One Website Claims 90% Cure Rate For Cancer

I continue to search the medical literature for interesting or important articles.

One website says, "...90% of prostate cancers can be cured...." - http://drcatalona.com/quest/quest_spring2002_2.htm

I think such statements are very misleading. They are misleading because approximately 80% of prostate cancer is slow growing and doesn't need to be cured (please check the latest statistics). Statistics generally show that the majority of men will die of something else before their slow growing prostate cancer gets big enough to kill them.

In a now famous quote, urologist Willet Whitmore described the situation perfectly, "Is cure possible for men in whom it is necessary? And is cure necessary for men in whom it is possible?"

Think about what Dr. Whitmore has said. His observation is the key to understanding all of the prostate cancer literature.

And understanding that will help you when it comes to researching whether you might have slow-growing prostate cancer or fast-growing, lethal, prostate cancer.

Image via Wikipedia

Two randomized controlled studies have shown that the radical prostatectomy does not extend life for men with prostate cancer:

1) Iversen P, Madsen PO, and Corle DK: Radical prostatectomy versus expectant treatment for early carcinoma of the prostate. Twenty-three year follow-up of a prospective randomized trial. Scandinavian Journal of Urology and Nephrology, supplement 1995, Jan 1;172:65-72.

2) Holmberg L, Bill-Axelson A, Helgesen F, Salo JO, Folmerz P, Haggman M, Andersson SO, Spangberg A, Busch C, Nordling S, Palmgren J, Adami HO, Johansson JE, Norlen BJ; Scandinavian Prostatic Cancer Group Study Number 4. A randomized trial comparing radical prostatectomy with watchful waiting in early prostate cancer. New England Journal of Medicine. 2002:Sep 12;347(11):781-789.

3) A third randomized controlled study, or a longer follow-up of the second study, only showed a 5.3% increase in survival for men who underwent the radical prostatectomy for prostate cancer. We have to do better than this!

Here is the abstract of the last paper describing some mortality benefits as well.

Radical prostatectomy versus watchful waiting in early prostate cancer.
Bill-Axelson A, Holmberg L, Ruutu M, Häggman M, Andersson SO, Bratell S, Spångberg A, Busch C, Nordling S, Garmo H, Palmgren J, Adami HO, Norlén BJ, Johansson JE; Scandinavian Prostate Cancer Group Study No. 4. N Engl J Med. 2005 May 12;352(19):1977-84.

Department of Urology, University Hospital, Uppsala, Sweden. anna.bill.axelson@akademiska.se

BACKGROUND: In 2002, we reported the initial results of a trial comparing radical prostatectomy with watchful waiting in the management of early prostate cancer. After three more years of follow-up, we report estimated 10-year results. METHODS: From October 1989 through February 1999, 695 men with early prostate cancer (mean age, 64.7 years) were randomly assigned to radical prostatectomy (347 men) or watchful waiting (348 men). The follow-up was complete through 2003, with blinded evaluation of the causes of death. The primary end point was death due to prostate cancer; the secondary end points were death from any cause, metastasis, and local progression. RESULTS: During a median of 8.2 years of follow-up, 83 men in the surgery group and 106 men in the watchful-waiting group died (P=0.04). In 30 of the 347 men assigned to surgery (8.6 percent) and 50 of the 348 men assigned to watchful waiting (14.4 percent), death was due to prostate cancer. The difference in the cumulative incidence of death due to prostate cancer increased from 2.0 percentage points after 5 years to 5.3 percentage points after 10 years, for a relative risk of 0.56 (95 percent confidence interval, 0.36 to 0.88; P=0.01 by Gray's test). For distant metastasis, the corresponding increase was from 1.7 to 10.2 percentage points, for a relative risk in the surgery group of 0.60 (95 percent confidence interval, 0.42 to 0.86; P=0.004 by Gray's test), and for local progression, the increase was from 19.1 to 25.1 percentage points, for a relative risk of 0.33 (95 percent confidence interval, 0.25 to 0.44; P<0.001 by Gray's test). CONCLUSIONS: Radical prostatectomy reduces disease-specific mortality, overall mortality, and the risks of metastasis and local progression. The absolute reduction in the risk of death after 10 years is small, but the reductions in the risks of metastasis and local tumor progression are substantial. Copyright 2005 Massachusetts Medical Society.

