Originally published as JCO Early Release 10.1200/JCO.2007.11.8869 on December 17 2007

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Lymphocyte-Predominant and Classical Hodgkin's Lymphoma: A Comprehensive Analysis From the German Hodgkin Study Group

Lucia Nogová, Thorsten Reineke, Corinne Brillant, Michal Sieniawski, Thomas Rüdiger, Andreas Josting, Henning Bredenfeld, Roman Skripnitchenko, Rolf-Peter Müller, Hans-Konrad Müller-Hermelink, Volker Diehl, Andreas Engert

From the Clinic I for Internal Medicine of University Hospital Cologne, Cologne; Department of Pathology, University Wuerzburg, Wuerzburg; Clinic of Radiotherapy, University Hospital Cologne; and the German Hodgkin Study Group, Cologne, Germany

Corresponding author: Lucia Nogová, MD, First Department of Internal Medicine, University Hospital Cologne, Kerpenerstr 62, 50924 Cologne, Germany; e-mail: lucia.nogova{at}uk-koeln.de

	ABSTRACT

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION Authors' Disclosures of... Author Contributions Appendix REFERENCES

 
Purpose Lymphocyte-predominant Hodgkin's lymphoma (LPHL) is rare and differs in histologic and clinical presentation from classical Hodgkin's lymphoma (cHL). To shed more light on the prognosis and outcome of LPHL, we reviewed all LPHL patients registered in the German Hodgkin Study Group (GHSG) database, comparing patient characteristics and treatment outcome with cHL patients.

Patients and Methods We analyzed retrospectively 8,298 HL patients treated within the GHSG trials HD4 to HD12, of whom 394 had LPHL and 7,904 had cHL.

Results Complete remission and unconfirmed complete remission after first-line treatment was achieved in 91.6% v 85.9% of patients in early favorable stages, 85.7% v 83.3% of patients in early unfavorable stages, and 76.8% v 77.8% of patients in advanced stages of LPHL compared with cHL, respectively. Tumor control (freedom from treatment failure [FFTF]) for LPHL and cHL patients at a median observation of 50 months was 88% and 82% (P = .0093) and overall survival (OS) was 96% and 92%, respectively (P = .0166). In LPHL patients, negative prognostic factors were advanced stage (P = .0092), Hb less than 10.5 g/dL (P = .0171), and lymphopenia (P = .010) for FFTF. Age 45 years (P = .0125), advanced stage (P = .0153), and Hb less than 10.5 g/dL (P = .0014) were negative prognostic factors for OS.

Conclusion The better prognosis of LPHL as compared with cHL might allow different treatment strategies, particularly for early-stage LPHL patients.

	INTRODUCTION

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION Authors' Disclosures of... Author Contributions Appendix REFERENCES

 
Lymphocyte-predominant Hodgkin's lymphoma (LPHL) is rare, accounting for approximately 5% of all Hodgkin's lymphoma (HL) cases in Western countries.¹ LPHL and classical HL (cHL) differ substantially in their histopathology and clinical course.^1,2 Histologically, LPHL can present with two distinct morphologic patterns: nodular and diffuse. The nodular subtype is characterized by the presence of atypical lymphocytic and histiocytic (L&H) or popcorn cells that are embedded in a nodular background composed of small B lymphocytes and other reactive cells. In the diffuse subtype, the L&H cells are set against a diffuse background consisting mainly of reactive T cells. However, it remains controversial whether diffuse subtype can be discriminated reliably.³ In addition, a purely diffuse subtype would be classified as diffuse large B-cell lymphoma or T-cell–rich B-cell lymphoma.⁴ According to the current WHO definition, at least a partial nodular pattern is required for the diagnosis of LPHL.⁵ L&H cells usually express the B-cell marker CD20 and lack expression of CD15 and CD30, which are the characteristic markers of cHL.^2,6

