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HIV Drugs Might Combat Two Other Diseases
Prostate Cancer And Chronic Fatigue Syndrome

Alan Cantwell MD

I have long wondered why prostate cancer was NOT a common cancer in male AIDS patients who have been on the "AIDS cocktail" (and sometimes added male hormones) for almost two decades, particularly when HIV is considered to be a "cancer-causing virus."
As the report below suggests, maybe HIV drugs are "protective" and the reason that PROSTATE CANCER is NOT a common cancer in ageing HIV/AIDS patients!!! (UNLIKE OTHER FORMS OF CANCER -- like Kaposi's sarcoma, various lymphomas, cervical cancer, etc -- which ARE
cancers commonly associated with AIDS. )
Also some AIDS patients are given testosterone "replacement" hormone therapy to treat the "wasting syndrome" sometimes associated with chronic AIDS. Doctors usually hesitate to give healthy ageing males "extra" testosterone for fear of CAUSING prostate cancer!! (There is recent evidence that the PROHIBITION of treating prostate cancer WITH testosterone is now being CHALLENGED -- see Morgentaler's partial paper from March, 2010, at the end of this email)
As you may know, "acid-fast" cell wall deficient pleomorphic BACTERIA have been discovered and reported in BOTH AIDS and prostate cancer. Although this research of mine has been ignored by the AIDS establishment (with HIV the supposed SOLE cause of AIDS) -- it may eventually prove that "HIV drugs" (and hormone therapy??) also have some killing or suppressive effect on the bacteria reported in prostate cancer and AIDS.
for more info on bacteria in AIDS and prostate cancer.....
GOOGLE: Cantwell + prostate cancer
and/or Cantwell + AIDS bacteria
HIV Drugs Might Combat Two Other Diseases
Prostate cancer, chronic fatigue are new research targets
(HealthDay News) -- Four anti-HIV drugs inhibit a retrovirus recently linked to prostate cancer and chronic fatigue syndrome (CFS), say U.S. researchers.
If further investigation proves that the retrovirus xenotropic murine leukemia virus-related virus (XMRV) causes prostate cancer or CFS, these HIV drugs may be an effective treatment for the two conditions.
In this study, researchers from the University of Utah and Emory University/Veterans Affair Medical Center tested how effectively 45 compounds used to treat HIV and other viral infections worked against XMRV. Raltegravir was the most effective, and three other drugs -- L-00870812, zidovudine (ZDV or AZT), and tenofovir disoproxil fumarate (TDF) -- also prevented XMRV replication.
"Our study showed that these drugs inhibited XMRV at lower concentrations when two of them were used together, suggesting that possible highly potent 'cocktail' therapies might inhibit the virus from replicating and spreading," Raymond F. Schinazi, a professor of pediatrics and chemistry and an investigator with the Center for AIDS Research at the Emory University School of Medicine and the Atlanta VA, said in a news release.
"This combination of therapies might also have the added benefit of delaying or even preventing the virus from mutating into forms that are drug-resistant," Schinazi added.
"These results offer hope to infected persons, but we are still at the early stages of our understanding of the potential link between XMRV and these diseases," Dr. Ila R. Singh, an associate professor of pathology at the University of Utah Medical School, said in the news release.
The study was published April 1 in the journal PLoS One.
More information
The U.S. Centers for Disease Control and Prevention outlines the possible causes of chronic fatigue syndrome.
-- Robert Preidt
SOURCE: University of Utah Health Sciences, news release, April 1, 2010
Copyright © 2010 HealthDay. All rights reserved.
Alan Cantwell M.D.
Oncol Rep. 2007 May;17(5):1121-6.
HIV infection and cancer in the era of highly active antiretroviral therapy (Review).
Barbaro G, Barbarini G.
