The data in Fig 1 is inconsistent with Table 2 (Jiayi Wang, 22 June 2012)
In Fig 1, the result of Asian subgroup is 0.84(0.73-0.97), while in Table 2 the same result changed into 0.85(0.77-0.94)(GG/TG vs.TT, Asian subgroup).
read full comment
New challenges in cancer communication (Ali Montazeri, 30 April 2012)
To understand what we are saying in this paper I refer the readers to a chapter (Chapter 33) in a new edition of the 'New Challenges in Communication with Cancer Patients' edited by Surbone et al. from Springer, 2012.
read full comment
errors in the articles (Elena Yakubovich, 20 February 2012)
The study by Wu et al shows the decreased expression of DUSP9 in ccRCC. The authors claim that DUSP9 may represent a novel and useful prognostic marker for ccRCC and that for their knowledge this is the first study to report the clinical significance of DUSP9 in ccRCC. In this connection we would like to refer to our similar results that have been published previously. The study reported in 2002 has revealed for the first time the down-regulation of DUSP9 in ccRCC [1]. In the study published in 2006 we determined DUSP9 mRNA level in clinical samples from patients at different stage of renal cancer [2]. It has been shown that DUSP9 inactivation was observed even in the early stage of the disease....
read full comment
Correction to recruitment data. (Janet de Moor, 26 January 2012)
The manuscript contains a typographical error on page 2, under Eligibility Criteria and Sample Recruitment. There were 773 survivors who were alive and eligible for PFH-2, not 733 as reported in the paper.
read full comment
incorrect model label - this is not a xenograft, it is an allograft (melinda hollingshead, 17 August 2011)
When tissues are transplanted from one species (e.g., human) into another species (e.g., mouse) you have prepared a xenograft (xeno- from the Greek for foreign and graft from Middle English for joining or transferring). When one transplants tissues within a species (e.g., mouse to mouse) it is referred to as an allograft. Thus, the title of this paper incorrectly refers to the test model as a xenograft. The authors did not prepare nor test a xenograft, they tested an allograft. The term syngeneic (used by the authors to describe the model) and the term xenograft are mutually exclusive. You cannot be syngeneic with another species. The correct title should not contain the word xenograft, it could contain the word allograft or syngeneic model.
read full comment
Corresponding author contact information (Jung-Young Shin, 31 May 2011)
Corresponding author: Jin-Hyoung Kang Correspondence : jinkang@catholic.ac.kr Seoul St. Mary’s Hospital, The Catholic University of Korea, Seoul, Korea.
the organizational affiliation is Department of Public Health, Erasmus MC (Lu Shi, 31 May 2011)
For Lu Shi, William J. McCarthy and Robert Boer, the organizational affiliation is "Department of Public Health, Erasmus MC, Rotterdam, The Netherlands"
read full comment
The authors wrote the methods as followed; 'The third (2005) KNHANES is composed of four parts: the Health Interview survey, the Health Examination survey, the Nutrition survey and the Health Promotion Knowledge, Attitude and Practice (HP-KAP) survey. As the item about breast cancer screening was included in HP-KAP survey, we started with cross-sectional data from the HP-KAP survey. HP-KAP survey was conducted in each household as face-to-face interviews by trained interviewers. In the third (2005) KNHANES, 8,417 individuals aged ≥ 19 year were sampled as subjects of the HP-KAP survey. Among them, 7,802 individuals participated in the examination: the response rate was 92.7%. Figure 2 shows the model used to select our study population. Subjects of male...
read full comment
There is a labelling mistake within the Figure 2B. (Dajun Deng, 20 May 2011)
CpG site markers (from "A" to "Q") within the Figure 2B were not labelled at their right positions. Each marker should be shift to its right neighborhood position. For example, the right position for the marker "A" is at the position for the marker "B", and so on.
read full comment
error in Figure 5C (Steven de Jong, 25 March 2011)
We have found an error in our article.
In Fig 5C the lane indicating treatment with MG alone has to be read as treatment with TRAIL alone. The lane indicating treatment with TRAIL alone is in fact treatment with MG alone.
Patient is the one who should choose the amount of information he/she wants to receive (Javad Shahidi, 06 January 2011)
The study by Montazeri et al. aims to explore the relationship between the disclosure of cancer diagnosis (and/or prognosis) and patient’s quality of life. Based on the study findings, authors make a conclusion that depending on the culture, in some cultures it might be better to conceal the truth from cancer patients.
