Your results provide clear evidence for the high level of overdiagnosis with consequent overtreatment due to mammographic screening: Thank you:
Italo Nenci, Professor of Pathology
read full comment
Are MDA-MB435 cells mammary carcinoma cells or melanoma cells? (Ulrich Pfeffer, 08 November 2011)
Holliday and Speirs discuss in their illuminating review on breast cancer cell lines as models for breast cancer research the cell line MDA-MB435, which has been considered as a breast cancer cell line until reports on their potential origin from a human melanoma (see ref. in Holliday and Speirs). More recent evidence shows that i) MDA-MB435 are indeed identical to M14 melanoma cells, ii) M14 were derived from a male melanoma patient but carry two X-chromosomes whereas MDA-MB435 were derived from a female patient (Chambers, Cancer Res. 2009, 5292; Hohestelle and Schutte, Cancer Res. 2009, 7893) and iii) 18% of human breast cancers express melan-A and other melanoma markers (Bachmeier et al. Int J Oncol. 2008, 1011). MDA-MB435 cells are therefore most likely breast cancer cells.
read full comment
Vitamin D deficiency may contribute to cause of death for those diagnosed with breast cancer (William B. Grant, 01 July 2011)
The paper by Patnaik et al. [1] is quite interesting. The conclusion, “Comorbid conditions contribute importantly to both total mortality and breast cancer-specific mortality among breast cancer survivors. Attention to reducing the risk of cardiovascular disease should be a priority for the long-term care of women following the diagnosis and treatment of breast cancer.” is correct, although other cancers, COPD, and diabetes should also be added to the list of diseases to be concerned about.
Missing from the paper, however, is any mention of how to go about reducing the risk of cardiovascular disease (CVD) or any other disease. A rather simple and straight forward approach is available: increase serum 25-hydroxyvitamin D [25(OH)D] levels. There is excellent evidence...
read full comment
Comment on: Patnaik et al. Breast Cancer Research, 13:R64
The follow-up time was too long to find a correlation (William B. Grant, 01 July 2011)
Breast cancer is characterized by rapidly growing tumors. For example, diagnoses are more common in spring and fall due to solar UVB and vitamin D reducing risk in summer and melatonin in winter (1). Thus, it should not be expected that a single serum 25(OH)D level measurement would have good prognostic value several years later. Indeed, a review of case-control and nested case-control studies of breast cancer incidence with respect to serum 25(OH)D level found that follow-up periods less than three years resulted in significant inverse correlations, while studies with longer follow-up periods did not (2).
In a nested case-control study of breast cancer incidence with respect to oral vitamin D intake, the relative risk of cancer decreased with increasing follow-up time: 0.66...
read full comment
It would very important to know how many of the 454 cases actually had ovarian cancer and how many had breast cancer. Now there is only short description of family histories.
read full comment
Comment on: Akbari et al. Breast Cancer Research, 12:404
Acknowledgement (Elizabeth O'Flynn, 20 April 2011)
Parametric images produced using Magnetic Resonance Imaging Workbench(MRIW) software (Institute of Cancer Research, London, United Kingdom)(1) by Dr Maria Schmidt and Mr Marco Borri.
1. d'Arcy J, Collins D, Padhani A, Walker-Samuel S, Suckling J, LeachM: informatics in radiology (infoRAD): magnetic resonance imaging workbench: analysis and visualisation of dynamic contrast-enhanced MR imaging data. Radiographics 2006;26(2):621-32. read full comment
Comment on: O'Flynn et al. Breast Cancer Research, 13:204
In defence of peer review (Dorothy Bishop, 04 January 2011)
Richard Smith seems not only to underestimate the benefits of peer review, but also to misrepresent its function, at least in the context of journal publishing. Thus he states that the process determines “which papers will be published…” etc. Unfortunately, all too often editors relinquish their responsibilities and treat the peer review process as a vote, but this is a distortion of the real function of peer review, which should be to offer advice to the editor and the author.
Of course, Dr Smith is right to point out the arbitrary and unreliable features of peer review, and the lack of hard evidence for its benefits. But most of those who’ve tried to evaluate the system seem to focus just on ‘scores’ given to papers. There should be much...
read full comment
It is wrong to encourage women to attend breast cancer screening (Paul Pharoah, 09 November 2010)
The the conclusion made by McCann and colleagues that "women should be encouraged to continue with screening" is not supported by their data. Women should be encouraged to decide for themselves whether the marginal reduction in breast cancer mortality associated with regular mammography is worth the harms. A false positives is an associated harm and if a woman decides that that harm, based on her own experience, outweighs any benefit, she should be encouraged to make the decision not to have screening that is right for her.