The last statement in this study is somewhat controversial, as are others, and this study generated many letters-to-the-editor.

a lesson in how to study the medical literature

This is a lesson in how to study the medical literature.

When studies were done on the radical prostatectomy and the transurethral resection of the prostate, it was found that the rates at which they are done vary greatly from region to region. This is the classic finding for operations that don't really work.

It is also very striking about how different the rates of medical procedures are around the world.

Image via Wikipedia

Surviving Prostate Cancer Without Surgery

Here is the information about my book, Surviving Prostate Cancer Without Surgery, from Amazon.com, which is properly formatted into paragraphs here. I hope to keep updating this book for the next twenty years or more. The current version at Amazon.com has been updated, although I did not feel that I made enough changes to warrant calling it a new edition.

Product Description
The niche bestseller "Surviving Prostate Cancer Without Surgery" begins with the shooting of a urologist and includes a World War II Battle. The book exposes the big lie about radical prostate surgery, is filled with cartoons and simple diagrams, and is written for the average layperson in easy-to-understand style.

"Surviving Prostate Cancer Without Surgery" quotes Dr. Gary Onik, M.D., Cryosurgeon and Director of Surgical Imaging at Celebration Health Hospital, Celebration, Florida, who says: "I expect that within five years we will see the death of the radical prostatectomy as a treatment for prostate cancer."

The author, Bradley Hennenfent, M.D., has seen five uncles suffer from prostate cancer and his book includes many uplifting stories about less harmful treatments than surgery.

Dr. Hennenfent also explains the problem of lies, damn lies, and prostate cancer statistics.

The adverse effects of surgery: impotence, sexual dysfunction, incontinence, and urethral strictures are explained in realistic fashion.

"Surviving Prostate Cancer Without Surgery" quotes oncologist Dr. Robert Leibowitz of Compassionate Oncology Medical Group, who says: "If radical prostatectomies worked, the data would be there. The reason the data is not there is because radical prostatectomies don't work."

Dr. Leibowitz adds: "No prospective randomized trial has ever found radical prostatectomy to be both necessary and effective."

Urologist W. Reid Pitts, Jr., M.D., FACS, wrote an outstanding letter-to-the-editor of the "Journal of Urology" lambasting the radical prostatectomy. When interviewed for "Surviving Prostate Cancer Without Surgery," Dr. Pitts said: "Although I did the first ever nerve sparing radical prostatectomy at New York-Cornell Hospital, I've abandoned the radical prostatectomy for my prostate cancer patients. There is always a better treatment option."

Dr. Hennenfent co-founded the Prostatitis Foundation (www.prostatitis.org). He also founded the Epididymitis Foundation (www.epididymitisfoundation.org), and the Acoustic Neuroma Foundation (www.acousticneuromafoundation.org).

He previously published "The Prostatitis Syndromes."

"Surviving Prostate Cancer Without Surgery" quotes urologist Ronald Wheeler, M.D. of the Prostatitis and Prostate Cancer Center, who says: "In my opinion, prostatitis resolution holds the key to the future of prostate cancer resolution."

“Two randomized, controlled studies suggest that 95% or more of all prostate cancer surgery done to date, has failed to extend the life of the patient,” says Dr. Bradley Hennenfent M.D., the book’s author.

“Surgery should no longer be presented or advertised as a cure-all for prostate cancer,” says Dr. Hennenfent. “My book is all about the options to harmful surgery."

“Surviving Prostate Cancer Without Surgery,” details the harm done by surgery, while explaining the pros and cons of watchful waiting, active noninvasive therapy, radiation seed implants, three-dimensional radiation therapy, herbal medications, cryosurgery, and hormone blockade. The website for the book is: www.SurvivingProstateCancerWithoutSurgery.org.