There are several issues to consider before making such a conclusion. First and foremost, this study with the current design cannot answer the question of whether or not the disclosure should happen. Even if we accept that the quality of life scores of those who know they have cancer is less, it does not necessarily mean that disclosure is not appropriate. As authors mention and similar studies in the similar settings (such as: Shahidi J...
read full comment
Difference between "emigrants" and those with "origins" (Amit Agrawal, 27 September 2010)
We must congratulate the authors in exploring this relatively under-reported area in breast cancer along with providing some factual data (albeit limited by the unavailability of histological subtypes in 20% and hormone receptors in approximately 50% of patients). It would have been more informative to see the actual differences between Indians/Pakistanis who are “emigrants” and those who have “origins” in India/Pakistan (i.e. born and raised in USA). If there was a difference between the 2 groups then socio-environmental factors could be further investigated as possible epidemiological factors in those with Indian/Pakistani roots. Genetic (excluding those with mixed-race parentage) and dietary factors may be the same between the two groups. Authors do mention the...
read full comment
GSTM1 and GSTT1 genes (Keith Grimaldi, 12 July 2010)
The study shows an impressive effect of cruciferous on lung cancer risk. I'm surprised though that the various work on GSTM1 and GSTT1 genes were not cited. In particular the Brennan 2005 article in Lancet is highly relevant, showing that the effect of cruciferous was limited to GSTT1 or GSTM1 null individuals (Brennan et al, Lancet, Volume 366, Issue 9496, Pages 1558 - 1560, 29 October 2005).
There is also a 2009 meta analysis reporting that higher cruciferous vegetable intake was consistently associated with lower lung cancer risk and was more marked in individuals with GSTM1 and GSTT1 null genotypes, emphasizing the potential importance of this gene-diet interaction. Lam et al, Cancer Epidemiol Biomarkers Prev...
read full comment
Inhibition of SDH in brain (Heikki Savolainen, 09 July 2010)
Dear Editor,
The highly interesting finding that the succinate dehydrogenase (SDH) activity was very low in malignant cells in brain while the enzyme activity was not affected in kidney cells (1) points at the possibility that a particular, possibly epigenetic, factor was involved.
The case is that alkoxyacetic acids which inhibit the SDH activity in kidney (2,3) do so also in brain (4). The low SDH acivity in tumor cells could be associated with the so-called Warburg effect. One may speculate that tumor cells can inhibit the enzyme or the translation of its gene by a hypothetical endogenous factor.
1 Feichtinger RG, Zimmermann F, Mayr JA, et al. BMC Cancer 2010;10:149
2 Laitinen J, Liesivuori J, Turunen T, Savolainen H. Chemosphere 1994;29:781...
read full comment
Is Biotinidase Really a Biomarker for Breast Cancer? (Barry Wolf, 08 July 2010)
Drs. Un-Beom Kang and colleagues recently reported that biotinidase may be a breast cancer biomarker [1]. The authors used affinity chromatography to select cysteine-containing peptides/proteins to identify a group of proteins in plasma that show differences between populations of women with breast cancer and those who are unaffected. The authors found that by comparing biotinidase in 21 patients with breast cancer and 21 normal healthy controls, biotinidase was statistically down-regulated in the plasmas from the women with breast cancer. The authors thereby concluded that biotinidase is a “potential seriological biomarker for the detection of breast cancer.” In the last paragraph of the discussion, the authors indicate that biotinidase catalyzes the release and recycles...
read full comment
This is a correction notice: On page 13, in the acknowledgements section, the following grant was not cited: U24-CA-114732, from the National Cancer Institute, National Institutes of Health, and Department of Health and Human Services.
read full comment
Model refinement on test data constitutes a dangerous case of overfitting (Olivier Gevaert, 05 August 2009)
Although already pointed out by the reviewers that the model refinement in this article is a dangerous case of overfitting, still the authors overemphasize that they improve prediction of progression free survival (PFS) of their model. In this article, the authors report that a 180-gene signature developed based on lung data and a different EGFR inhibitor, is predictive of therapy response in metastatic colorectal cancer independent of KRAS mutation status. This constitutes an important finding since these results show that their original signature is independent of disease and anti-EGFR monoclonal antibodies. Next, the researchers attempted to reduce the number of genes in the original signature to a suitable number manageable with other methods besides microarray such as qRT-PCR. This is...