The concept that a successful screening programme depends on a high uptake rate needs to be revisited. The benefits and harms of mammography are individual based and uptake rates are of no consequence to a woman who decides to undergo mammography or not....
read full comment
Comment on: McCann et al. Breast Cancer Research, 4:R11
PREDICT prognostication tool now available online (David Greenberg, 08 September 2010)
The new web-based prognostication and treatment benefit tool for early breast cancer in the UK referred to in the conclusions of this paper is now freely accessible online at http://www.predict.nhs.uk/ read full comment
Comment on: Wishart et al. Breast Cancer Research, 12:R1
No proven correlation (Dene Godfrey, 18 February 2010)
The review states:
"Any increase in the disproportionality of breast cancer in the upper outer quadrant would be inconsistent with an explanation relating to the greater amount of target epithelial tissue in that region but does parallel the increasing use of cosmetics in the underarm area [2-5]."
All four references are to studies/reviews by this author and do not appear to be directly related to any market information on the increase in use of underarm products. There does not, therefore, appear to be any tangible evidence to support the author's assertion that there is specifically a parallel increase in both use of underarm products and cancer in the upper outer quadrant. Unless specific market information is quoted on any increase in underarm product volumes...
read full comment
Authors have not cited articles that are absolutely relevant to this paper (Malathy Shekhar, 19 February 2009)
I read the article, "Novel multicellular organotypic models of normal and malignant breast: tools for dissecting the role of the microenvironment in breast cancer progression" by Holliday et al with great interest. However, I was disappointed to note that while the authors included references for homotypic three-dimensional cultures, citations pertinent to their paper were omitted. Specifically, original articles describing heterotypic interactions between breast cancer cells and stromal cells (the microenvironment), and the dominant role the microenvironment plays in breast tumorigenesis were omitted. Although citing these papers would indicate that the authors of this paper are not the first to report on multicellular interactions in three-dimensional tricultures, inclusion of these...
read full comment
Bi-Modal Hazard (BMH) an epidemiological hallmark of cancer (Gershom Zajicek, 13 November 2008)
The phenomenon described by the authors is known as bi-modal hazard rate (BMH).In an detailed analysis based of SEER data I have shown that hazard rate in breast cancer proceeds through three phases. Following diagnosis and treatment hazard rate rises (AB). By the third year it reaches its maximum whereupon it declines to a minimum (BC). from there and on it gradually rises to a second maximum whereupon the patient dies (CD). This pattern appears in many cancers and is unique to cancer and does not appear in other chronic diseases. It is an epidemiological hallmark of cancer. It is so typical of cancer that it distinguishes cancer from other chronic diseases.http://www.what-is-cancer.com/papers/newmedicine/epidemiologyFrame.htmData source: Surveillance, Epidemiology, and End Results (SEER)...
read full comment
Additional data for this article (Claire Hansford, 13 November 2008)
Due to a technical fault the additional file links have become unavailable for this article.They are now available from:Additional file 1: http://www.biomedcentral.com/content/supplementary/bcr1836-S1.xlsAdditional file 2: http://www.biomedcentral.com/content/supplementary/bcr1836-S2.xlsAdditional file 3: http://www.biomedcentral.com/content/supplementary/bcr1836-S3.xls
read full comment
Comment on: Esteva et al. Breast Cancer Research, 9:R87
Relationship of Ox-E/ER signature expression with clinical parameters and outcome in age-stratified cohorts (Christina Yau, 22 September 2008)
In their recent editorial (Breast Cancer Res 2008, 10:109), Neven et al. highlight our recent finding (Breast Cancer Res 2008, 10:R61) that an experimentally derived oxidative stress gene expression signature, ‘Ox-E/ER’, identifies an aggressive subset of primary estrogen receptor (ER)-positive breast cancers associated with poor clinical outcome, and appears to outperform loss of progesterone receptor (PR) expression as a prognostic variable. Given their earlier studies suggesting an age-related association between PR status and HER2 overexpression in ER-positive breast cancers that could confound our oxidative stress analysis, they suggested that we further explore the prognostic relationship between our Ox-E/ER signature index and breast cancer PR status, stratifying for age-...
