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Ch P Chen - One of the best experts on this subject based on the ideXlab platform.
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the diagnostic utility of moc31 berep4 rcc marker and cd10 in the classification of renal cell carcinoma and renal oncocytoma an immunohistochemical analysis of 328 cases
Histopathology, 2004Co-Authors: Ch P Chen, Mt D HoAbstract:Aims: To demonstrate the diagnostic utility of MOC31, BerEP4, renal cell carcinoma marker (RCC Ma) and CD10 in the classification of RCC and renal oncocytoma, based upon a comprehensive immunohistochemical analysis. Methods and results: Immunohistochemistry was performed on 328 samples consisting of 256 clear cell/conventional, 27 papillary, 28 chromophobe, five collecting duct, five unclassified RCCs and seven renal oncocytomas using antibodies MOC31, BerEP4 and antibodies against cytokeratins (KL-1, CAM5.2, 34βE12, cytokeratin 7), RCC Ma, epithelial membrane antigen, E-cadherin, CD10, CD15 and vimentin. Multivariate analysis showed that MOC31, BerEP4, RCC Ma and CD10 have discriminatory value. MOC31 and BerEP4 chiefly labelled distal tubules of normal kidney while RCC Ma and CD10 labelled the proximal tubules. Twenty-three chromophobe RCCs (82%) were reactive for MOC31, while only four clear cell RCCs and three papillary RCCs were positive for this marker. Clear cell RCCs were characterized by a high positive rate for CD10 (82%) and a low positive rate for BerEP4 (27%). Papillary RCCs frequently coexpressed RCC Ma and BerEP4 (51%). All renal oncocytomas were negative for MOC31 and CD10. Conclusions: MOC31 has diagnostic merit in discerning chromophobe RCC. The CD10+/BerEP4– profile and RCC Ma+/BerEP4+ profile achieve moderate sensitivity and good specificity for clear cell RCC and papillary RCC, respectively. The non-reactivity for both MOC31 and CD10 is helpful in distinguishing renal oncocytoma from RCC. When properly selected, antibodies have immunohistochemical diagnostic utility for the classification of renal cortical epithelial tumours.
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the diagnostic utility of moc31 berep4 rcc marker and cd10 in the classification of renal cell carcinoma and renal oncocytoma an immunohistochemical analysis of 328 cases
Histopathology, 2004Co-Authors: Cc Pan, Ch P ChenAbstract:Aims To demonstrate the diagnostic utility of MOC31, BerEP4, renal cell carcinoma marker (RCC Ma) and CD10 in the classification of RCC and renal oncocytoma, based upon a comprehensive immunohistochemical analysis. Methods and results Immunohistochemistry was performed on 328 samples consisting of 256 clear cell/conventional, 27 papillary, 28 chromophobe, five collecting duct, five unclassified RCCs and seven renal oncocytomas using antibodies MOC31, BerEP4 and antibodies against cytokeratins (KL-1, CAM5.2, 34betaE12, cytokeratin 7), RCC Ma, epithelial membrane antigen, E-cadherin, CD10, CD15 and vimentin. Multivariate analysis showed that MOC31, BerEP4, RCC Ma and CD10 have discriminatory value. MOC31 and BerEP4 chiefly labelled distal tubules of normal kidney while RCC Ma and CD10 labelled the proximal tubules. Twenty-three chromophobe RCCs (82%) were reactive for MOC31, while only four clear cell RCCs and three papillary RCCs were positive for this marker. Clear cell RCCs were characterized by a high positive rate for CD10 (82%) and a low positive rate for BerEP4 (27%). Papillary RCCs frequently coexpressed RCC Ma and BerEP4 (51%). All renal oncocytomas were negative for MOC31 and CD10. Conclusions MOC31 has diagnostic merit in discerning chromophobe RCC. The CD10+/BerEP4- profile and RCC Ma+/BerEP4+ profile achieve moderate sensitivity and good specificity for clear cell RCC and papillary RCC, respectively. The non-reactivity for both MOC31 and CD10 is helpful in distinguishing renal oncocytoma from RCC. When properly selected, antibodies have immunohistochemical diagnostic utility for the classification of renal cortical epithelial tumours.
A Claudy - One of the best experts on this subject based on the ideXlab platform.