read full comment
It has come to our attention that one of the 95% CIs included in our analyses was incorrect. For the Nine Hospital Study the RR (95% CI) for chewing tobacco, given in Table 3 as 2.82 (0.95-9.39), should in fact be 2.82 (0.85-9.39). The error has no substantive effect on the conclusions drawn in the paper, and does not affect the wording of the text. It does, however, slightly affect some of the relative risks and 95% confidence intervals in the eta-analyses reported in Tables 4 and 5. With the corrected values of the meta-analyses, the fifth paragraph of the abstract should read: “Giving preference to estimates for never smokers, if available, and overall population estimates otherwise, the estimate was 1.13 (0.67-1.92), again based on heterogeneous estimates....
read full comment
Targeting EGFR, HER2 and VEGF (Michael Hölling, 23 January 2009)
Dear Sir,<br><br>my first comment is just a technical one, as for the time being the provisional pdf of the article is not accessible.<br><br>Secondly, in the abstract the monoclonal antibody (MAB)Bevacizumab is erroneously described as targeting the human epidermal growth factor receptor (EGFR), while in fact it targets the vascular endothelial growth factor (VEGF) (but not its receptor). The MAB targeting the EGFR is named Cetuximab.<br><br>Yours faithfully<br>Michael Hölling
read full comment
Krainick-Strobel et al. provide detail of their single-arm trial of preoperative letrozole in stage T2 – T4b, N0 breast cancer patients. The authors observed that over 50% of the study population became eligible for breast conserving surgery within four months of neoadjuvant letrozole and that letrozole had a favourable safety and tolerability profile. They indicate that no patients showed evidence of metastatic disease at the final assessment. The authors indicate, however, that ‘no or a very few’ patients did end up having ‘affected’ lymph nodes by the time of their final clinical assessment. It would be helpful to have clear documentation of the number of patients who were found to have positive nodes in table 7. Also, it is not clear from the article...
read full comment
Psychological distress and breast cancer-is there any correlation with response to therapy (. Chintamani, 14 October 2008)
We read with interest the article by Ronid Pelet et al. The increased incidence of adverse and depressing life style events in breast cancer cases as compared to the age matched control group further highlights the already known relationship of increased stress with higher incidence of breast cancer. We are presently working on the correlation of the levels of depression and stress with response to neoadjuvant chemotherapy in patients with locally advanced breast cancers. The intial results(not yet published)indicate a statistically significant correlation between the two. Patients with higher levels of happiness or lower depression and anxiety levels(measured using HADS score) responded better to their therapy.We would therefore like to know, if there was any correlation observed in this...
read full comment
The effect of smoking on cancer risk and ultraviolet wavelengths on melanoma risk (William B. Grant, 30 September 2008)
The study of variation of cancer incidence by socioeconomic group in England by Shack et al. [1] presents some interesting results; however, the interpretation of the findings overlooks two important factors: the role of smoking in risk for some types of cancer and the different roles of solar ultraviolet-B (UVB) and UVA in the etiology of melanoma and non-melanoma skin cancer (NMSC). This letter presents results in the relevant journal literature regarding these oversights.As mentioned in [1], those with lower socioeconomic status (SES) have higher rates of smoking. Thus, the effect of smoking on the cancers discussed should be evaluated to determine whether smoking rates, rather than SES per se might explain the findings. Lower SES is associated with increased risk of cervical cancer...
read full comment
Choice of effect measure – was it appropriate? (Sandro José Martins, 10 December 2007)
The analytic method and the specific formulas used in meta-analysis are affected by the choice of effect measures. Main outcome measures in adjuvant trials are the ratio of cumulative incidence rates (e.g. recurrence, death), and are statistically modeled as time-to-event data (risk ratio and hazard ratio). In this article, authors have chosen to handle such measures as plain odds ratios, using the Peto method. This implies that it was available data to complete 2 x 2 table of outcome by treatment, and confounding was negligible. Unfortunately, this may not be true. Let us examine consequences of author's choice in the main outcome measure (DFS) of the largest trial (HERA). In Figure 3, we are informed that there were 347 recurrences in the HERA trial. It was assumed that remaining patients...