read full comment
Comment on: Neven et al. Breast Cancer Research, 10:109
Loss of TYMS in sporadic breast cancer (Barry Barclay, 14 September 2007)
It is becoming increasingly clear that both loss of heterozygosity at 18p11.3 and amplification of TYMS at its normal locus or on extra-chromosomal elements serve not only as useful diagnostic and prognostic indicators in breast cancer as suggested here but may at least in some cases be causally related to breast tumor initiation and disease progression. Loss of TYMS gives rise to gross chromosome rearrangements including translocations, loss of chromosome arms, interstital deletions and amplifications. Thus low TYMS activity could be considered a molecular "driver" of subsequent cytogenetic events and an important early event in breast carcinogenesis that channels cells into histopathological subtypes. On the other hand amplification of TYMS (including a mutant polymorphic allele) could...
read full comment
Characterization of our 1998 report as indirect evidence for existence of mammary epithelial stem cells (Gilbert Smith, 09 March 2007)
In this commentary, Max Wicha incorrectly characterizes our work published in 1998[2]in Development as providing INDIRECT evidence forthe existence of mammary epithelial stem cells. We feel this is an inappropriate portrayal of our seminal discovery as it diminishes its realimpact upon the mammary stem cell field while elevating the recent Nature publications from Shackleton et al and Stingl et al as the ONLYdemonstration for the fact that a single mammary stem cell can give rise to a complete functional mammary gland. This is misleading and gratuitous. In addition, he ignores the demonstration both in our original paper and subsequently in Mech. Aging and Develop., Boulanger and Smith 2002, that serial transplantation of our retrovirally-tagged mammary outgrowths gaverise...
read full comment
Clarification of the Malmö study (Sophia Zackrisson, 15 February 2007)
Overdiagnosis is a potentially harmful effect of screening. Every effort to assess the magnitude of the problem is essential. Therefore, the paper by Paci et al is welcome.(1) As the validity of the Malmö study of overdiagnosis (2) was questioned we would like to make a few comments. Ideally, the rate of overdiagnosis at screening should be estimated by direct observation in a randomised trial where the control group was not invited at the end of the trial and during a long follow-up. This was the case in the Malmö Mammographic Screening Trial (MMST). Most other estimates were based on various sorts of modelling (3) or from non-randomised settings. (1;4-7) In the MMST the control group of the age cohort 55-69 years at entry was never invited. The follow-up comprised 15 years after...
read full comment
Comment on: Paci et al. Breast Cancer Research, 8:R68
Release of tumor cells during neoadjuvant therapy (Katharina Pachmann, 01 November 2006)
The present report by Dr. Fehm confirms our previous results about dissemination of tumor cells during the course of neoadjuvant therapy presented already at the 2004 San Antonio Breast cancer symposium (Pachmann K., Camara O., Pachmann UA. Influence of primary tumor chemotherapy in breast cancer on circulating tumor cells. Indications for massive cell release into circulations concurrent with tumor size reduction. (2004) Breast Cancer Research and Treatment 88: S224), which was commented in several publications: "An article in the May 2005 issue of Oncology News International (Vol. 14, No. 5) reports that neoadjuvant chemotherapy* may cause the release of cancer cells into the blood. Katharina Pachmann, MD, of Friedrich-Schiller University in Germany said that "ironically, paclitaxel...
read full comment
Comment on: Fehm et al. Breast Cancer Research, 8:R60
suggesting a specific role for elastography (Asem Al-Rifai, 23 August 2006)
my comment concers technical details about how to improve the imaging data sensitivity of detecting the 2 % of malignancies in the group 3 of the ACR classification.(BI-RADS)As Mr. Stavros indicated , the aim of relatively short term follow up is to detect teh rapidly growing cancer which in most cases is grade 3 infiltrating ductal carcinoma .So my comment is the following : in order to try to recognize these cases of early malignancy ( which will appear after six months to show atypical characters on ultrasound ) , wouldn't it be possible to use elastograpy to try to find hard areas into the concerned nodule ( in the early phase of infiltrating ductal carcinoma a reaction of the surrounding tissue yields a hard area around it ) . the aim is to have better criteria allowing for more...