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differential expression of the cd10 antigen neutral endopeptidase in primary versus metastatic malignant melanomas of the skin
Melanoma Research, 2002Co-Authors: Jean Kanitakis, D Narvaez, A ClaudyAbstract:The CD10 antigen is a neutral endopeptidase expressed by a variety of mesenchymal tumours (haemopoietic or not), including a subset of malignant melanomas. We investigated the expression of CD10 in formalin-fixed, paraffin-embedded tissue specimens of 72 cutaneous melanomas (28 primary, 26 metastatic to the skin and 18 lymph node metastases). The CD10 antigen was expressed by 18 of the 26 (69%) and 11 of the 18 (61%) melanomas metastatic to the skin or lymph nodes, respectively; in contrast, only six of the 28 primary melanomas (21.4%) expressed appreciable CD10 reactivity, and expression was usually lower (in terms of the percentage of immunoreactive cells) than that found in metastatic tumours. The sensitivity, specificity, and positive and negative predictive values of CD10 positivity for metastatic malignant melanoma were calculated to be 0.66, 0.79, 0.83 and 0.6, respectively. Our results suggest that the CD10 antigen is upregulated during the process of metastasis in melanomas. From a diagnostic point of view, the expression of CD10 appears to be an additional feature for the histological differential diagnosis between primary and metastatic melanomas.
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expression of the cd10 antigen neutral endopeptidase by mesenchymal tumors of the skin
Anticancer Research, 2000Co-Authors: Jean Kanitakis, Dominique Bourchany, A ClaudyAbstract:Background: The CD10 (or CALLA) antigen is a neutral endopeptidase expressed by a variety of non-hemopoietic cells, including fibroblasts in various tissues. So far little or conflicting data exist concerning the expression of CD10 in normal and pathologic skin. Methods. We investigated the immunohistochemical expression of the CD10 antigen on formalin-fixed, paraffin-embedded tissue specimens of normal skin and 162 cutaneous proliferative lesions, mostly mesenchymal tumors. Results: In normal skin CD10 immunoreactivity was found in periadnexal mesenchymal cells. In skin tumors, CD10+ cells were found mainly in dermatofibromas and, to a lesser extent, in Dermatofibrosarcoma protuberans and neurofibromas. Metastatic (and to a lesser extent primary) melanomas also occasionally expressed CD10. Conclusion: Our results show that the CD10 antigen is expressed by mesenchymal cells of normal human dermis, presumably encompassing a subset of CD34+ dermal dendrocytes and/or periadnexal fibroblasts. The CD10 antigen could be used as an adjunct to the diagnosis of some spindle-cell cutaneous tumors such as dermatofibromas and Dermatofibrosarcoma protuberans, but its value as a single marker is rather limited. The possible role of CD10 as a progression marker in melanoma is interesting and merits further study.
Sigit Kirana Lintang Bhima - One of the best experts on this subject based on the ideXlab platform.
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perbandingan pemberian brodifakum ld50 dan LD100 terhadap perubahan gambaran histopatologi usus halus tikus wistar
DIPONEGORO MEDICAL JOURNAL ( JURNAL KEDOKTERAN DIPONEGORO ), 2016Co-Authors: Alfian Salahudin Al Ayoubi, Tuntas Dhanardhono, Sigit Kirana Lintang BhimaAbstract:Background : Brodifacoum is an anticoagulant substance which usually used as pest control, but this substance has a poisoning effect the body. Brodifacoum is absorbed through gastrointestinal tract which can cause the disorder of blod clotting by slowing down the process of epoxide reductase of vitamin-K. Aim : To know the comparison of Histopathology Rattus norvegicus Intestine against brodifacoum administration LD50 and LD100. Methods : This study was an experimental study with post test only group design. The sample of this study are 27 Rattus norvegicus which given per oral administration of brodifacoum. Barthel Manja scores were used to assess changes in intestine Histopatology. Normal and desquamation are a minor damage, while erosion and ulcers are major damage. Non-parametric test of Mann-Whitney to the results are revealed significant if p <0.05. Results : On LD50, 2 rats died on days 3, 5 on day 5, and 2 rats terminated on day 7. In LD100 2 rats died on day 3, 2 on day 5, and 5 rats terminated on day 7. On LD50 groups there are 66,67% minor damage and 33,33% major damage, while in LD100 groups there are 55,56% minor damage and 44,44% major damage. Test non parametric Mann-Whitney in the control group with LD50 was found p = 0.269, in control group with LD100 was found p = 0106, then group with the LD50 and LD100 found p = 0.159. Conclusion : There are not significant differentiation of histopatology picture between LD50 and LD100 dose ( p = 0.159 )