Prostate Cancer in Black Men of African Descent

I continue to search the medical literature for interesting or important articles about prostate cancer. Here is an abstract. I have made some text bold for emphasis.

Prostate cancer disparities in Black men of African descent: a comparative literature review of prostate cancer burden among Black men in the United States, Caribbean, United Kingdom, and West Africa
Infect Agent Cancer. 2009; 4(Suppl 1): S2.
Published online 2009 February 10. doi: 10.1186/1750-9378-4-S1-S2.
Folakemi T Odedina,corresponding author1 Titilola O Akinremi,#2 Frank Chinegwundoh,#3 Robin Roberts,#4 Daohai Yu,#1 R Renee Reams,#5 Matthew L Freedman,#6 Brian Rivers,#1 B Lee Green,#1 and Nagi Kumar1

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract
Background
African American men have the highest prostate cancer morbidity and mortality rates than any other racial or ethnic group in the US. Although the overall incidence of and mortality from prostate cancer has been declining in White men since 1991, the decline in African American men lags behind White men. Of particular concern is the growing literature on the disproportionate burden of prostate cancer among other Black men of West African ancestry in the Caribbean Islands, United Kingdom and West Africa. This higher incidence of prostate cancer observed in populations of African descent may be attributed to the fact that these populations share ancestral genetic factors. To better understand the burden of prostate cancer among men of West African Ancestry, we conducted a review of the literature on prostate cancer incidence, prevalence, and mortality in the countries connected by the Transatlantic Slave Trade.

Results
Several published studies indicate high prostate cancer burden in Nigeria and Ghana. There was no published literature for the countries Benin, Gambia and Senegal that met our review criteria. Prostate cancer morbidity and/or mortality data from the Caribbean Islands and the United Kingdom also provided comparable or worse prostate cancer burden to that of US Blacks.

Conclusion
The growing literature on the disproportionate burden of prostate cancer among other Black men of West African ancestry follows the path of the Transatlantic Slave Trade. To better understand and address the global prostate cancer disparities seen in Black men of West African ancestry, future studies should explore the genetic and environmental risk factors for prostate cancer among this group.

Introduction
In the United States (US), an estimated 30,870 cases of prostate cancer are expected to occur among African American men in 2007, accounting for 37% of all cancers diagnosed in African American men [1]. Between 2000 and 2003, the average annual prostate cancer rate was 60% higher in African American men compared to White men [1]. In addition, African American men have the highest mortality rate compared to any other racial or ethnic group in the US, and 2.4 times higher than in White men. Although prostate cancer incidence and mortality rates have been declining in both African American and White men since 1991, possibly due to improved diagnostic techniques, better screening and improved surgical and radiologic treatments, the rates remain comparably higher among African American men. Why does this disparity continue to exist among African American men in spite of the significant research to eliminate this disparity?
The population-based studies on prostate cancer disparity have traditionally studied African American men only or compared African American men to other racial groups within the US. Although these studies have provided vital insights necessary to understanding the primary differences among the ethnic groups in the US, we are left with more questions than answers. With the problem of prostate cancer disparity persisting, it is crucial that we begin to use new paradigms to examine the problem of prostate cancer disparity from new perspectives. The prospect for a new paradigm/new perspectives emerge with the growing literature on the disproportionate burden of prostate cancer among other Black men (in other parts of the world, other than the US) who are related to African American men through the Transatlantic Slave Trade (TAS) [2-7], especially Black men of West African ancestry. Based on the World Health Organization (WHO)'s worldwide cancer data, West African men have much lower prostate cancer incidence and mortality compared to African American men. For example, compared to Nigerian men, African-American men are >10 times likely to develop prostate cancer and 3.5 times likely to die from the disease [8]. On the other hand, Silverberg and Lubera [9] reported high rates of prostate cancer mortality in Martinique, Trinidad & Tobago; while Glover et al. [10]reported high rates of prostate cancer incidence in the predominantly Afro-Caribbean population of Jamaica. Thus the variability in risk and mortality across these populations of West African descent suggests a potential and important influence of environmental/lifestyle factors acting on prostate cancer risk in these already susceptible populations. Can this evolving international data hold the key to our better understanding of the etiology of unequal burden of this disease in African American men?