read full comment
Importance of Familial and inherited breast cancers in preventive paradigm. (parvin mehdipour, 13 June 2006)
Many thanks for the valuable contribution to the breast cancer word.You have written the following description in the Introduction:" ..other 90–95% is assumed to be 'sporadic', with no apparent family history. A large proportion of familial breast cancer (<40%) can be attributed to mutations in the high-risk genes BRCA1 and BRCA2 [1]".My comment: the sporadic figure of 90%-95% doesn't indicate that the proband has no family history.There are many families in my database having 3-8 and 4-12 relatives affected with Breast cancer and other malignancies, respectively, who had no mutation in BRCA1&2.So, Familial BC is not representive of inherited BC. Many of our early onset probands with no family history could be positive ( i.e.,inherited, or new mutation)or negative for BRCA-...
read full comment
Comment on: Lose et al. Breast Cancer Research, 8:R26
Alcohol verses mitigating folic acid intake in mineral density verse BC risk profiles, confounding geological environment. (Bernhard Hochwimmer, 25 May 2006)
It is possible alcohol (in moderation) adds mineral density through stimulating growth hormone, yet alcohol by itself increases breast cancer (BC) risk. Then mitigating circumstances would be folic acid against alcohol induced BC risk, while still enhancing bone mineral density. One assumes naturally breast density may not dictate BC risk, if at all. So it’s worth speculating on mineral density and BC risk directly, rather than focusing only on breast density. While this response dose not address breast and bone mineral density association directly, it highlights potential utility of a multidisciplinary approach in BC risk that may under some circumstances include bone mineral density and interplay of non anthropogenic factors, including the geological environment. Moderate exercise...
read full comment
BLV as an agent involved in Breast Cancer (Elisabeth Rieping, 23 March 2006)
There are some additional features of BLV which qualify it as a causal agent for breast cancer: It induces monocytes to form giant cells.The osteoclasts physiologically active in bone resorption and during breast cancer metastasis develop from monocytes, too. Bone metastasis is an important feature of human, feline and canine breast cancer. All three species are frequently raised with bovine milk, although neither physians nor vets propagate it.HTLV-1 the close relative of BLV is found in acut T-cell leukemia ATL. A disease for which hypercalcemia is as typical as for breast cancer.MMTV induced tumors in mice rarely metastasize and they do not not show bone metastases.Traces of an MMTV like, not identical retrovirus are often found in human breast cancer. BLV is not identical. That would...
read full comment
Long-chain polyunsaturated fatty acids and cancer (Undurti Das, 13 June 2005)
I read with interest the study by Siddiqui et al.In a series of studies, previously I reported that long-chain polyunsaturated fatty acids (LCPUFAs) have selective tumoricidal action on a variety of tumor cells with little or no effects on normal cells both in vitro and in vivo (1-5). Our studies showed that human breast cancer cells ZR-75-1 are killed by LCPUFAs. Of all the fatty acids tested gamma-linolenic acid (GLA) was found to be the most effective compared to EPA and DHA. Subsequent studies revealed that LCPUFAs are able to enhance free radical generation and lipid roxidation process in tumor cells but not in normal cells and that this could be one of the main, if not the sole, mechanism of their tumoricidal action. It was also observed that anti-oxidants such as BHA, BHT and vitamin...
read full comment
Low risk HPV types and malignancy (Janet Buchanan, 02 February 2005)
The findings by deVilliers et al. regarding the prevalence of HPV 6 and HPV 11 in both breast tumor tissue and nipples is interesting. The finding by deVilliers et al that HPV 11 was the most prevalent type and that it was detected in 19 carcinomas and 8 nipples may be evidence that HPV 11 is a high risk type for certain types of carcinomas. HPV 11 in patients with recurrent respiratory papillomatosis (RRP) has not only been been found to be a predictor of aggressive disease, but has also been documented to be associated with pulmonary malignancy in patients with RRP. Future studies may be more revealing in the association of HPV 11 and malignancies.