Department of Medical Pathophysiology, University La Sapienza, 00174 Rome, Italy. g.barbaro@tin.it
The majority of cancers affecting HIV-infected subjects are those established as acquired immunodeficiency syndrome (AIDS)-defining: Kaposi's sarcoma (KS), non-Hodgkin's lymphoma (NHL), and invasive cervical cancer (ICC). However, other types of cancer, such as Hodgkin's disease (HD), anal cancer, lung cancer and testicular germ cell tumors appear to be more common among HIV-infected subjects compared to the general population. While not classified as AIDS-defining, these malignancies have been referred to as AIDS-associated malignancies. The mechanisms by which depressed immunity could increase the risk for cancer are unclear, except for in KS and most subtypes of NHL, where it is strictly associated with a low CD4 count. Although it remains unclear whether HIV-1 acts directly as an oncogenic agent, it may contribute to the development of malignancies through several mechanisms (e.g., infection by oncogenic viruses, impaired immune surveillance, imbalance between cellular proliferation and differentiation). Studies of the effect of highly active antiretroviral therapy (HAART) on the incidence and progression of HIV/AIDS-associated cancers provided contrasting data. While a significant decrease in the incidence of KS has been observed, HAART has not had a significant impact on NHL incidence, particularly systemic NHL, or on ICC, HD, anal cancers and other non-AIDS-defining cancers. Regardless of whether these cancers are directly related to HIV-induced immunodeficiency, treating cancer in HIV-infected patients remains a challenge because of drug interactions, compounded side effects, and the potential effect of chemotherapy on CD4 count and HIV-1 viral load. A better knowledge of viral mechanisms of immune evasion and manipulation will provide the basis for a better management and treatment of the malignancies associated with chronic viral infections.
PMID: 17390054 [PubMed - indexed for MEDLINE]
J Natl Med Assoc. 2008 Jul;100(7):817-20.
Malignancies in HIV: pre- and post-highly active antiretroviral therapy.
Nutankalva L, Wutoh AK, McNeil J, Frederick WR, Reddy RB, Daftary M, Gentles A, Addae-Afoakwa K.
College of Medicine, Howard University, Washington, DC 20059, USA.
OBJECTIVES: A study was conducted at a large metropolitan tertiary-care teaching hospital to investigate the incidence of cancers among HIV-infected patients over a 13-year period. DESIGN: Retrospective cohort study. METHODS: A retrospective cohort study was conducted among HIV-infected patients diagnosed with cancer between January 1990 and December 2003 at a large metropolitan teaching hospital. Any HIV-infected patient who also had a confirmed diagnosis of Kaposi's sarcoma, primary central nervous system lymphoma, invasive cervical cancer or non-Hodgkin's lymphoma was categorized as having AIDS-defining cancer (ADC) according to the CDC's initial case definition for AIDS, while patients with other malignancies were classified as having non-ADCs. A clinical database was created consisting of HIV patients diagnosed with cancer at this teaching hospital, and data were abstracted for the current project. RESULTS: A total of 203 HIV-infected patients diagnosed with cancer were identified during the study period. Ninety-three cases occurred before 1995 and 110 after 1996. The median age of patients (at cancer diagnosis) in the era before highly active antiretroviral therapy (HAART) was 37 years and in the post-HAART era was 43 years (p<0.05). Mean CD4 count at cancer diagnosis in the pre-HAART era was 101 cells/mm3, and 183 cells/mm3 in the post-HAART period (p<0.05). Six patients had diagnoses of both ADC and NADC during the study period. Of the 197 remaining cases, 129 (65.4%) were ADCs and 68 (34.6%) were NADCs (p<0.05). The incidence of Kaposi's sarcoma decreased significantly, while the incidence of lung cancer increased significantly. CONCLUSIONS: Of 197 patients with a single diagnosis of either ADC or NADC, there was statistically a larger proportion of NADC cases diagnosed in the post-HAART period compared to the pre-HAART period. The number of ADC diagnoses decreased between the pre- and post-HAART period.