read full comment
CD105 (endoglin) expression: an unfavorable prognostic marker in hepatocellular carcinoma? (Koert de Jong, 22 June 2007)
Koert P. de Jong and Annette S.H. Gouw Working in the field of angiogenesis in hepatocellular carcinoma we read with interest the paper by Yang et al (BMC Cancer 2006, 6:110). They concluded that CD105 is superior to CD34 as a marker for new microvessels in HCC and that CD105 is a better prognostic indicator for recurrence and metastasis of HCC. These conclusions were based on three major findings. After partial liver resection for HCC there was a significantly lower patient survival if their tumors contained a higher microvessel density (MVD), quantified by CD105 expression. However, the authors did not find a significant influence on patient survival when tumor MVD was quantified by CD34. Secondly, CD105-MVD correlated with venous invasion whereas CD34-MVD did not. And thirdly, in...
read full comment
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Latest comments
The data in Fig 1 is inconsistent with Table 2 (Jiayi Wang, 22 June 2012)
In Fig 1, the result of Asian subgroup is 0.84(0.73-0.97), while in Table 2 the same result changed into 0.85(0.77-0.94)(GG/TG vs.TT, Asian subgroup). read full comment
Comment on: Zhou et al. BMC Cancer, 11:521
New challenges in cancer communication (Ali Montazeri, 30 April 2012)
To understand what we are saying in this paper I refer the readers to a chapter (Chapter 33) in a new edition of the 'New Challenges in Communication with Cancer Patients' edited by Surbone et al. from Springer, 2012. read full comment
Comment on: Montazeri et al. BMC Cancer, 4:21
errors in the articles (Elena Yakubovich, 20 February 2012)
The study by Wu et al shows the decreased expression of DUSP9 in ccRCC. The authors claim that DUSP9 may represent a novel and useful prognostic marker for ccRCC and that for their knowledge this is the first study to report the clinical significance of DUSP9 in ccRCC. In this connection we would like to refer to our similar results that have been published previously. The study reported in 2002 has revealed for the first time the down-regulation of DUSP9 in ccRCC [1]. In the study published in 2006 we determined DUSP9 mRNA level in clinical samples from patients at different stage of renal cancer [2]. It has been shown that DUSP9 inactivation was observed even in the early stage of the disease.... read full comment
Comment on: Wu et al. BMC Cancer, 11:413
Correction to recruitment data. (Janet de Moor, 26 January 2012)
The manuscript contains a typographical error on page 2, under Eligibility Criteria and Sample Recruitment. There were 773 survivors who were alive and eligible for PFH-2, not 733 as reported in the paper. read full comment
Comment on: de Moor et al. BMC Cancer, 11:165
incorrect model label - this is not a xenograft, it is an allograft (melinda hollingshead, 17 August 2011)
When tissues are transplanted from one species (e.g., human) into another species (e.g., mouse) you have prepared a xenograft (xeno- from the Greek for foreign and graft from Middle English for joining or transferring). When one transplants tissues within a species (e.g., mouse to mouse) it is referred to as an allograft. Thus, the title of this paper incorrectly refers to the test model as a xenograft. The authors did not prepare nor test a xenograft, they tested an allograft. The term syngeneic (used by the authors to describe the model) and the term xenograft are mutually exclusive. You cannot be syngeneic with another species. The correct title should not contain the word xenograft, it could contain the word allograft or syngeneic model. read full comment
Comment on: Shibata et al. BMC Cancer, 10:566
Corresponding author contact information (Jung-Young Shin, 31 May 2011)
Corresponding author: Jin-Hyoung Kang
Correspondence
: jinkang@catholic.ac.kr
Seoul St. Mary’s Hospital,
The Catholic University of Korea, Seoul, Korea.
If you have any questions please contact him. read full comment
Comment on: Shin et al. BMC Cancer, 10:425
the organizational affiliation is Department of Public Health, Erasmus MC (Lu Shi, 31 May 2011)
For Lu Shi, William J. McCarthy and Robert Boer, the organizational affiliation is "Department of Public Health, Erasmus MC, Rotterdam, The Netherlands" read full comment
Comment on: Shi et al. BMC Cancer, 11:92
Errors in Methods (Jun-Pyo Myong, 31 May 2011)
Dear Dr. Park.