read full comment
RSS
Latest comments
Overdiagnosis!!! (italo nenci, 03 January 2012)
Your results provide clear evidence for the high level of overdiagnosis with consequent overtreatment due to mammographic screening: Thank you:
Italo Nenci, Professor of Pathology read full comment
Comment on: Lehtimäki et al. Breast Cancer Research, 13:R134
Are MDA-MB435 cells mammary carcinoma cells or melanoma cells? (Ulrich Pfeffer, 08 November 2011)
Holliday and Speirs discuss in their illuminating review on breast cancer cell lines as models for breast cancer research the cell line MDA-MB435, which has been considered as a breast cancer cell line until reports on their potential origin from a human melanoma (see ref. in Holliday and Speirs). More recent evidence shows that i) MDA-MB435 are indeed identical to M14 melanoma cells, ii) M14 were derived from a male melanoma patient but carry two X-chromosomes whereas MDA-MB435 were derived from a female patient (Chambers, Cancer Res. 2009, 5292; Hohestelle and Schutte, Cancer Res. 2009, 7893) and iii) 18% of human breast cancers express melan-A and other melanoma markers (Bachmeier et al. Int J Oncol. 2008, 1011). MDA-MB435 cells are therefore most likely breast cancer cells. read full comment
Comment on: Holliday et al. Breast Cancer Research, 13:215
Vitamin D deficiency may contribute to cause of death for those diagnosed with breast cancer (William B. Grant, 01 July 2011)
The paper by Patnaik et al. [1] is quite interesting. The conclusion, “Comorbid conditions contribute importantly to both total mortality and breast cancer-specific mortality among breast cancer survivors. Attention to reducing the risk of cardiovascular disease should be a priority for the long-term care of women following the diagnosis and treatment of breast cancer.” is correct, although other cancers, COPD, and diabetes should also be added to the list of diseases to be concerned about.
Missing from the paper, however, is any mention of how to go about reducing the risk of cardiovascular disease (CVD) or any other disease. A rather simple and straight forward approach is available: increase serum 25-hydroxyvitamin D [25(OH)D] levels. There is excellent evidence... read full comment
Comment on: Patnaik et al. Breast Cancer Research, 13:R64
The follow-up time was too long to find a correlation (William B. Grant, 01 July 2011)
Breast cancer is characterized by rapidly growing tumors. For example, diagnoses are more common in spring and fall due to solar UVB and vitamin D reducing risk in summer and melatonin in winter (1). Thus, it should not be expected that a single serum 25(OH)D level measurement would have good prognostic value several years later. Indeed, a review of case-control and nested case-control studies of breast cancer incidence with respect to serum 25(OH)D level found that follow-up periods less than three years resulted in significant inverse correlations, while studies with longer follow-up periods did not (2).
In a nested case-control study of breast cancer incidence with respect to oral vitamin D intake, the relative risk of cancer decreased with increasing follow-up time: 0.66... read full comment
Comment on: Eliassen et al. Breast Cancer Research, 13:R50
Cases description (Mikko Vuorela, 19 May 2011)
It would very important to know how many of the 454 cases actually had ovarian cancer and how many had breast cancer. Now there is only short description of family histories. read full comment
Comment on: Akbari et al. Breast Cancer Research, 12:404
Acknowledgement (Elizabeth O'Flynn, 20 April 2011)
Parametric images produced using Magnetic Resonance Imaging Workbench(MRIW) software (Institute of Cancer Research, London, United Kingdom)(1) by Dr Maria Schmidt and Mr Marco Borri.
1. d'Arcy J, Collins D, Padhani A, Walker-Samuel S, Suckling J, LeachM: informatics in radiology (infoRAD): magnetic resonance imaging workbench: analysis and visualisation of dynamic contrast-enhanced MR imaging data. Radiographics 2006;26(2):621-32.
read full comment
Comment on: O'Flynn et al. Breast Cancer Research, 13:204
In defence of peer review (Dorothy Bishop, 04 January 2011)
Richard Smith seems not only to underestimate the benefits of peer review, but also to misrepresent its function, at least in the context of journal publishing. Thus he states that the process determines “which papers will be published…” etc. Unfortunately, all too often editors relinquish their responsibilities and treat the peer review process as a vote, but this is a distortion of the real function of peer review, which should be to offer advice to the editor and the author.
Of course, Dr Smith is right to point out the arbitrary and unreliable features of peer review, and the lack of hard evidence for its benefits. But most of those who’ve tried to evaluate the system seem to focus just on ‘scores’ given to papers. There should be much... read full comment
Comment on: Smith Breast Cancer Research, 12:S13
It is wrong to encourage women to attend breast cancer screening (Paul Pharoah, 09 November 2010)
The the conclusion made by McCann and colleagues that "women should be encouraged to continue with screening" is not supported by their data. Women should be encouraged to decide for themselves whether the marginal reduction in breast cancer mortality associated with regular mammography is worth the harms. A false positives is an associated harm and if a woman decides that that harm, based on her own experience, outweighs any benefit, she should be encouraged to make the decision not to have screening that is right for her.