PMID: 18672558 [PubMed - indexed for MEDLINE]
March 1, 2010
Use of testosterone therapy in hypogonadal men with prostate cancer
By Abraham Morgentaler, MD
The long-standing prohibition against testosterone therapy (TTh) in men with prostate cancer is now being challenged. New evidence indicates that TTh in these men is not as risky as once believed, and a number of studies have reported good symptomatic results from TTh without cancer recurrence in men who were treated for prostate cancer.
Abraham Morgentaler, MD
Just a few years ago, it would have been unthinkable to offer testosterone therapy (TTh) to men with a history of prostate cancer. Yet several changes have occurred to make TTh (also known as testosterone replacement therapy) a reasonable treatment option in men who are symptomatic from testosterone (T) deficiency. The greatest stimulus has been the desire of men to improve their health and quality of life. A re-evaluation of the historical prohibition against TTh in men with prostate cancer has been prompted by increased awareness of the benefits of TTh, including improvement in sexual desire and function, energy, vitality, mood, and physical performance.1Evidence now indicates that TTh in men with prostate cancer is not nearly as risky as once believed2 (figure 1).
Figure 1. Serum T and PCa growth: Extrapolation vs. evidence
Indeed, a number of publications have now reported good symptomatic results from TTh without cancer recurrence in men following various types of prostate cancer treatments.3-7 Although the total number of men in these studies is limited, the historical fear that higher T must necessarily lead to prostate cancer recurrence or progression is clearly incorrect.
The relationship between T and prostate cancer has been a primary interest of mine, and it has been fascinating to watch the transformation in thought and practice over the last 20 years. In this article, I will present our current understanding of this topic and its impact on clinical practice.
'Feeding a hungry tumor'
At the time of my urology residency in 1984-'88, it was axiomatic that higher T was responsible for prostate cancer development. My fellow residents and I learned that giving T to men with prostate cancer was like "pouring gasoline on a fire" or "feeding a hungry tumor." We saw with our own eyes that men who presented with bony pain from prostate cancer metastases responded nicely to bilateral orchiectomy, often within hours. It was obvious that prostate cancer was androgen-dependent, and there was no reason to doubt that less T was a good thing for men with prostate cancer. Subsequent experience, in which discontinuation of luteinizing hormone-releasing hormone agonist treatment was associated with a steady rise in PSA, appeared to close the circle; lowering T caused prostate cancer to regress, and raising T caused prostate cancer to grow.
After my residency, I became interested in TTh for men with sexual dysfunction. I was impressed by how many of my patients responded well to TTh with improved erections and libido, and was surprised when several of my first TTh patients reported a renewed sense of vitality and resolution of chronic fatigue. Some of these patients asked to stay on TTh even when their ED persisted because they felt better overall. However, I was concerned about the risk of stimulating occult prostate cancer, and a few years later began to require prostate biopsy prior to initiating TTh in order to exclude the presence of prostate cancer.
At the time, it was believed that high T led to prostate cancer and low T was protective against prostate cancer. So it was confusing to all when my colleagues and I in 1996 found prostate cancer in 11 of 77 (14%) T-deficient men with normal PSA (<4.0 ng/mL), a cancer rate in an otherwise normal population that was far higher than anything published at the time.8 A subsequent series in 345 T-deficient men (mean age, 58 years) with PSA <4.0 ng/mL found a similar prostate cancer rate of 15%. Moreover, men with the most severe degree of T deficiency had twice the degree of risk as men with milder T deficiency.9 These results indicated that low T was not protective against prostate cancer, and even suggested paradoxically that low T may represent a risk for prostate cancer.
