego A, Belmonte A. Effects of amphetamine on the development of MTV-induced mammary tumors in female mice. Life Sci 1992;51(6):PL37-40

Female C3H/He mice carrying the mammary tumor virus (MTV) were monitored for mammary tumor incidence and latent periods while submitted to a daily subcutaneous injection with amphetamine (0.4 mg/kg/day). Results show that amphetamine caused an increase in incidence and a decrease in latency of tumors compared with placebo. There was also appreciated a correlation with the lethality of mice.

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Akintonwa DA. Mechanistic biotransformations of some amphetamine drugs. Journal of Theoretical Biology. 120(3):303-8, 1986 Jun 7.

Amphetamine, fenfluramine and benzphetamine were the drugs investigated for the isolation of toxic metabolites using the biochemical mechanism of cytochrome P-450 monooxygenase mediated reaction. NH3 derived from amphetamine should be innocuous unless the in vivo ammonia detoxifying mechanism is overwhelmed thus culminating in ammonia intoxication in cerebral tissues with consequent concomitant convulsion. +CF3 electrophile derived from fenfluramine is potentially reactive with nucleophiles of proteins, carbohydrates, lipids, DNA and RNA. The derivation of .CF3 was discussed. Methylbenzylamine was derived from benzphetamine. This, in the nitrosating environment of the gastrointestinal tract, could yield the carcinogenic methylbenzylnitrosamine.

Tutton PJ. Barkla DH. Cytotoxicity of p-chloroamphetamine in dimethylhydrazine-induced carcinomata of rat colon. Cancer Chemotherapy & Pharmacology. 2(2):137-8, 1979.

Previous studies have shown that several serotonin-related compounds are cytotoxic to dimethylhydrazine-induced carcinomata of the colon of rat. This paper reports the cytotoxicity of another serotonin-related compound, p-chloroamphetamine.

Larez A, Briceno E, Ochoa Y, Montenegro M, Aponte N. Mutagenicity obtained experimentally by oral administration of dextroamphetamine sulphate to the rat Bull Narc 1979 Jan-Mar;31(1):67-70

Research work on the possible mutagenic effects of the amphetamine, sympathomimetic amine, was carried out on the rat. The method used was the dominant lethal assay, in its sub-acute form. Dextroamphetamine sulphate was administered orally. At the dosage and frequency of the test, dextroamphetamine sulphate was found to be a significantly mutogenic agent. The over-all mutagenic index was13.92% (P less than 0.01) for the test group and 8.90% for the control group.

MA Assis MS, AM Pacchioni MS, C Collino MS, B Salido-Rentería MS, V Molina PhD, AM Basso PhD, C Sotomayor PhD and L Cancela PhD. Repeated administration of d-amphetamine facilitates stress-induced immunosuppression: a multiparameter T and B cells analysis by flow cytometry. Paper presented at the International Symposium on Predictive Oncology and Intervention Strategies; Paris, France; February 9 - 12, 2002; in the section on Carcinogenesis.

http://www.cancerpre...6/101/1010/4284

http://www.cancerpre...6/101/1010/4284


AIMS: Drug addiction and stress are associated with immunosuppression states that altering the vulnerability to a wide variety of diseases, including neoplasia. Repeated exposure to psychostimulants like amphetamine (AMPH) is characterized by enhanced neurochemical and behavioural responses to a subsequent administration of the same drug (sensitization) or to stress (cross-sensitization) involving the activation of central dopaminergic (DA) pathways. We previously demonstrated that chronic AMPH treatment facilitates the immunosuppression following the exposure to an aversive stimulus. This facilitation is reverted by a pre-treatment with haloperidol (HAL), a nonselective D1/D2 DA receptor antagonist. The main goal of this study was to determine the influence of d-amphetamine and/or haloperidol repeated treatment, on stress-induced effects on lymphocyte subpopulations. METHODS: Wistar rats were treated with AMPH (2mg/kg/day IP during 9 days), and subsequently exposed to a footshock stress. Other group was administered with HAL (1mg/kg IP, 30 min previous to each daily AMPH injection). Then, blood cells were stained with monoclonal antibodies against CD3-FITC, CD4-Cy-Chrome, CD8-PE and CD45RA-Cy-Crhome and were analyzed by multiparameter flow cytometry. RESULTS: The absolute number of peripheral lymphocyte decreased, as well as CD4+ and CD8+ T-cells and B-cells in chronically AMPH-pretreated rats relative to vehicle-treated controls. That immunosuppressive response was abolished by HAL administration. CONCLUSIONS: The present findings complement our previous evidence and are indicative of a modulatory role for DA in the facilitating process induced by AMPH on stress-induced immunosuppressive effects.

AMPHETAMINE INDUCED GENETIC AND CHROMOSOMAL DAMAGE

1) Li JH, Hu HC, Chen WB, Lin SK. Genetic toxicity of methamphetamine in vitro and in human abusers. Environ Mol Mutagen. 2003;42(4):233-42.