The concept that a successful screening programme depends on a high uptake rate needs to be revisited. The benefits and harms of mammography are individual based and uptake rates are of no consequence to a woman who decides to undergo mammography or not.... read full comment
Comment on: McCann et al. Breast Cancer Research, 4:R11
PREDICT prognostication tool now available online (David Greenberg, 08 September 2010)
The new web-based prognostication and treatment benefit tool for early breast cancer in the UK referred to in the conclusions of this paper is now freely accessible online at
http://www.predict.nhs.uk/
read full comment
Comment on: Wishart et al. Breast Cancer Research, 12:R1
No proven correlation (Dene Godfrey, 18 February 2010)
The review states:
"Any increase in the disproportionality of breast cancer in the upper outer quadrant would be inconsistent with an explanation relating to the greater amount of target epithelial tissue in that region but does parallel the increasing use of cosmetics in the underarm area [2-5]."
All four references are to studies/reviews by this author and do not appear to be directly related to any market information on the increase in use of underarm products. There does not, therefore, appear to be any tangible evidence to support the author's assertion that there is specifically a parallel increase in both use of underarm products and cancer in the upper outer quadrant. Unless specific market information is quoted on any increase in underarm product volumes... read full comment
Comment on: Darbre Breast Cancer Research, 11:S5
Leptin-signaling inhibition trial (Kathleen Riley, 12 November 2009)
Are there currently any clinical trials involving leptin-signaling inhibition for Stage IV breast cancer patients? read full comment
Comment on: Rene Gonzalez et al. Breast Cancer Research, 11:R36
Authors have not cited articles that are absolutely relevant to this paper (Malathy Shekhar, 19 February 2009)
I read the article, "Novel multicellular organotypic models of normal and malignant breast: tools for dissecting the role of the microenvironment in breast cancer progression" by Holliday et al with great interest. However, I was disappointed to note that while the authors included references for homotypic
three-dimensional cultures, citations pertinent to their paper were omitted. Specifically, original articles describing heterotypic interactions between breast cancer cells and stromal cells (the microenvironment), and the dominant role the microenvironment plays in breast tumorigenesis were omitted. Although citing these papers would indicate that the authors of this paper are not the first to report on multicellular interactions in three-dimensional tricultures, inclusion of these... read full comment
Comment on: Holliday et al. Breast Cancer Research, 11:R3
Bi-Modal Hazard (BMH) an epidemiological hallmark of cancer (Gershom Zajicek, 13 November 2008)
The phenomenon described by the authors is known as bi-modal hazard rate (BMH).In an detailed analysis based of SEER data I have shown that hazard rate in breast cancer proceeds through three phases. Following diagnosis and treatment hazard rate rises (AB). By the third year it reaches its maximum whereupon it declines to a minimum (BC). from there and on it gradually rises to a second maximum whereupon the patient dies (CD). This pattern appears in many cancers and is unique to cancer and does not appear in other chronic diseases. It is an epidemiological hallmark of cancer. It is so typical of cancer that it distinguishes cancer from other chronic diseases.http://www.what-is-cancer.com/papers/newmedicine/epidemiologyFrame.htmData source: Surveillance, Epidemiology, and End Results (SEER)... read full comment
Comment on: Demicheli et al. Breast Cancer Research, 10:R83
Additional data for this article (Claire Hansford, 13 November 2008)
Due to a technical fault the additional file links have become unavailable for this article.They are now available from:Additional file 1: http://www.biomedcentral.com/content/supplementary/bcr1836-S1.xlsAdditional file 2: http://www.biomedcentral.com/content/supplementary/bcr1836-S2.xlsAdditional file 3: http://www.biomedcentral.com/content/supplementary/bcr1836-S3.xls read full comment
Comment on: Esteva et al. Breast Cancer Research, 9:R87
Relationship of Ox-E/ER signature expression with clinical parameters and outcome in age-stratified cohorts (Christina Yau, 22 September 2008)
In their recent editorial (Breast Cancer Res 2008, 10:109), Neven et al. highlight our recent finding (Breast Cancer Res 2008, 10:R61) that an experimentally derived oxidative stress gene expression signature, ‘Ox-E/ER’, identifies an aggressive subset of primary estrogen receptor (ER)-positive breast cancers associated with poor clinical outcome, and appears to outperform loss of progesterone receptor (PR) expression as a prognostic variable. Given their earlier studies suggesting an age-related association between PR status and HER2 overexpression in ER-positive breast cancers that could confound our oxidative stress analysis, they suggested that we further explore the prognostic relationship between our Ox-E/ER signature index and breast cancer PR status, stratifying for age-... read full comment