The authors wrote the methods as followed;
'The third (2005) KNHANES is composed of four parts: the Health Interview survey, the Health Examination survey, the Nutrition survey and the Health Promotion Knowledge, Attitude and Practice (HP-KAP) survey. As the item about breast cancer screening was included in HP-KAP survey, we started with cross-sectional data from the HP-KAP survey. HP-KAP survey was conducted in each household as face-to-face interviews by trained interviewers. In the third (2005) KNHANES, 8,417 individuals aged ≥ 19 year were sampled as subjects of the HP-KAP survey. Among them, 7,802 individuals participated in the examination: the response rate was 92.7%. Figure 2 shows the model used to select our study population. Subjects of male... read full comment
Comment on: Lee et al. BMC Cancer, 10:144
There is a labelling mistake within the Figure 2B. (Dajun Deng, 20 May 2011)
CpG site markers (from "A" to "Q") within the Figure 2B were not labelled at their right positions. Each marker should be shift to its right neighborhood position. For example, the right position for the marker "A" is at the position for the marker "B", and so on. read full comment
Comment on: Xiang et al. BMC Cancer, 10:44
error in Figure 5C (Steven de Jong, 25 March 2011)
We have found an error in our article.
In Fig 5C the lane indicating treatment with MG alone has to be read as treatment with TRAIL alone. The lane indicating treatment with TRAIL alone is in fact treatment with MG alone.
We apologies for this error. read full comment
Comment on: van Geelen et al. BMC Cancer, 11:39
Patient is the one who should choose the amount of information he/she wants to receive (Javad Shahidi, 06 January 2011)
The study by Montazeri et al. aims to explore the relationship between the disclosure of cancer diagnosis (and/or prognosis) and patient’s quality of life. Based on the study findings, authors make a conclusion that depending on the culture, in some cultures it might be better to conceal the truth from cancer patients.
There are several issues to consider before making such a conclusion. First and foremost, this study with the current design cannot answer the question of whether or not the disclosure should happen. Even if we accept that the quality of life scores of those who know they have cancer is less, it does not necessarily mean that disclosure is not appropriate. As authors mention and similar studies in the similar settings (such as: Shahidi J... read full comment
Comment on: Montazeri et al. BMC Cancer, 9:39
Difference between "emigrants" and those with "origins" (Amit Agrawal, 27 September 2010)
We must congratulate the authors in exploring this relatively under-reported area in breast cancer along with providing some factual data (albeit limited by the unavailability of histological subtypes in 20% and hormone receptors in approximately 50% of patients). It would have been more informative to see the actual differences between Indians/Pakistanis who are “emigrants” and those who have “origins” in India/Pakistan (i.e. born and raised in USA). If there was a difference between the 2 groups then socio-environmental factors could be further investigated as possible epidemiological factors in those with Indian/Pakistani roots. Genetic (excluding those with mixed-race parentage) and dietary factors may be the same between the two groups. Authors do mention the... read full comment
Comment on: Kakarala et al. BMC Cancer, 10:191
GSTM1 and GSTT1 genes (Keith Grimaldi, 12 July 2010)
The study shows an impressive effect of cruciferous on lung cancer risk. I'm surprised though that the various work on GSTM1 and GSTT1 genes were not cited. In particular the Brennan 2005 article in Lancet is highly relevant, showing that the effect of cruciferous was limited to GSTT1 or GSTM1 null individuals (Brennan et al, Lancet, Volume 366, Issue 9496, Pages 1558 - 1560, 29 October 2005).
There is also a 2009 meta analysis reporting that higher cruciferous vegetable intake was consistently associated with lower lung cancer risk and was more marked in individuals with GSTM1 and GSTT1 null genotypes, emphasizing the potential importance of this gene-diet interaction. Lam et al, Cancer Epidemiol Biomarkers Prev... read full comment
Comment on: Tang et al. BMC Cancer, 10:162
to consider an even better study medication ? (k tseng, 09 July 2010)
You have been innovative in showing a common medication has the prospect of reducing tumor size and metastasis.
Would it be even better to study a medication in the same group, and yet clinically have less side effects, eg. pioglitazone in the future?
