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No such thing as homeopathy? (Lee Turnpenny, 03 May 2013)

This paper was recently cited in a short article entitled `Homeopathy is more than placebo¿, in the February 2013 edition of the magazine What Doctors Don¿t Tell You, on sale in various UK outlets. (It also formed the basis for an article... read full comment

Comment on: Rostock et al. BMC Cancer, 11:19

Without homeopathic remedies, is care 'homeopathic'? (Lee Turnpenny, 18 March 2013)

Without homeopathic remedies, is care 'homeopathic'?

I came across this reference in an article entitled 'Homeopathy is more than placebo' in the February 2013 issue of the magazine 'What Doctor's Don't Tell You', on sale in various supermarkets in the UK.

Do the authors consider that the title of this magazine piece is used appropriately; ie do they concur with it as a statement, and with the citing of this paper in a magazine endorsing homeopathy? read full comment

Comment on: Rostock et al. BMC Cancer, 11:19

No convincing evidence for efficacy of homeopathic care, let alone homeopathic treatment. (Kausik Datta, 10 March 2013)

I started reading this paper with interest, particularly since I was intrigued by the assertion by the authors that they wanted to focus on homeopathic care, and not the efficacy of homeopathic remedies per se (an interesting assertion pointed out by someone else). I found this study largely disappointing, scientifically speaking. Several points have been discussed in the blog this hyperlink points to. I made a few additional observations which indicate, to me, that this paper did not present convincing evidence for efficacy of homeopathic care as... read full comment

Comment on: Rostock et al. BMC Cancer, 11:19

Alternative explanation (Janusz Kaczorowski, 08 March 2013)

I have reviewed the stats from Google Trends with respect to 'breast cancer' searches and it appears that the internet search activity peeks in September - that is before the start of the awareness campaigns. There is also some data suggesting that incidence of breast cancer is seasonal (higher in fall and spring - both hemispheres) -- perhaps there is more to increased search activity than just breast cancer awareness campaigns. read full comment

Comment on: Glynn et al. BMC Cancer, 11:442

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