Compared with cHL, LPHL has been associated with less aggressive tumor growth and lymphadenopathy often preceding the diagnosis for many years.^1,7-9 Treatment of LPHL using standard HL protocols leads to CR in more than 95% of patients. Particularly, early favorable LPHL patients without risk factors have an excellent prognosis compared with those in early stages with risk factors (early unfavorable) or advanced stages.¹ Patients with early unfavorable and advanced stages are usually included in treatment protocols for cHL.^1,8 In contrast, treatment of early LPHL is less defined and includes radiotherapy, combined-modality treatment, and, more recently, the anti-CD20 monoclonal antibody rituximab.^10-12 Furthermore, watch-and-wait strategies have been used in selected pediatric LPHL patients to avoid adverse effects of treatment.^13,14

To shed more light on open clinically relevant questions regarding LPHL, we revisited our database to analyze patient characteristics, risk factors, and outcome in a large cohort of LPHL patients.

	PATIENTS AND METHODS

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION Authors' Disclosures of... Author Contributions Appendix REFERENCES

 
Patient Selection
We analyzed 8,298 HL patients retrospectively in all clinical stages treated within the German Hodgkin Study Group (GHSG) trials HD4 to HD12 (Appendix Table A1, online only). Overall, there were 394 LPHL and 7,904 cHL patients.

To be eligible for the GHSG trials, patients aged between 16 and 75 years had to have biopsy-proven HL histology at diagnosis, adequate organ function as defined by a creatinine clearance more than 60 mL/min, serum aminotransferases less than 3x the upper normal limit, bilirubin less than 2 mg/dL, left ventricular ejection fraction more than 0.45, and forced expiratory volume in the first second or diffusion capacity of carbon monoxide more than 60% of predicted. Required blood cells count was defined as WBCs 3,500/µL, platelets 100,000/µL, and hemoglobin level 8 g/dL. Randomly assigned patients were negative for antibodies against HIV and free of active infection. All patients signed informed consent based on the institutional review board guidelines and were treated in accordance with the declaration of Helsinki.

Patients in clinical stage I or II without risk factors, such as large mediastinal mass, extranodal lesions, massive spleen involvement, elevated erythrocyte sedimentation rate (ESR; 50 mm without "B" symptoms and 30 mm with B symptoms), and three nodal areas (GHSG risk factors), were included in studies for early favorable stages. Patients in clinical stages I or II with risk factors were treated on trials for early unfavorable stages and patients in clinical stage IIB with risk factors (mediastinal and/or extranodal involvement) and in clinical stages III and IV were allocated to advanced stages and treated accordingly.

Staging Procedures
The extent of disease was assessed by chest x-ray, abdominal ultrasound, computed tomography, bone scintigraphy, and bone marrow biopsy. Histopathologic diagnosis of both cHL and LPHL was reassessed by an expert pathology review panel.

Outcome Definitions
Complete remission (CR) was defined as a disappearance of all symptoms (clinical and radiologic). Patients with radiologic residues that did not meet the criteria for partial remission (PR) were considered unconfirmed CR (CRu) if there were no other signs of lymphoma activity. PR was defined as presence of lymphoma with significant reduction of lymph nodes by 50% and reduction of a large mediastinal tumor by at least 25%. No change was defined as a presence of lymph node tissue that did not fulfill the criteria of PR and did not increase by more than 25%. Progressive disease (PD) meant occurrence of new lesions, B symptoms, or increase of already known lesions by more than 25% during 3 months after CR/CRu or PR. Relapse was defined as an appearance of new or reappearance of initial tumors or symptoms after a remission period (CR or PR) of 3 months at least. Relapse during the first year after completed therapy was defined as an early relapse. Relapse as late as 1 year after the completed therapy was defined as a late relapse.

Risk Factors
Risk factors were evaluated using the international prognostic score (IPS)¹⁵ and the Follicular Lymphoma International Prognostic Score (FLIPI).¹⁶ Because the FLIPI risk factors such as age, Ann Arbor stage, and hemoglobin level were already included in the analysis using IPS, we added the number of nodal areas involved and increased serum lactate dehydrogenase (above normal) to the risk factors analysis. In addition, we adapted the risk factor number of nodal sites to the GHSG risk factors and modified the nodal areas factor from more than four to three areas. In addition, we evaluated ESR ( 50 mm without B symptoms and 30 mm with B symptoms) and extranodal involvement.