A similar success will enhance the chance of an already useful medication. read full comment
Comment on: Aizawa et al. BMC Cancer, 10:51
Inhibition of SDH in brain (Heikki Savolainen, 09 July 2010)
Dear Editor,
The highly interesting finding that the succinate dehydrogenase (SDH) activity was very low in malignant cells in brain while the enzyme activity was not affected in kidney cells (1) points at the possibility that a particular, possibly epigenetic, factor was involved.
The case is that alkoxyacetic acids which inhibit the SDH activity in kidney (2,3) do so also in brain (4). The low SDH acivity in tumor cells could be associated with the so-called Warburg effect. One may speculate that tumor cells can inhibit the enzyme or the translation of its gene by a hypothetical endogenous factor.
1 Feichtinger RG, Zimmermann F, Mayr JA, et al. BMC Cancer 2010;10:149
2 Laitinen J, Liesivuori J, Turunen T, Savolainen H. Chemosphere 1994;29:781... read full comment
Comment on: Feichtinger et al. BMC Cancer, 10:149
Is Biotinidase Really a Biomarker for Breast Cancer? (Barry Wolf, 08 July 2010)
Drs. Un-Beom Kang and colleagues recently reported that biotinidase may be a breast cancer biomarker [1]. The authors used affinity chromatography to select cysteine-containing peptides/proteins to identify a group of proteins in plasma that show differences between populations of women with breast cancer and those who are unaffected. The authors found that by comparing biotinidase in 21 patients with breast cancer and 21 normal healthy controls, biotinidase was statistically down-regulated in the plasmas from the women with breast cancer. The authors thereby concluded that biotinidase is a “potential seriological biomarker for the detection of breast cancer.” In the last paragraph of the discussion, the authors indicate that biotinidase catalyzes the release and recycles... read full comment
Comment on: Kang et al. BMC Cancer, 10:114
Grant acknowledgement (Wendy Rea, 09 June 2010)
This is a correction notice:
On page 13, in the acknowledgements section, the following grant was not cited: U24-CA-114732, from the National Cancer Institute, National Institutes of Health, and Department of Health and Human Services. read full comment
Comment on: Fumagalli et al. BMC Cancer, 10:101
Model refinement on test data constitutes a dangerous case of overfitting (Olivier Gevaert, 05 August 2009)
Although already pointed out by the reviewers that the model refinement in this article is a dangerous case of overfitting, still the authors overemphasize that they improve prediction of progression free survival (PFS) of their model. In this article, the authors report that a 180-gene signature developed based on lung data and a different EGFR inhibitor, is predictive of therapy response in metastatic colorectal cancer independent of KRAS mutation status. This constitutes an important finding since these results show that their original signature is independent of disease and anti-EGFR monoclonal antibodies. Next, the researchers attempted to reduce the number of genes in the original signature to a suitable number manageable with other methods besides microarray such as qRT-PCR. This is... read full comment
Comment on: Balko et al. BMC Cancer, 9:145
Correction of an error (Peter Lee, 23 June 2009)
It has come to our attention that one of the 95% CIs included in our analyses was incorrect. For the Nine Hospital Study the RR (95% CI) for chewing tobacco, given in Table 3 as 2.82 (0.95-9.39), should in fact be 2.82 (0.85-9.39). The error has no substantive effect on the conclusions drawn in the paper, and does not affect the wording of the text. It does, however, slightly affect some of the relative risks and 95% confidence intervals in the eta-analyses reported in Tables 4 and 5.