Methamphetamine (METH) is a widely abused psychomotor stimulant. Although numerous studies have examined METH-induced neurotoxicity, its ability to produce genotoxic effects has not been evaluated. In this article, we report on the genotoxicity of METH in vitro and in human METH abusers. METH induced his(+) revertants in Salmonella typhimurium strains TA98 and TA100, and increased the frequency of hprt mutants, micronuclei, and sister chromatid exchange (SCE) in cultured Chinese hamster ovary K1 (CHO-K1) cells. These METH-induced genotoxic effects were eliminated if METH exposure was conducted in the presence of rat liver S9, indicating that the genotoxicity was caused by METH, and not by metabolites of METH. In addition, reactive oxygen species (ROS) scavengers inhibited the METH-induced micronuclei in CHO-K1 cells. Further investigation with 76 human long-term METH abusers and 98 unexposed controls demonstrated that total METH exposure correlated with micronucleus and SCE frequencies in cultured lymphocytes. [/b]The results of this study indicate that METH is a genotoxic agent and that ROS may play a role in METH-induced genotoxicity. [/b]

In this study the authors state that "Methamphetamine is genotoxic in Salmonella typhimurium and in cultured (CHO-K1) cells." They also state that human exposure to methamphetamine is genotoxic and there is a correlation between the total amount of methamphetamine consumed and the frequency of MN (micronucleus) and SCE (sister chromatid exchange) in human subjects.

In addition the authors state "The induction of MN and SCE by methamphetamine in both CHO-K1 cells and human abusers indicates that the genotoxicity of methamphetamine occurs not only in vitro but also in human subjects, and further confirms that methamphetamine-induced genotoxic effects are dose dependant.

Agarwal K, Mukherjee A, Sharma A, Sharma R, Bhardwaj KR, Sen S. Clastogenic effect of fenfluramine in mice bone marrow cells in vivo. Environ Mol Mutagen 1992;19(4):323-6

Fenfluramine, an amphetamine derivative used in the treatment of obesity, has been evaluated in vivo in the bone marrow cells of Swiss albino mice using two cytogenetic endpoints for assessing its genotoxic and clastogenic potentials. Fenfluramine showed a significant increase in the percentage of damaged cells over that of the vehicle control. The degree of clastogenicity was directly proportional to the dosage used and inversely related with the duration of treatment. This study evaluated the drug for its genotoxicity and showed that Fenfluramine is moderately clastogenic and a DNA damaging agent in vivo.

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Tariq M, Parmar NS, Qureshi S, el-Feraly FS, Al-Meshal IA. Clastogenic evaluation of cathinone and amphetamine in somatic cells of mice. Mutat Res 1987 Feb;190(2):153-7

Clastogenic effects of cathinone, the active principle from khat (Catha edulis) and amphetamine, a compound having similar chemical structure and pharmacological activity, have been studied on the somatic cells of mice. Both of them produced marked clastogenic activity and affected the cell proliferation in the bone marrow of mice. They induced a significant increase in the frequency of micronucleated polychromatic erythrocytes at higher doses. These results substantiate our earlier observations on the clastogenic and mitodepressive activity of cathinone on the meristematic region of Allium cepa, and indicate that cathinone may be responsible for the mutagenic effect of khat reported by other workers. The clastogenic effects of amphetamine are being reported for the first time.

Akintonwa DA Mechanistic biotransformation of some amphetamine drugs. J theor Biol 1986; 120:303-308

A study of benzphetamine showed that the potentially carcinogenic agent methylbenzylnitrosamine could be formed in a nitrosating envirement (Akintonwa 1986).

Petrakis NL, Maack CA, Lee RE, Lyon M. Mutagenic activity in nipple aspirates of human breast fluid. Cancer Res 1980 Jan;40(1):188-9

Breast fluid samples from women attending breast screening clinics were assayed for mutagenic activity using the Ames Samonella mutagenesis test. Two of the positive breast fluids were from women taking Eskatrol, an anorectic containing prochlorperazine and dextroamphetamine.

GENOTOXICITY

From Meditext off of Micromedex. A phamaceutical service Allina offers Medical Health Professionals.

7) DNA DAMAAGE/REPAIR: DNA damage was observed in E COLI exposed to amphetamine (RTEC, 1991)

8) CHROMOSOMAL ABERRATIONS: The micronucleus test showed chromosomal aberrations in thee mouse exposed to amphetamine (RTEC, 1991)

PARENTAL AMPHETAMINES USE AND SUBSEQUENT TUMOR OR LEUKEMIA DEVELOPMENT IN ANIMALS AND HUMANS

Martin JC. The effects of maternal use of tobacco products or amphetamines on offspring. In the book: Perinatal Substance Abuse: Research Findings and Clinical Implications 1992; Chapter 12 :279-305 Edited by Theo B Sondereg.