Statistics
Statistical analyses were performed with the SAS Software (SAS Institute Inc, Cary, NC), Version 8.2 for Microsoft Windows. Differences in the distribution of variables were assessed using Wilcoxon rank sum test for numeric data and Fisher's exact test for categoric data. Kaplan-Meier estimates were calculated for overall survival (OS) and freedom from treatment failure (FFTF); comparisons of failure-time data used the log-rank test. All reported P values are two sided. OS and FFTF are defined as the time from diagnosis to death or the time from diagnosis to an event, respectively. IPS, FLIPI, ESR, and extranodal involvement were tested within a multiple Cox regression model.

	RESULTS

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Patient Characteristics
The median age of LPHL and cHL patients was 37 and 33 years, respectively. LPHL patients were predominantly of male sex (75%); 9% of LPHL patients had B symptoms compared with 40% of cHL patients. Of 394 LPHL patients, 63% were in early favorable stage, 16% were in early unfavorable stage, and 21% were in advanced stage of disease. Of the 7904 cHL patients analyzed, 22% were in early favorable, 39% were in early unfavorable stages, and 39% were in advanced stages, respectively. As compared with cHL, fewer LPHL than cHL patients had involvement of three nodal areas (28% v 55%), LPHL patients presented more often with normal ESR (96% v 55%), and were less likely to have an elevated lactate dehydrogenase level (84% v 68%), a mediastinal bulky tumor (31% v 55%), or extranodal involvement (6% v 14%), respectively. All of these differences in patient characteristics were significant (Appendix Table A2, online only).

Treatment Outcome
Treatment outcome is shown in Table 1. There were significant differences in CR/CRu between the total group of LPHL and cHL patients (87.5% v 81.7%; P = .0034) and between those presenting with early favorable stages (91.6% v 85.9%; P = .0145). Other significantly different outcome measures between LPHL and cHL patients included PD (0.3% v 3.9%; P < .0001), mortality (4.6% v 9.6%; P = .0004), and early (0.8% v 3.2%; P = .0037) and late relapses (7.4% v 4.7%; P = .0226).

View larger version (10K): [in this window] [in a new window] [PowerPoint Slide for Teaching]   Fig 1. Freedom from treatment failure (FFTF) in lymphocyte-predominant Hodgkin's lymphoma (LPHL) and classical Hodgkin's lymphoma (cHL) patients in the GHSG trials (1988 to 2002).

View larger version (12K): [in this window] [in a new window] [PowerPoint Slide for Teaching]   Fig 2. Lymphocyte-predominant Hodgkin's lymphoma freedom from treatment failure (FFTF) according to clinical stage.

View larger version (10K): [in this window] [in a new window] [PowerPoint Slide for Teaching]   Fig 3. Overall survival in lymphocyte-predominant Hodgkin's lymphoma (LPHL) and classical Hodgkin's lymphoma (cHL) patients in German Hodgkin Study Group trials (1988 to 2002).

	DISCUSSION

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION Authors' Disclosures of... Author Contributions Appendix REFERENCES

Earlier studies suggested that LPHL and cHL differ in pathology and clinical behavior, and that other treatment strategies for LPHL patients might be needed. However, due to the small number of LPHL cases and difficulties in obtaining reliable and reproducible diagnostic tools, there are only few studies comparing disease characteristics, treatment outcome, and prognostic factors among patients with LPHL and cHL.^1,2,4,8,17 The paucity of data has left the most relevant clinical questions on the best treatment of these patients open.