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perbandingan pemberian brodifakum dosis ld50 dan LD100 terhadap residu brodifakum pada hepar tikus wistar
DIPONEGORO MEDICAL JOURNAL ( JURNAL KEDOKTERAN DIPONEGORO ), 2016Co-Authors: Nugraha Adiyasa, Tuntas Dhanardhono, Sigit Kirana Lintang BhimaAbstract:Latar Belakang : Brodifakum adalah senyawa yang umumnya digunakan sebagai racun tikus. Namun, sering disalah gunakan pada kasus kriminal. Brodifakum akan di metabolisme tubuh melalui organ ekskresi diantaranya hepar. Paparan brodifakum dalam dosis yang berbeda akan menghasilkan kadar residu yang berbeda pula. Tujuan: Mengetahui perbandingan pemberian brodifakum dosis LD50 dan LD100 terhadap jumlah residu brodifakum pada hepar tikus wistar. Metode: Penelitian ini merupakan penelitian eksperimental dengan menggunakan pendekatan post test only control group design. 27 sampel tikus wistar diberikan perlakuan pemberian brodifakum secara per oral. Residu brodifakum dideteksi menggunakan High Performance Liquid Chromatography. Dilakukan analisa deskriptif, uji non parametrik Mann-Whitney terhadap data. Hasil analisis dinyatakan bermakna bila nilai p<0,05. Hasil: Konsentrasi brodifakum pada hepar hewan coba meningkat berdasarkan jumlah brodifakum yang dimakan. Tikus mati pada hari ke-3 sebanyak 4, pada hari ke-5 sebanyak 7 dan pada hari terminasi sebanyak 16 tikus diterminasi. Kadar residu terendah didapatkan pada angka 0,00002 mg/kg dan tertinggi pada angka 0,00100 mg/kg. Uji Mann-Whitney didapatkan hasil perbandingan residu brodifakum pada hepar tikus pada dosis kontrol dan LD50 (p=0,001) dan pada kontrol dan LD100 (p=0,000). Antara jumlah residu brodifakum pada hepar tikus pada dosis LD50 dan LD100 (p=0,539). Simpulan: Tidak ada perbedaan bermakna antara jumlah residu brodifakum pada hepar tikus pada dosis LD50 dan LD100 (p=0,539).
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perbandingan pemberian brodifakum ld50 dan LD100 terhadap perubahan gambaran patologi anatomi gaster tikus wistar
Jurnal Kedokteran Diponegoro, 2015Co-Authors: Ricky P Renardi, Tuntas Dhanardhono, Sigit Kirana Lintang BhimaAbstract:Background : Brodifakum is a substance that often used as rat poison and disrupt the process of blood coagulation.As a result of this disorder can cause bleeding in vital organs of rat. This study was conducted to assess the gastric anatomic pathology due to Brodifakum. Aim : To know the comparison of Anatomical Pathology Rattus norvegicus Gastric againstbrodifacoum administration LD50 and LD100. Methods :This study was an experimental study with post test only group design. The sample of this study are 27 Rattus norvegicus which given per oral administration of brodifacoum. Barthel Manja scores were used to assess changes in gastric Anatomical Pathology.Normal and desquamation are a minor damage, while erosion and ulcers are major damage.Non-parametric test of Mann-Whitney to the results are revealed significant if p <0.05. Results :On LD50, 2 rats died on days 3, 5 on day 5, and 2 rats terminated on day 7. In LD100 2 rats died on day 3, 2 on day 5, and 5 rats terminated on day 7. On LD50 groups there are 44.44% minor damage and55.56% major damage,whilein LD100 discovered at 100% major damage. Test non parametric Mann-Whitney in the control group with LD50was found p = 0.106, in control group with LD100was found p = 0.001, then group with the LD50and LD100 found p = 0.028. Conclusion :There are significant differentiation of anatomic pathology picture between LD50 and LD100 dose ( p = 0.028 )
Mt D Ho - One of the best experts on this subject based on the ideXlab platform.