With the corrected values of the meta-analyses, the fifth paragraph of the abstract should read:
“Giving preference to estimates for never smokers, if available, and overall population estimates otherwise, the estimate was 1.13 (0.67-1.92), again based on heterogeneous estimates.... read full comment
Comment on: Sponsiello-Wang et al. BMC Cancer, 8:356
Targeting EGFR, HER2 and VEGF (Michael Hölling, 23 January 2009)
Dear Sir,<br><br>my first comment is just a technical one, as for the time being the provisional pdf of the article is not accessible.<br><br>Secondly, in the abstract the monoclonal antibody (MAB)Bevacizumab is erroneously described as targeting the human epidermal growth factor receptor (EGFR), while in fact it targets the vascular endothelial growth factor (VEGF) (but not its receptor). The MAB targeting the EGFR is named Cetuximab.<br><br>Yours faithfully<br>Michael Hölling read full comment
Comment on: Kavanagh et al. BMC Cancer, 9:1
Nodal status (John Fralick, 15 January 2009)
Krainick-Strobel et al. provide detail of their single-arm trial of preoperative letrozole in stage T2 – T4b, N0 breast cancer patients. The authors observed that over 50% of the study population became eligible for breast conserving surgery within four months of neoadjuvant letrozole and that letrozole had a favourable safety and tolerability profile. They indicate that no patients showed evidence of metastatic disease at the final assessment. The authors indicate, however, that ‘no or a very few’ patients did end up having ‘affected’ lymph nodes by the time of their final clinical assessment. It would be helpful to have clear documentation of the number of patients who were found to have positive nodes in table 7. Also, it is not clear from the article... read full comment
Comment on: Krainick-Strobel et al. BMC Cancer, 8:62
Psychological distress and breast cancer-is there any correlation with response to therapy (. Chintamani, 14 October 2008)
We read with interest the article by Ronid Pelet et al. The increased incidence of adverse and depressing life style events in breast cancer cases as compared to the age matched control group further highlights the already known relationship of increased stress with higher incidence of breast cancer. We are presently working on the correlation of the levels of depression and stress with response to neoadjuvant chemotherapy in patients with locally advanced breast cancers. The intial results(not yet published)indicate a statistically significant correlation between the two. Patients with higher levels of happiness or lower depression and anxiety levels(measured using HADS score) responded better to their therapy.We would therefore like to know, if there was any correlation observed in this... read full comment
Comment on: Peled et al. BMC Cancer, 8:245
The effect of smoking on cancer risk and ultraviolet wavelengths on melanoma risk (William B. Grant, 30 September 2008)
The study of variation of cancer incidence by socioeconomic group in England by Shack et al. [1] presents some interesting results; however, the interpretation of the findings overlooks two important factors: the role of smoking in risk for some types of cancer and the different roles of solar ultraviolet-B (UVB) and UVA in the etiology of melanoma and non-melanoma skin cancer (NMSC). This letter presents results in the relevant journal literature regarding these oversights.As mentioned in [1], those with lower socioeconomic status (SES) have higher rates of smoking. Thus, the effect of smoking on the cancers discussed should be evaluated to determine whether smoking rates, rather than SES per se might explain the findings. Lower SES is associated with increased risk of cervical cancer... read full comment
Comment on: Shack et al. BMC Cancer, 8:271
Choice of effect measure – was it appropriate? (Sandro José Martins, 10 December 2007)
The analytic method and the specific formulas used in meta-analysis are affected by the choice of effect measures. Main outcome measures in adjuvant trials are the ratio of cumulative incidence rates (e.g. recurrence, death), and are statistically modeled as time-to-event data (risk ratio and hazard ratio). In this article, authors have chosen to handle such measures as plain odds ratios, using the Peto method. This implies that it was available data to complete 2 x 2 table of outcome by treatment, and confounding was negligible. Unfortunately, this may not be true. Let us examine consequences of author's choice in the main outcome measure (DFS) of the largest trial (HERA). In Figure 3, we are informed that there were 347 recurrences in the HERA trial. It was assumed that remaining patients... read full comment
Comment on: Viani et al. BMC Cancer, 7:153
CD105 (endoglin) expression: an unfavorable prognostic marker in hepatocellular carcinoma? (Koert de Jong, 22 June 2007)
Koert P. de Jong and Annette S.H. Gouw Working in the field of angiogenesis in hepatocellular carcinoma we read with interest the paper by Yang et al (BMC Cancer 2006, 6:110). They concluded that CD105 is superior to CD34 as a marker for new microvessels in HCC and that CD105 is a better prognostic indicator for recurrence and metastasis of HCC. These conclusions were based on three major findings. After partial liver resection for HCC there was a significantly lower patient survival if their tumors contained a higher microvessel density (MVD), quantified by CD105 expression. However, the authors did not find a significant influence on patient survival when tumor MVD was quantified by CD34. Secondly, CD105-MVD correlated with venous invasion whereas CD34-MVD did not. And thirdly, in... read full comment
Comment on: Yang et al. BMC Cancer, 6:110