The largest data collection was performed by the European Task Force on Lymphoma Project on LPHL and included data from 426 patients initially diagnosed as having LPHL from 17 European and United States centers.¹ Importantly, after expert pathology revision, only 219 patients were confirmed as having LPHL (51%). Other histologies included lymphocyte-rich cHL (n = 115), non-Hodgkin's lymphoma (n = 12), cHL (n = 19), and reactive lesions (n = 14). Of the 219 LPHL patients analyzed, 74% were male, 53% had stage I, 28% had stage II, 13% had bulky disease, 10% had B symptoms, 7% had mediastinal mass, and 8% had splenic involvement. A formal assessment of risk factors was not performed. The most relevant finding from this study was the surprisingly high rate of reclassified patients (49%), which emphasizes the need for expert pathology confirmation in LPHL and questions the validity of past results, particularly in older series that did not apply immunohistology. Another more recent analysis in which prior reclassification was applied defined the clinical characteristics and treatment outcome of 100 patients having confirmed lymphocyte-rich cHL.¹⁸ In this series, 2,470 patients with cHL and 145 patients with proven LPHL were included to allow comparisons of clinical characteristics. Of the LPHL patients, 75% were in early favorable stages, 10% had B symptoms, 6% had extranodal involvement, 35% had more than three nodal areas involved, and 3% had elevated ESR. These data are similar to the findings presented in our present study. Tests for prognostic factors were not performed in these patients.

Wirth et al¹⁹ analyzed 202 Australian LPHL patients treated between 1969 and 1995, and identified age 45 years, B symptoms, and number of involved sites as negative prognostic factors for OS. However, this analysis included patients who were treated with radiotherapy only, and unfortunately, did not apply pathology expert confirmation using immunohistology. This is also true for most other published series, which were performed usually on a small number of patients, making analysis of prognostic factors impossible.^7-9,17,20

The majority of published trials on LPHL relate to the different treatment options available, including radiotherapy in extended-field and involved-field techniques, combined-modality treatment, and monoclonal antibodies.^{10-12,17,19,20} Pediatric study groups reported small case studies suggesting that a watch-and-wait strategy after complete lymphadenectomy may be appropriate in a few selected children.^13,14 Treatment of LPHL in pediatric patients is aimed at avoiding adverse events such as growth retardation, infertility, hypothyroidism, cardiopulmonary complications, and others by administering as little treatment as possible.

In adults with early favorable LPHL, radiotherapy can be curative, and recent clinical trials suggest that limited-field radiotherapy could be used without loss of efficacy.^12,17,19 Although longer follow-up is needed, based on the European Orgnisation for Research and Treatment of Cancer H7 trial (1988 to 1993)²¹ and earlier GHSG analysis,¹² involved-field radiotherapy was introduced as the GHSG standard for adult LPHL stage IA patients.

Given that both the malignant L&H cells as well as the reactive background is strongly positive for CD20 in LPHL patients, the chimeric anti-CD20 monoclonal antibody rituximab was evaluated in phase II studies in this patient population, demonstrating impressive activity in patients who had experienced multiple relapses.^10,11 A recent update of the GSHG trial confirmed these earlier reports, with 92% of patients alive and 50% progression free after a median observation time of 63 months.²² On the basis of on these provocative data, the GHSG is currently conducting a phase II study with standard-dose rituximab in stage IA LPHL patients. Thus, rituximab is becoming an interesting new treatment approach in early-stage LPHL patients, and will eventually be combined with small-field radiotherapy in future trials. In early unfavorable-stage and advanced-stage LPHL, rituximab might also be explored in future studies. Younes et al²³ reported on newly diagnosed cHL patients who received a combination of rituximab plus doxorubicin, bleomycin, vinblastine, and dacarbazine: 65 assessable patients in clinical stages II to IV received standard-dose rituximab for 6 weeks combined with ABVD. With a median follow-up of 32 months, the estimated event-free survival for the entire group was 85% and OS was 98%. Although this combination needs additional study in randomized trials, this regimen also might be an interesting option for LPHL patients.

In conclusion, our study showed differences in prognostic factors, disease characteristics, and treatment outcomes between LPHL and cHL that might allow treatment algorithms to be changed, especially for early-stage LPHL patients.

	Authors' Disclosures of Potential Conflicts of Interest

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION Authors' Disclosures of... Author Contributions Appendix REFERENCES

 
The author(s) indicated no potential conflicts of interest.