Metamphetamine-exposed offspring (of Sprague-Dawley rats) developed significantly more tumors in middle and late maturity than saline or untreated offspring.

Martin JC, Martin DD, Radow B and Day HE. Life Span and Pathology in Offspring Following Nicotine and Methamphetamine Exposure. Experimental Aging Research. 1979, Vol 5, No 6, 509-522

Primiparous Sprague-Dawley rats received S.C. injections of either 3.0 mg/kg of pure nicotine, 5.0 mg/kg of methamphetamine HCL, 5.0 mg/kg of saline vehicle, or received no injection during the 21 day gestational period and 19 day nursing period. None (0 of 16) of rats receiving saline had tumors while 25% (4 of 16) of the rats receiving methamphetamine developed tumors. The authors stated there was "possible greater susceptibility to tumor formation (in rats) following methamphetamine administration in utero."

Martin JC, Martin DD, Radow B and Day HE. Life Span and Pathology in Offspring Following Nicotine and Methamphetamine Exposure. Experimental Aging Research. 1979, Vol 5, No 6, 509-522

Primiparous Sprague-Dawley rats received S.C. injections of either 3.0 mg/kg of pure nicotine, 5.0 mg/kg of methamphetamine HCL, 5.0 mg/kg of saline vehicle, or received no injection during the 21 day gestational period and 19 day nursing period. None (0 of 16) of rats receiving saline had tumors while 25% (4 of 16) of the rats receiving methamphetamine developed tumors. The authors stated there was "possible greater susceptibility to tumor formation (in rats) following methamphetamine administration in utero."

HUMAN DATA:

Parental medication use and risk of childhood acute lymphoblastic leukemia. Wen WQ; Shu XO; Potter J; Severson RK; Buckley J; Reaman G; Robison L Am J Epidemiol 1999 Jun;149(11 Suppl):S70 [DART]

Few studies have examined the risk of childhood acute lymphoblastic leukemia (ALL) associated with parental medication use. As part of a large case-control study recently conducted by the children's Cancer Group, we evaluated the relationship between maternal and paternal medication use and risk of ALL in offspring. Paternal and maternal use of amphetamines were associated with an increased risk of childhood ALL, with a significant dose-response relationship found for paternal exposure (trend p value less than 0.01). The associations observed were strongest among children whose parents both used these medications (OR = 3.61, 95% CI = 1.00-13.09 for amphetamines) compared to those for whom neither parent was exposed.

Shu XO, Perentesis JP, Wen W, Buckley JD, Boyle E, Ross JA, Robison LL; Children's Oncology Group. Parental exposure to medications and hydrocarbons and ras mutations in children with acute lymphoblastic leukemia: a report from the Children's Oncology Group. Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1230-5

"Ras proto-oncogene mutations have been implicated in the pathogenesis of many malignancies, including leukemia. While both human and animal studies have linked several chemical carcinogens to specific ras mutations, little data exist regarding the association of ras mutations with parental exposures and risk of childhood leukemia. Using data from a large case-control study of childhood acute lymphoblastic leukemia (ALL; age <15 years) conducted by the Children's Cancer Group, we used a case-case comparison approach to examine whether reported parental exposure to … use of specific medications are related to ras gene mutations in the leukemia cells of children with ALL." … "Paternal use of amphetamines or diet pills was associated with N-ras mutations (OR 4.1, 95% CI 1.1-15.0)"; "This study suggests that parental exposure to specific chemicals may be associated with distinct ras mutations in children who develop ALL."

IN VITRO TEST PREDICT AMPHETAMINE IS A CARCINOGEN
TEST SHOWN TO BE ABLE TO PREDICT POTENTIAL CARCINOGENS


1) Kubinski H, Gutzke GE, and Kubinski ZO. DNA-Cell-Binding (DCB) Assay for suspected carcinogens and mutagens. Mutation Research 89 (1981) 95-136.

The authors took known carcingens (by animal test) and performed a in vitro test called DNA-cell-binding assay. This test is based on the finding that DNA and other nucleic acids exposed to active carcinogens strongly react with macromolecules producing nucleic acid--nucleic acid and nucleic acid—protein adducts.

Of the 65 known carcinogens the DCB assay was positive in 62 providing a 95.4% agreement with animal data.

Of the 70 known non-carcinogens the DCB assay was negative in 67 providing 95.7% agreement with animal studies.

****** The DCB assay for Amphetamine was positive.

The positive DCB for amphetamines is in agreement with the subsequent human and animal studies showing that amphetamines are carcinogens.

[truecolor10]

this is the best site ever regarding the topic Amphetamines Cause Cancer .
Very useful
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Edited by truecolor10, 08 June 2009 - 01:23 AM.

[Anewlife]

I was a heavy amphetamine user for a year at 20 and developed cancer towards the end of it.
After researching how cancer works I doubt it's related until I read this, then I realised all these studies aren't really conclusive. Cancer develops way before it is detected.

Edited by Anewlife, 12 May 2015 - 01:49 AM.