The Transatlantic Slave Trade (TAS) Relations
Based on the TAS, about 15 million people were transported as slaves from Africa, not counting those who died en-route to the Americas, Caribbean and Europe [7]. The TAS comprised the following three journeys: (1) Outward passage from Europe to Africa carrying manufactured goods; (2) Middle passage from Africa to the Americas/Caribbean carrying African captives and other commodities; and (3) Homeward passage carrying sugar, tobacco, rum, rice, cotton and other goods back to Europe. These slave routes included diverse countries. The European countries involved in the TAS were Portugal, France, Netherlands, Spain, Denmark, Norway and United Kingdom. Slaves were primarily imported from the African countries – Benin, Nigeria, Ghana, Gambia, Senegal, Mozambique, and Angola. The middle passage took the slaves from Africa to the American and Caribbean countries – Barbados, Cuba, Haiti, Dominican Republic, Netherlands Antilles, Trinidad and Tobago, Jamaica, Brazil, and the US. Most of the slaves ended up in South America or the Caribbean with about 500,000 transported to North America. Unfortunately, most of the slaves in the Caribbean, Central America and South America died while the slave population in North America had higher life expectancy [7].

Objective
In this manuscript, we explored the burden of prostate cancer among the TAS population targeting Black men of West African Ancestry to answer the question:Does the prostate cancer disparities seen in Black men around the world follow the path of the TAS?

Publication supported in part by the University Of Pittsburgh Graduate School Of Public Health, the University of Pittsburgh Cancer Institute, and by the National Institute of Health, grant number R13CA130596A.
http://www.biomedcentral.com/content/pdf/1750-9378-4-S1-info.pdf
Conference
Second Annual International African-Caribbean Cancer Consortium Conference
12–13 May 2008
Miami, FL, USA

PMCID: PMC2638461
Copyright © 2009 Odedina et al; licensee BioMed Central Ltd.

1H. Lee Moffitt Cancer Center, Tampa, Florida, USA
2Federal Medical Center (FMC), Abeokuta, Nigeria
3Barts and The London NHS Trust and Newham University NHS Trust, London UK
4Princess Margaret Hospital in Nassau, The Bahamas
5Florida A&M University, Tallahassee, Florida, USA
6Dana-Farber Cancer Institute, Boston, Massachusetts, USA
corresponding authorCorresponding author.
#Contributed equally.
Folakemi T Odedina: Folakemi.odedina@moffitt.org ; Titilola O Akinremi: bakinremi2@aol.com; Frank Chinegwundoh: Frank.Chinegwundoh@nhs.net; Robin Roberts: robinnassau50@yahoo.com; Daohai Yu: Daohai.Yu@moffitt.org; R Renee Reams: Renee.reams@famu.edu; Matthew L Freedman: freedman@broad.mit.edu; Brian Rivers: brian.rivers@moffitt.org; B Lee Green: lee.green@moffitt.org; Nagi Kumar: Nagi.kumar@moffitt.org

Supplement
Second Annual International African-Caribbean Cancer Consortium Conference
Camille Ragin and Emanuela Taioli

Image via Wikipedia

Vitamin D and Prostate Cancer

I search the medical literature for pertinent articles as often as I can. Like this one:

A Prospective Study of Plasma Vitamin D Metabolites, Vitamin D Receptor Polymorphisms, and Prostate Cancer
PLoS Med. 2007 March; 4(3): e103.

Abstract
Background
Vitamin D insufficiency is a common public health problem nationwide. Circulating 25-hydroxyvitamin D3 (25[OH]D), the most commonly used index of vitamin D status, is converted to the active hormone 1,25 dihydroxyvitamin D3 (1,25[OH]2D), which, operating through the vitamin D receptor (VDR), inhibits in vitro cell proliferation, induces differentiation and apoptosis, and may protect against prostate cancer. Despite intriguing results from laboratory studies, previous epidemiological studies showed inconsistent associations of circulating levels of 25(OH)D, 1,25(OH)2D, and several VDR polymorphisms with prostate cancer risk. Few studies have explored the joint association of circulating vitamin D levels with VDR polymorphisms.