	Author Contributions

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION Authors' Disclosures of... Author Contributions Appendix REFERENCES

 
Conception and design: Lucia Nogová, Thorsten Reineke, Corinne Brillant, Andreas Josting, Rolf-Peter Müller, Hans-Konrad Müller-Hermelink, Volker Diehl, Andreas Engert

Administrative support: Roman Skripnitchenko

Provision of study materials or patients: Lucia Nogová, Michal Sieniawski, Thomas Rüdiger, Andreas Josting, Henning Bredenfeld, Roman Skripnitchenko, Rolf-Peter Müller, Hans-Konrad Müller-Hermelink, Volker Diehl, Andreas Engert

Collection and assembly of data: Lucia Nogová, Thorsten Reineke, Corinne Brillant, Michal Sieniawski, Thomas Rüdiger, Henning Bredenfeld, Roman Skripnitchenko, Hans-Konrad Müller-Hermelink, Volker Diehl, Andreas Engert

Data analysis and interpretation: Lucia Nogová, Thorsten Reineke, Corinne Brillant, Volker Diehl, Andreas Engert

Manuscript writing: Lucia Nogova, Thorsten Reineke, Michal Sieniawski, Andreas Engert

Final approval of manuscript: Lucia Nogova, Thorsten Reineke, Corinne Brillant, Thomas Rüdiger, Michal Sieniawski, Andreas Engert

	Appendix

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION Authors' Disclosures of... Author Contributions Appendix REFERENCES

 
The Appendix is included in the full-text version of this article, available online at www.jco.org. It is not included in the PDF version (via Adobe® Reader®).

	NOTES

 
published online ahead of print at www.jco.org on December 17, 2007.

Supported by the Deutsche Krebshilfe (German Cancer Aid), the German Federal Ministry of Education and Research (BMBF), and the Kompetenznetz Maligne Lymphome (Competence Network Malignant Lymphoma).

Presented in part at the Hodgkin Lymphoma Simultaneous Session at the 48th American Society of Hematology Annual Meeting, December 9-12, 2006, Orlando, FL.

L.N. and T.R. contributed equally to this article.

Authors' disclosures of potential conflicts of interest and author contributions are found at the end of this article.

	REFERENCES

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION Authors' Disclosures of... Author Contributions Appendix REFERENCES

 
1. Diehl V, Sextro M, Franklin J, et al: Clinical presentation, course, and prognostic factors in lymphocyte-predominant Hodgkin's disease and lymphocyte-rich classical Hodgkin's disease: Report from the European Task Force on Lymphoma Project on Lymphocyte-Predominant Hodgkin's Disease. J Clin Oncol 17:776-783, 1999[Abstract/Free Full Text]

2. Anagnostopoulos I, Hansmann ML, Franssila K, et al: European Task Force on Lymphoma project on lymphocyte predominance Hodgkin disease: Histologic and immunohistologic analysis of submitted cases reveals 2 types of Hodgkin disease with a nodular growth pattern and abundant lymphocytes. Blood 96:1889-1899, 2000[Abstract/Free Full Text]

3. Boudová L, Torlakovic E, Delabie J, et al: Nodular lymphocyte-predominant Hodgkin lymphoma with nodules resembling T-cell/histiocyte-rich B-cell lymphoma: Differential diagnosis between nodular lymphocyte-predominant Hodgkin lymphoma and T-cell/histiocyte-rich B-cell lymphoma. Blood 102:3753-3758, 2003[Abstract/Free Full Text]

4. Nicholas DS, Harris S, Wright DH: Lymphocyte predominance Hodgkin's disease: An immunohistochemical study. Histopathology 16:157-165, 1990[Medline]

5. Jaffe E, Harris NL, Stein H, et al: Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. Lyon, France, IARC Press, 2001, pp 240-243

6. Thomas RK, Re D, Wolf J, et al: Part I: Hodgkin's lymphoma-molecular biology of Hodgkin and Reed-Sternberg cells. Lancet Oncol 5:11-18, 2004[CrossRef][Medline]

7. Trudel MA, Krikorian JG, Neiman RS: Lymphocyte predominance Hodgkin's disease: A clinicopathologic reassessment. Cancer 59:99-106, 1987[CrossRef][Medline]

8. Pappa VI, Norton AJ, Gupta RK, et al: Nodular type of lymphocyte predominant Hodgkin's disease: A clinical study of 50 cases. Ann Oncol 6:559-565, 1995[Abstract/Free Full Text]