Comment on: Neven et al. Breast Cancer Research, 10:109
Loss of TYMS in sporadic breast cancer (Barry Barclay, 14 September 2007)
It is becoming increasingly clear that both loss of heterozygosity at 18p11.3 and amplification of TYMS at its normal locus or on extra-chromosomal elements serve not only as useful diagnostic and prognostic indicators in breast cancer as suggested here but may at least in some cases be causally related to breast tumor initiation and disease progression. Loss of TYMS gives rise to gross chromosome rearrangements including translocations, loss of chromosome arms, interstital deletions and amplifications. Thus low TYMS activity could be considered a molecular "driver" of subsequent cytogenetic events and an important early event in breast carcinogenesis that channels cells into histopathological subtypes. On the other hand amplification of TYMS (including a mutant polymorphic allele) could... read full comment
Comment on: Kittiniyom et al. Breast Cancer Research, 3:192
Characterization of our 1998 report as indirect evidence for existence of mammary epithelial stem cells (Gilbert Smith, 09 March 2007)
In this commentary, Max Wicha incorrectly characterizes our work published in 1998[2]in Development as providing INDIRECT evidence forthe existence of mammary epithelial stem cells. We feel this is an inappropriate portrayal of our seminal discovery as it diminishes its realimpact upon the mammary stem cell field while elevating the recent Nature publications from Shackleton et al and Stingl et al as the ONLYdemonstration for the fact that a single mammary stem cell can give rise to a complete functional mammary gland. This is misleading and gratuitous. In addition, he ignores the demonstration both in our original paper and subsequently in Mech. Aging and Develop., Boulanger and Smith 2002, that serial transplantation of our retrovirally-tagged mammary outgrowths gaverise... read full comment
Comment on: Wicha Breast Cancer Research, 8:109
Clarification of the Malmö study (Sophia Zackrisson, 15 February 2007)
Overdiagnosis is a potentially harmful effect of screening. Every effort to assess the magnitude of the problem is essential. Therefore, the paper by Paci et al is welcome.(1) As the validity of the Malmö study of overdiagnosis (2) was questioned we would like to make a few comments. Ideally, the rate of overdiagnosis at screening should be estimated by direct observation in a randomised trial where the control group was not invited at the end of the trial and during a long follow-up. This was the case in the Malmö Mammographic Screening Trial (MMST). Most other estimates were based on various sorts of modelling (3) or from non-randomised settings. (1;4-7) In the MMST the control group of the age cohort 55-69 years at entry was never invited. The follow-up comprised 15 years after... read full comment
Comment on: Paci et al. Breast Cancer Research, 8:R68
Release of tumor cells during neoadjuvant therapy (Katharina Pachmann, 01 November 2006)
The present report by Dr. Fehm confirms our previous results about dissemination of tumor cells during the course of neoadjuvant therapy presented already at the 2004 San Antonio Breast cancer symposium (Pachmann K., Camara O., Pachmann UA. Influence of primary tumor chemotherapy in breast cancer on circulating tumor cells. Indications for massive cell release into circulations concurrent with tumor size reduction. (2004) Breast Cancer Research and Treatment 88: S224), which was commented in several publications: "An article in the May 2005 issue of Oncology News International (Vol. 14, No. 5) reports that neoadjuvant chemotherapy* may cause the release of cancer cells into the blood. Katharina Pachmann, MD, of Friedrich-Schiller University in Germany said that "ironically, paclitaxel... read full comment
Comment on: Fehm et al. Breast Cancer Research, 8:R60
suggesting a specific role for elastography (Asem Al-Rifai, 23 August 2006)
my comment concers technical details about how to improve the imaging data sensitivity of detecting the 2 % of malignancies in the group 3 of the ACR classification.(BI-RADS)As Mr. Stavros indicated , the aim of relatively short term follow up is to detect teh rapidly growing cancer which in most cases is grade 3 infiltrating ductal carcinoma .So my comment is the following : in order to try to recognize these cases of early malignancy ( which will appear after six months to show atypical characters on ultrasound ) , wouldn't it be possible to use elastograpy to try to find hard areas into the concerned nodule ( in the early phase of infiltrating ductal carcinoma a reaction of the surrounding tissue yields a hard area around it ) . the aim is to have better criteria allowing for more... read full comment