Methods and Findings
During 18 y of follow-up of 14,916 men initially free of diagnosed cancer, we identified 1,066 men with incident prostate cancer (including 496 with aggressive disease, defined as stage C or D, Gleason 7–10, metastatic, and fatal prostate cancer) and 1,618 cancer-free, age- and smoking-matched control participants in the Physicians' Health Study. We examined the associations of prediagnostic plasma levels of 25(OH)D and 1,25(OH)2D, individually and jointly, with total and aggressive disease, and explored whether relations between vitamin D metabolites and prostate cancer were modified by the functional VDR FokI polymorphism, using conditional logistic regression. Among these US physicians, the median plasma 25(OH)D levels were 25 ng/ml in the blood samples collected during the winter or spring and 32 ng/ml in samples collected during the summer or fall. Nearly 13% (summer/fall) to 36% (winter/spring) of the control participants were deficient in 25(OH)D (<20 style="font-weight: bold;">Men whose levels for both 25(OH)D and 1,25(OH)2D were below (versus above) the median had a significantly increased risk of aggressive prostate cancer (odds ratio [OR] = 2.1, 95% confidence interval [CI] 1.2–3.4), although the interaction between the two vitamin D metabolites was not statistically significant (pinteraction = 0.23). We observed a significant interaction between circulating 25(OH)D levels and the VDR FokI genotype (pinteraction < 0.05). Compared with those with plasma 25(OH)D levels above the median and with the FokI FF or Ff genotype, men who had low 25(OH)D levels and the less functional FokI ff genotype had increased risks of total (OR = 1.9, 95% CI 1.1–3.3) and aggressive prostate cancer (OR = 2.5, 95% CI 1.1–5.8). Among men with plasma 25(OH)D levels above the median, the ff genotype was no longer associated with risk. Conversely, among men with the ff genotype, high plasma 25(OH)D level (above versus below the median) was related to significant 60%∼70% lower risks of total and aggressive prostate cancer.

Conclusions
Our data suggest that a large proportion of the US men had suboptimal vitamin D status (especially during the winter/spring season), and both 25(OH)D and 1,25(OH)2D may play an important role in preventing prostate cancer progression. Moreover, vitamin D status, measured by 25(OH)D in plasma, interacts with the VDR FokI polymorphism and modifies prostate cancer risk. Men with the less functional FokI ff genotype (14% in the European-descent population of this cohort) are more susceptible to this cancer in the presence of low 25(OH)D status.

Copyright : © 2007 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Published online 2007 March 20. doi: 10.1371/journal.pmed.0040103. PMCID: PMC1831738
Haojie Li,1* Meir J Stampfer,1,2,3,4,5 J. Bruce W Hollis,6 Lorelei A Mucci,1 J. Michael Gaziano,4,5 David Hunter,1,2,3 Edward L Giovannucci,1,2,3 and Jing Ma1

1 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
2 Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America
3 Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, United States of America
4 Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
5 Massachusetts Veterans Epidemiology Research and Information Center, Veterans Administration Boston Healthcare System, Massachusetts, United States of America
6 Department of Pediatrics, Medical University of South Carolina, Charleston, South Carolina, United States of America
Eduardo L Franco, Academic Editor
McGill University, Canada

* To whom correspondence should be addressed. E-mail: haojie.li@channing.havard.edu
Received September 12, 2006; Accepted January 24, 2007.
-----------------------------------------------------------
This is another important study that gets at the risk of being deficient in vitamin D perhaps causing prostate cancer. It does not tell us how to fix that deficiency.

Related articles by Zemanta

• The ABCs of Vitamin D: What Are its Real Benefits? (blogs.wsj.com)
• Vitamin D and Fish Oil - Time to Put Up or Shut Up (singularityhub.com)