9. Connors JM: Lymphocyte-predominant Hodgkin's lymphoma, in American Society of Hematology Education Program Book, Washington, DC, American Society of Hematology, 2001, pp 187-190

10. Rehwald U, Schulz H, Reiser M, et al: Treatment of relapsed CD20+ Hodgkin lymphoma with the monoclonal antibody rituximab is effective and well tolerated: Results of a phase 2 trial of the German Hodgkin Lymphoma Study Group. Blood 101:420-424, 2003[Abstract/Free Full Text]

11. Ekstrand BC, Lucas JB, Horwitz SM, et al: Rituximab in lymphocyte-predominant Hodgkin disease: Results of a phase 2 trial. Blood 101:4285-4289, 2003[Abstract/Free Full Text]

12. Nogová L, Reineke T, Eich HT, et al: Extended field radiotherapy, combined modality treatment or involved field radiotherapy for patients with stage IA lymphocyte-predominant Hodgkin's lymphoma: A retrospective analysis from the German Hodgkin Study Group (GHSG). Ann Oncol 16:1683-1687, 2005[Abstract/Free Full Text]

13. Pellegrino B, Terrier-Lacombe MJ, Oberlin O, et al: Lymphocyte-predominant Hodgkin's lymphoma in children: Therapeutic abstention after initial lymph node resection—A Study of the French Society of Pediatric Oncology. J Clin Oncol 21:2948-2952, 2003[Abstract/Free Full Text]

14. Murphy SB, Morgan ER, Katzenstein HM, et al: Results of little or no treatment for lymphocyte-predominant Hodgkin disease in children and adolescents. J Pediatr Hematol Oncol 25:684-687, 2003[CrossRef][Medline]

15. Hasenclever D, Diehl V: A prognostic score for advanced Hodgkin's disease: International Prognostic Factors Project on Advanced Hodgkin's Disease. N Engl J Med 339:1506-1514, 1998[Abstract/Free Full Text]

16. Solal-Celigny P: Follicular Lymphoma International Prognostic Index. Curr Treat Options Oncol 7:270-275, 2006[CrossRef][Medline]

17. Wilder RB, Schlembach PJ, Jones D, et al: European Organization for Research and Treatment of Cancer and Groupe d'Etude des Lymphomes de l'Adulte very favorable and favorable, lymphocyte-predominant Hodgkin disease. Cancer 94:1731-1738, 2002[CrossRef][Medline]

18. Shimabukuro-Vornhage A, Haverkamp H, Engert A, et al: Lymphocyte-rich classical Hodgkin's Lymphoma: Clinical presentation and treatment outcome in 100 patients treated within German Hodgkin's Study Group trials. J Clin Oncol 23:5739-5745, 2005[Abstract/Free Full Text]

19. Wirth A, Yuen K, Barton M, et al: Long-term outcome after radiotherapy alone for lymphocyte-predominant Hodgkin lymphoma: A retrospective multicenter study of the Australasian Radiation Oncology Lymphoma Group. Cancer 104:1221-1229, 2005[CrossRef][Medline]

20. Schlembach PJ, Wilder RB, Jones D, et al: Radiotherapy alone for lymphocyte-predominant Hodgkin's disease. Cancer J 8:377-383, 2002[Medline]

21. Raemaekers J, Kluin-Nelemans H, Teodorovic I, et al: The achievements of the EORTC Lymphoma Group: European Organisation for Research and Treatment of Cancer. Eur J Cancer 38:S107-S113, 2002 (suppl 4)[Medline]

22. Schulz H, Rehwald U, Morschhauser F, et al: Rituximab in relapsed lymphocyte predominant Hodgkin lymphoma: Long-term results of a phase 2 trial of the German Hodgkin Lymphoma Study Group (GHSG). Blood [epub ahead of print on October 15, 2007]

23. Younes A FL, Goy A, et al: Results of rituximab plus ABVD in 65 newly diagnosed patients with classical Hodgkin lymphoma: Improvement of event free survival in all International Prognostic Score groups. Presented at 48th American Society of Hematology Annual Meeting, December 9-12, 2006, Orlando, FL. Abstract Book, 2006, p 776a (abstr 2742)

Submitted April 8, 2007; accepted October 11, 2007.

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