Erratum

Ravindranath MH, Muthugounder S, Presser N, Ye X, Brosman S, Morton DL. Endogenous immune response to gangliosides in patients with confined prostate cancer. Int J Cancer.2005 Sep 1;116(3):368–377 doi: 10.1002/ijc.21023. Epub 2005 Mar 30.

This paper contains two parts. Part # 1 defines ganglioside profiles of CaP cell lines which include Figures 1,2,3 & 4. Part # 2 provides the results of a double-blind analyses with Tables 1, 2, 3 to show the differences in the IgM antibodies to the gangliosides among healthy controls, patients with benign prostatic hyperplasia (BPH) and stages of Prostate Cancer.

The IRB of John Wayne Cancer Institute, Santa Monica CA, where the original research was carried, brought to our attention that the consent forms of some patients listed in Table 1 are wanting. Consent forms revealed the discovery of serial bleeds of the same prostate cancer patients, erroneously entered as different patients due to difference in the patient characteristics. This inadvertent error has led to change of sample size in Table 1 and consequently altered the mean values of sera analyses of the cohort presented in Tables 2 & 3. In the following sections, detailed error corrections of the tables are presented. In addition, a minor line shift error is clarified in the revised Table 2 involving the anti-GD3 IgM of healthy cohort, which altered the statistical inference for anti-GD3 IgM in both Tables 2 and 3.

Table 1 CORRECTION OF PRIMARY ERROR

The original Table 1 contains information regarding 11 normal healthy controls, 11 patients with BPH and 36 “patients” with organ-confined CaP (stages T1 and T2) and 27 “patients” with unconfined CaP (stages T3 and T4). After deleting the error of serial bleeds in both organ-confied and unconfined CaP patients, the table is corrected to include 31 patients with organ-confined CaP (stages T1 and T2) and 20 patients with unconfined CaP (stages T3 and T4). Consequently, the sample size indicated in Material and Methods section in page 369, column 1, para 4, lines 2 and 3 should be corrected as above.

Table 2 CORRECTION IN LOG TITER VALUES DUE TO CHANGE IN SAMPLE SIZE OF CaP STAGES.

Based on the corrections carried out in Table 1, the results of analyses of anti-ganglioside IgM antibodies change as follows:

The corrected Table 2 is based on 11 normal healthy controls, 11 patients with BPH and 31 patients with organ-confined CaP (stages T1 and T2) and 20 patients with unconfined CaP (stages T3 and T4). The statistical analyses of the revised values were carried out by an independent Statistician from University of California, Los Angeles, who concurred and followed the statistical methodology used in the original manuscript. Most importantly, the corrections did not anyway change the statistical inferences or conclusions derived regarding the primary antibody anti-GD1a IgM as an early biomarker of CaP.

Another correction involved a single line shift error for log titers for IgM against GD3/GD2 for Healthy cohort as indicated in the revised table, the ANOVA revealed no any significant reduction in anti-GD3. Therefore, under the Results section in page 374, column 1, para 1, lines 4–6, should read as follows: “Two tailed p-values revealed significant intergroup differences in titers of anti-GD1a but not anti-GM1, anti-GM2, anti-GM3, anti-GD3…” and also under Discussion section in page 375, column 2, para 1, lines 8–11 should be deleted. The word GD3 should be inserted after GM3 in line 11 to read as follows: Although GM3, GD3 and GM2 are the major gangliosides of Cap, they failed to induce significant immune response….”

Table 3 CORRECTED

The corrected Table 3 reiterates and confirms the statistical inferences or conclusions derived regarding anti-GD1a IgM as an early biomarker. Consequent to corrections made in the table, the results described under subheading Endogenous IgM response to gangliosides, page 374, column 1, Lines 9–13 change as follows:: “Log titers of anti-GD1a were significantly higher in patients with confined CaP (T1/T2) than in healthy controls (p=0.048), patients with BPH (p = 0.022) or patients with unconfined CaP (p = 0.03) Table 3”.

The following lines in the discussion (page 376, column 2, para 2, line 9–13) should be corrected as “In our study, this ELISA revealed that serum levels of anti-GD1a IgM antibody were significantly higher in patients with organ-confined CaP than in healthy controls (p= 0.048), patients with BPH (0.022) or patients with unconfined CaP (p = 0.03).

Correction of the shift error for log titers for IgM against GD3/GD2 for Healthy cohort, the text under Results in page 374, column 1, para 1, lines 7–11, the sentence referring to anti-GD3 IgM, “The LSD method used….than in controls” should be deleted.

Discussion section under the heading Endogenous immune response to gangliosides needs to be corrected as follows; The following lines from page 375, column 1, last two lines commencing from “In the present investigation of….”, which continues to column 2, lines 1–3 ending in which considers differences in sample size” should be deleted.

Finally it may be noted that the sample size corrections did not anyway change the primary conclusion of this publication regarding the anti-GD1a IgM as an early biomarker of CaP. A secondary finding emerging after correction of the line shift error in healthy cohort is that the log titer of anti-GD3 IgM in CaP cohort do not differ from that of the healthy cohort, again reaffirming that the anti-GD1a IgM can serve as an anti-ganglioside IgM with diagnostic potential in CaP patients.