In 2004, my colleague Ernani Rhoden, MD, and I published a review on the risks of TTh in the New England Journal of Medicine. 10 We were stunned to discover that we could not find a single article in the PSA era that clearly showed a link between higher serum T and prostate cancer. On the contrary, multiple studies showed that men with higher endogenous serum T were at no greater risk for prostate cancer than men with low endogenous serum T. And prostate cancer rates in TTh trials were no different than for the general population.10 Even men with prostatic intraepithelial neoplasia, believed to be a pre-malignant condition, did not develop prostate cancer at a worrisome rate after 12 months of TTh.11
Furthermore, PSA has been shown in several population studies to be unrelated to serum T,12 and the administration of supraphysiologic T doses for up to 40 weeks did not cause an increase in either PSA or prostate volume.13
This was confusing. How was it possible that androgen deprivation and its discontinuation cause such major changes in PSA, yet so many other studies showed no influence of T on PSA, prostate volume, or prostate cancer risk? In the archives of the Countway Medical Library at Harvard Medical School, I found the original landmark paper from 1941 by Huggins and Hodges, which showed that castration or estrogen treatment (which lowers T) resulted in a rapid and substantial decline in the serum marker acid phosphatase in men with metastatic prostate cancer.14 This was the paper that established androgen deprivation as the mainstay of treatment for advanced prostate cancer.
In addition, the authors reported that every man who received T administration developed an elevation of acid phosphatase, causing the authors to conclude that T caused "activation" of prostate cancer and more rapid growth.14However, the number of men who received T was only three, and results were only given for two men. One of these men had already been castrated.14 The acid phosphatase curve for the hormonally intact man was erratic. Amazingly, the origin of the general assertion that higher T led to greater prostate cancer growth was based on equivocal results in a single non-castrated man!2
Other investigators in the pre-PSA era also reported results of T administration in men with metastatic prostate cancer.15,16 Two quite different sets of results were seen. Men with recurrent disease after castration uniformly did poorly with T administration, whereas T administration in men who were previously untreated or newly castrated appeared to have a benign course when T was administered. The authors of one of these studies speculated that perhaps normal T concentrations were sufficient to produce maximal prostate cancer growth.16 Unfortunately, this prescient concept did not survive into the modern prostate cancer era.2
The saturation model: Water for a thirsty tumor
It is now clear that prostate tissue, whether benign or malignant, does not have an endless capacity for increased growth as androgen concentrations increase. There is no doubt that prostate tissue requires androgen for optimal growth, but once the requirement for androgens has been satisfied, additional androgen has little, if any, further effect on growth or PSA response.17 Prostate cancer cell lines demonstrate a dose-response growth curve with increasing concentrations of T or dihydrotestosterone (DHT), but then plateau and demonstrate no further growth even with log increases in androgen concentration.17 A saturation model has been described to account for the biphasic response of prostate tissue to androgens, with exquisite sensitivity to androgens at very low T concentrations and indifference to changes in androgens at higher concentrations.17-18
There are at least two possible mechanisms to account for the saturation model. One is that the androgen receptor (AR) in benign human prostate tissue becomes maximally bound to androgen at approximately 120 ng/dL.19 Since it is the complex of androgen-AR that binds to androgen response elements of nuclear DNA, T concentrations above this saturation point no longer have AR-mediated mechanisms to influence growth. It is rare for men to have naturally occurring T concentrations less than 120 ng/dL, although the saturation model would suggest that men who do might still demonstrate prostate growth or PSA increase with additional T.
Another possibility is suggested by a study in which intraprostatic concentrations of T and DHT were measured before and after 6 months of TTh.20 Although serum T levels increased markedly, intraprostatic concentrations of T and DHT were no different from those seen at baseline. This suggests that the intraprostatic hormonal microenvironment is relatively protected from changes in serum T.
Figure 2. The saturation model of serum T and PCa growth
I no longer describe the relationship of T to prostate cancer as "food for a hungry tumor." Instead, I now describe the relationship as "water for a thirsty tumor" (figure 2). Once the thirst has been satisfied, additional water is simply excess.
