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Advocacy > Standards in Abstracts

Last update: 04/27/2010

We propose that all medical journals adopt standards for published abstracts in order to make the reports more informative, easier to read, evaluate, and compare

Specifically, we recommend that all medical journals adopt standards for labeled content and structure, and divide the sections into separate paragraphs to improve readability.  

Adopting standards for required labeled categories will help reviewers to: 

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Locate areas of interest quickly:  
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Study Title, Study question, Statistical significance, Study type/method, Endpoints

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Patients, Disease type, Sample size, Clinical setting,  

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Results, Statistical significance, Toxicities (significance order), Validation

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Conclusion,  Discussion,  Disclosures

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Compare similar articles or outcomes.

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Quickly identify weaknesses and strengths of the study.

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Identify potential biases if Disclosure information is included or omitted.

Please feel free to comment by email by clicking here.

We've provided an example below by selecting an abstract at random to see what categories would emerge for standardization. 

See Diagnostic Abstract Type: Before | After


DIAGNOSTIC "Run-on" Paragraph Type

Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7259-64. Epub 2003 May 19.


Involvement of multiple signaling pathways in follicular lymphoma transformation: p38-mitogen-activated protein kinase as a target for therapy.

Elenitoba-Johnson KS, Jenson SD, Abbott RT, Palais RA, Bohling SD, Lin Z, Tripp S, Shami PJ, Wang LY, Coupland RW, Buckstein R, Perez-Ordonez B, Perkins SL, Dube ID, Lim MS.

Department of Pathology, Associated Regional and University Pathologists Institute for Clinical and Experimental Pathology, University of Utah, Salt Lake City, UT 84132, USA. kojo.elenitobaj@path.utah.edu

Follicular lymphoma (FL) is the most common form of low-grade non-Hodgkin's lymphoma. Transformation to diffuse large B cell lymphoma (DLBCL) is an important cause of mortality. Using cDNA microarray analysis we identified 113 transformation-associated genes whose expression differed consistently between serial clonally related samples of FL and DLBCL occurring within the same individual. Quantitative RT-PCR validated the microarray results and assigned blinded independent group of 20 FLs, 20 DLBCLs, and five transformed lymphoma-derived cell lines with 100%, 70%, and 100% accuracy, respectively. Notably, growth factor cytokine receptors and p38beta-mitogen-activated protein kinase (MAPK) were differentially expressed in the DLBCLs. Immunohistochemistry of another blinded set of samples demonstrated expression of phosphorylated p38MAPK in 6/6 DLBCLs and 1/5 FLs, but not in benign germinal centers. SB203580 an inhibitor of p38MAPK specifically induced caspase-3-mediated apoptosis in t(14;18)+/p38MAPK+-transformed FL-derived cell lines. Lymphoma growth was also inhibited in SB203580-treated NOD-SCID mice. Our results implicate p38MAPK dysregulation in FL transformation and suggest that molecular targeting of specific elements within this pathway should be explored for transformed FL therapy.

PMID: 12756297


DIAGNOSTIC Structured Type

Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7259-64. Epub 2003 May 19

Title: Involvement of multiple signaling pathways in follicular lymphoma transformation: p38-mitogen-activated protein kinase as a target for therapy. PMID: 12756297

Authors: Elenitoba-Johnson KS, Jenson SD, Abbott RT, Palais RA, Bohling SD, Lin Z, Tripp S, Shami PJ, Wang LY, Coupland RW, Buckstein R, Perez-Ordonez B, Perkins SL, Dube ID, Lim MS.

Centers: Department of Pathology, Associated Regional and University Pathologists Institute for Clinical and Experimental Pathology, University of Utah, Salt Lake City, UT 84132, USA.

Study questions: 1) What genes are associated with transformation from FL to DLBCL? 2) Are identified genes potential targets for treatment?

Background: Follicular lymphoma (FL) is the most common form of low-grade non-Hodgkin's lymphoma. Transformation to diffuse large B cell lymphoma (DLBCL) is an important cause of mortality..

Methods: Using cDNA microarray analysis we identified 113 transformation-associated genes whose expression differed consistently between serial clonally related samples of FL and DLBCL occurring within the same individual.

Sample: 20 FLs, 20 DLBCLs, and five transformed lymphoma-derived cell lines

Findings: 1) 113 transformation-associated genes whose expression differed consistently between serial clonally related samples of FL and DLBCL occurring within the same individual. 2) Growth factor cytokine receptors and p38beta-mitogen-activated protein kinase (MAPK) were differentially expressed in the DLBCLs

Conclusion: 1) Our results implicate p38MAPK dysregulation in FL transformation. 2) Notably, growth factor cytokine receptors and p38beta-mitogen-activated protein kinase (MAPK) were differentially expressed in the DLBCLs.

Validation: 1) Quantitative RT-PCR validated the microarray results and assigned blinded independent group of 20 FLs, 20 DLBCLs, and five transformed lymphoma-derived cell lines with 100%, 70%, and 100% accuracy, respectively. 2) Immunohistochemistry of another blinded set of samples demonstrated expression of phosphorylated p38MAPK in 6/6 DLBCLs and 1/5 FLs, but not in benign germinal centers. 3) SB203580 an inhibitor of p38MAPK specifically induced caspase-3-mediated apoptosis in t(14;18)+/p38MAPK+-transformed FL-derived cell lines. Lymphoma growth was also inhibited in SB203580-treated NOD-SCID mice.

Statistical significance: Not specified/calculated

Discussion: Our results implicate p38MAPK dysregulation in FL transformation and suggest that molecular targeting of specific elements within this pathway should be explored for transformed FL therapy.

Disclosures: None specified.

 

 
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