Comment on: Stavros Breast Cancer Research, 6:P3
Importance of Familial and inherited breast cancers in preventive paradigm. (parvin mehdipour, 13 June 2006)
Many thanks for the valuable contribution to the breast cancer word.You have written the following description in the Introduction:" ..other 90–95% is assumed to be 'sporadic', with no apparent family history. A large proportion of familial breast cancer (<40%) can be attributed to mutations in the high-risk genes BRCA1 and BRCA2 [1]".My comment: the sporadic figure of 90%-95% doesn't indicate that the proband has no family history.There are many families in my database having 3-8 and 4-12 relatives affected with Breast cancer and other malignancies, respectively, who had no mutation in BRCA1&2.So, Familial BC is not representive of inherited BC. Many of our early onset probands with no family history could be positive ( i.e.,inherited, or new mutation)or negative for BRCA-... read full comment
Comment on: Lose et al. Breast Cancer Research, 8:R26
Alcohol verses mitigating folic acid intake in mineral density verse BC risk profiles, confounding geological environment. (Bernhard Hochwimmer, 25 May 2006)
It is possible alcohol (in moderation) adds mineral density through stimulating growth hormone, yet alcohol by itself increases breast cancer (BC) risk. Then mitigating circumstances would be folic acid against alcohol induced BC risk, while still enhancing bone mineral density. One assumes naturally breast density may not dictate BC risk, if at all. So it’s worth speculating on mineral density and BC risk directly, rather than focusing only on breast density. While this response dose not address breast and bone mineral density association directly, it highlights potential utility of a multidisciplinary approach in BC risk that may under some circumstances include bone mineral density and interplay of non anthropogenic factors, including the geological environment. Moderate exercise... read full comment
Comment on: Crandall et al. Breast Cancer Research, 8:404
BLV as an agent involved in Breast Cancer (Elisabeth Rieping, 23 March 2006)
There are some additional features of BLV which qualify it as a causal agent for breast cancer: It induces monocytes to form giant cells.The osteoclasts physiologically active in bone resorption and during breast cancer metastasis develop from monocytes, too. Bone metastasis is an important feature of human, feline and canine breast cancer. All three species are frequently raised with bovine milk, although neither physians nor vets propagate it.HTLV-1 the close relative of BLV is found in acut T-cell leukemia ATL. A disease for which hypercalcemia is as typical as for breast cancer.MMTV induced tumors in mice rarely metastasize and they do not not show bone metastases.Traces of an MMTV like, not identical retrovirus are often found in human breast cancer. BLV is not identical. That would... read full comment
Comment on: Buehring et al. Breast Cancer Research, 3:A14
Long-chain polyunsaturated fatty acids and cancer (Undurti Das, 13 June 2005)
I read with interest the study by Siddiqui et al.In a series of studies, previously I reported that long-chain polyunsaturated fatty acids (LCPUFAs) have selective tumoricidal action on a variety of tumor cells with little or no effects on normal cells both in vitro and in vivo (1-5). Our studies showed that human breast cancer cells ZR-75-1 are killed by LCPUFAs. Of all the fatty acids tested gamma-linolenic acid (GLA) was found to be the most effective compared to EPA and DHA. Subsequent studies revealed that LCPUFAs are able to enhance free radical generation and lipid roxidation process in tumor cells but not in normal cells and that this could be one of the main, if not the sole, mechanism of their tumoricidal action. It was also observed that anti-oxidants such as BHA, BHT and vitamin... read full comment
Comment on: Siddiqui et al. Breast Cancer Research, 7:R645
Low risk HPV types and malignancy (Janet Buchanan, 02 February 2005)
The findings by deVilliers et al. regarding the prevalence of HPV 6 and HPV 11 in both breast tumor tissue and nipples is interesting. The finding by deVilliers et al that HPV 11 was the most prevalent type and that it was detected in 19 carcinomas and 8 nipples may be evidence that HPV 11 is a high risk type for certain types of carcinomas. HPV 11 in patients with recurrent respiratory papillomatosis (RRP) has not only been been found to be a predictor of aggressive disease, but has also been documented to be associated with pulmonary malignancy in patients with RRP. Future studies may be more revealing in the association of HPV 11 and malignancies. read full comment
Comment on: de Villiers et al. Breast Cancer Research, 7:R1