Experience with TTh after PCa Tx
A small number of studies have investigated the effects of TTh in men after various forms of treatment for localized prostate cancer. Three have reported results of TTh after radical prostatectomy, with a total of 74 men, all with undetectable PSA prior to TTh. None developed biochemical recurrence.3-5
Sarosdy reported the results of 4.5 years of TTh in 31 men following brachytherapy. None developed biochemical recurrence.6 In addition, a small study reported no recurrences in five men who received TTh after external beam radiation.7
Figure 3. T therapy and PCa incidence: Traditional, current views
One possible reason that none of these men developed cancer recurrence is because of complete eradication of cancer. Another possibility, as suggested by the saturation model,17 is that any existing but occult prostate cancer cells had already been maximally stimulated by the relatively low but still quite appreciable T in the bodies of these men (figure 3).
An interesting case that lends support to this concept is the response to TTh in an 84-year-old man with untreated prostate cancer.21 This active, elderly man underwent biopsy for a PSA of 8.1 ng/mL (repeat 8.5) revealing Gleason 6 cancer in two of six cores. He elected surveillance for his prostate cancer and requested TTh for his sexual dysfunction. His PSA gradually declined, and he continues on TTh 3 years later without evidence of prostate cancer progression.
Although it may seem risky to raise T concentrations in men with untreated prostate cancer, it must be recognized that we already treat a great many men with untreated prostate cancer, since one in seven hypogonadal men with normal PSA has biopsy-detectable prostate cancer.8,9 Yet there is no evidence to suggest these men are at any greater risk of developing prostate cancer than if they remained untreated. In fact, higher T may even turn out one day to be beneficial, since laboratory studies have shown that T promotes a less aggressive, better-differentiated phenotype in some prostate cancer cell lines.17
In fact, it is possible that we have been chasing the wrong suspect when it comes to hormonal risk factors for prostate cancer. Although multiple studies have failed to provide any solid data linking high T to worrisome prostate cancer features or outcomes, a number of studies (but not all) have reported associations between low T and aggressive features of prostate cancer, including high Gleason grade, advanced stage at presentation, biochemical recurrence after radical prostatectomy, and survival.22 Perhaps we should be more concerned with low T than high T when it comes to prostate cancer. After all, men tend to get prostate cancer when they are old and their T concentrations are low; they never get prostate cancer during their late teens and twenties, representing their peak T years.
Summary: Putting it all together
There are many beneficial effects of TTh in T-deficient men, including improvements in sexual function, libido, vitality, and mood. This is no less true in the T-deficient man with a history of prostate cancer. As more and more men are diagnosed with prostate cancer, the dilemma becomes more acute. Is it reasonable to withhold a treatment known to have beneficial effects when the cancer risk is theoretical, unproven, and based on observations in previously castrated men? A moderately large placebo-controlled study sponsored by the National Institute on Aging has been initiated to examine several aspects of TTh, but prostate cancer outcomes are not a primary endpoint due to the relatively short time of treatment (1 year). In the meantime, clinicians must make their own best judgment as to the safety of TTh based on available information.
In my opinion, it is reasonable to offer TTh to men with prostate cancer who are symptomatic from T deficiency and have a PSA value indicative of cure or of favorable prognosis after definitive cancer treatment. However, it is critical to inform men of the limited safety data available at the present time, and that there can thus be no guarantee regarding safety. It must also be recognized that some men with prostate cancer will experience disease recurrence or progression even without TTh; if a negative outcome occurs during T treatment, one therefore cannot assume the cause was TTh. Special caution should be exercised in men who are severely T deficient (<200 ng/dL), since these men still may have ample remaining potential for androgenic stimulation of existing prostate cancer cells, especially those who have undergone androgen deprivation.
Dr. Morgentaler is Director of Men's Health Boston, Brookline, MA, and Associate Clinical Professor of Urology, Harvard Medical School, Boston. Dr. Morgentaler discloses that he has served as a paid consultant for Slate Pharmaceuticals; has provided promotional services for Solvay, Watson, and Auxilium; and has conducted contracted research for GlaxoSmithKline.
1. Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in adult men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2006; 91:1995-2010.
2. Morgentaler A. Testosterone and Prostate Cancer: An Historical Perspective On A Modern Myth. Eur Urol 2006; 50:935-9.
3. Kaufman JM, Graydon RJ. Androgen replacement after curative radical prostatectomy for prostate cancer in hypogonadal men. J Urol 2004; 172:920-2.
4. Agarwal PK, Oefelein MG. Testosterone replacement therapy after primary treatment for prostate cancer. J Urol2005; 173:533-6.
5. Khera M, Grober ED, Najari B, et al. Testosterone replacement therapy following radical prostatectomy. J Sex Med2009; 6:1165-70.
6. Sarosdy MF. Testosterone replacement for hypogonadism after treatment of early prostate cancer with brachytherapy. Cancer 2007; 109:536-41.
7. Morales A, Black AM, Emerson LE. Testosterone administration to men with testosterone deficiency syndrome after external beam radiotherapy for localized prostate cancer: preliminary observations. BJU Int 2009; 103:62-4.
8. Morgentaler A, Bruning CO, III, DeWolf WC. Incidence of occult prostate cancer among men with low total or free serum testosterone. JAMA 1996; 276:1904-6.
9. Morgentaler A, Rhoden EL. Prevalence of prostate cancer among hypogonadal men with prostate-specific antigen of 4.0 ng/mL or less. Urology 2006; 68:1263-7.
10. Rhoden EL, Morgentaler A. Risks of testosterone-replacement therapy and recommendations for monitoring. N Engl J Med 2004; 350:482-92.
11. Rhoden EL, Morgentaler A. Testosterone replacement therapy in hypogonadal men at high risk for prostate cancer: results of 1 year of treatment in men with prostatic intraepithelial neoplasia. J Urol 2003; 170:2348-51.
12. Monath JR, McCullough DL, Hart LJ, et al. Physiologic variations of serum testosterone within the normal range do not affect serum prostate-specific antigen. Urology 1995; 46:58-61.
13. Cooper CS, Perry PJ, Sparks AE, et al. Effect of exogenous testosterone on prostate volume, serum and semen prostate specific antigen levels in healthy young men. J Urol. 1998; 159:441-3.
14. Huggins C, Hodges CV. Studies on prostatic cancer. I. The effect of castration, of estrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate. Cancer Res 1941; 1:293-7.
15. Prout GR, Brewer WR. Response of men with advanced prostatic carcinoma to exogenous administration of testosterone. Cancer 1967; 20:1871-8.
16. Fowler JE, Whitmore WF, Jr. The response of metastatic adenocarcinoma of the prostate to exogenous testosterone. J Urol 1981; 126:372-5.
17. Morgentaler A, Traish AM. Shifting the paradigm of testosterone and prostate cancer: the Saturation Model and the limits of androgen stimulation of prostate cancer. Eur Urol 2009; 55:310-21.
18. Morgentaler A. Testosterone replacement therapy and prostate cancer. Urol Clin N Am 2007; 34:555-63.
19. Traish AM, Williams DF, Hoffman ND, et al. Validation of the exchange assay for the measurement of androgen receptors in human and dog prostates. Prog Clin Biol Res 1988; 262:145-60.
20. Marks LS, Andriole GL, Fitzpatrick JM, et al. The interpretation of serum prostate specific antigen in men receiving 5alpha-reductase inhibitors: a review and clinical recommendations. J Urol 2006; 176:868-74.
21. Morgentaler A. Two years of testosterone therapy associated with decline in serum prostate-specific antigen in a man with untreated prostate cancer. J Sex Med 2009; 6:574-7.
22. Morgentaler A. Testosterone deficiency and prostate cancer: emerging recognition of an important and troubling relationship. Eur Urol 2007; 52:623-5.
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