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the diagnostic utility of moc31 berep4 rcc marker and cd10 in the classification of renal cell carcinoma and renal oncocytoma an immunohistochemical analysis of 328 cases
Histopathology, 2004Co-Authors: Ch P Chen, Mt D HoAbstract:Aims: To demonstrate the diagnostic utility of MOC31, BerEP4, renal cell carcinoma marker (RCC Ma) and CD10 in the classification of RCC and renal oncocytoma, based upon a comprehensive immunohistochemical analysis. Methods and results: Immunohistochemistry was performed on 328 samples consisting of 256 clear cell/conventional, 27 papillary, 28 chromophobe, five collecting duct, five unclassified RCCs and seven renal oncocytomas using antibodies MOC31, BerEP4 and antibodies against cytokeratins (KL-1, CAM5.2, 34βE12, cytokeratin 7), RCC Ma, epithelial membrane antigen, E-cadherin, CD10, CD15 and vimentin. Multivariate analysis showed that MOC31, BerEP4, RCC Ma and CD10 have discriminatory value. MOC31 and BerEP4 chiefly labelled distal tubules of normal kidney while RCC Ma and CD10 labelled the proximal tubules. Twenty-three chromophobe RCCs (82%) were reactive for MOC31, while only four clear cell RCCs and three papillary RCCs were positive for this marker. Clear cell RCCs were characterized by a high positive rate for CD10 (82%) and a low positive rate for BerEP4 (27%). Papillary RCCs frequently coexpressed RCC Ma and BerEP4 (51%). All renal oncocytomas were negative for MOC31 and CD10. Conclusions: MOC31 has diagnostic merit in discerning chromophobe RCC. The CD10+/BerEP4– profile and RCC Ma+/BerEP4+ profile achieve moderate sensitivity and good specificity for clear cell RCC and papillary RCC, respectively. The non-reactivity for both MOC31 and CD10 is helpful in distinguishing renal oncocytoma from RCC. When properly selected, antibodies have immunohistochemical diagnostic utility for the classification of renal cortical epithelial tumours.
Jana Markova - One of the best experts on this subject based on the ideXlab platform.
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treatment of stage i ii a non bulky hodgkin s lymphoma hl an individual patient data comparison of german hodgkin study group ghsg hd10 and hd11 combined modality therapy cmt and ncic clinical trials group ncic ctg hd 6 abvd alone
Blood, 2012Co-Authors: Annette E Hay, Beate Klimm, Bingshu E Chen, Helen Goergen, Lois E Shepherd, Michael Fuchs, Mary K Gospodarowicz, Peter Borchmann, Joseph M Connors, Jana MarkovaAbstract:Abstract 548 Background: Excellent results are seen in HL patients with stage I-IIA disease treated with CMT that includes involved field radiation therapy (IFRT), as per GHSG HD10 [Engert NEJM 2010] and HD11 [Eich JCO 2010] or with ABVD alone, as per NCIC CTG/ECOG HD.6 [Meyer NEJM 2012]. Comparing these reports is complicated by differences in eligibility, staging, endpoints and follow-up duration. Our objectives were to use individual patient data from these 3 trials to compare outcomes after standardizing patient eligibility. Methods: Potentially eligible patients were those treated with 2 cycles of ABVD/20 Gy IFRT on GHSG HD10, 4 cycles of ABVD/30 Gy IFRT on GHSG HD11 and 4–6 cycles of ABVD alone on NCIC CTG HD.6. To be included in analysis, patients were required to be eligible for GHSG HD10 or HD11 and NCIC CTG HD.6. Eligibility of HD10/11 patients for HD.6 was determined by the GHSG by applying HD.6 protocol criteria. Anonymized individual patient data of eligible patients was forwarded to NCIC CTG along with reasons for ineligibility of other patients. Eligibility of HD.6 patients for HD10/11 was determined by NCIC CTG by applying HD10/11 protocol criteria with listing of reasons for ineligibility. Eligibility questions were resolved through consensus. Patients meeting mutually inclusive eligibility criteria were stratified by a propensity score (PSc) based on age, gender, stage, ESR and number of disease sites. Outcomes were based on Revised Response Criteria for Malignant Lymphoma [Cheson JCO 2007]; no trial incorporated PET scanning. The primary outcome measure was progression-free survival (PFS), which includes disease progression and death from any cause as events. Secondary outcomes included overall survival (OS) and time to progression (TTP), which includes disease progression and death from HL as events. A priori subsets for analysis included eligibility for HD10 vs. HD11 and CR/CRu status after 2 cycles of ABVD among those eligible for both HD10 and HD.6. Cox models stratified by PSc were used to obtain hazard ratios (HR) for PFS, OS and TTP; HRs are expressed as GHSG HD10/11 relative to NCIC CTG HD.6. Results: Of 655 patients eligible for selected arms of HD10/HD11, 406 were eligible when applying the inclusion criteria for HD.6 (HD10 = 254; HD11 = 152). Most common reasons for ineligibility were B symptoms (n=127) and large mediastinal mass (n=80). Of 196 HD.6 patients, 182 were eligible for HD10 (n=110) or HD11 (n=71; 1 patient not assignable). Median follow-up for both HD10 and HD11 was 91 months and for HD.6 was 134 months. Results that include all eligible patients are shown in table; TTP was superior in GHSG trials. In the HD10/HD.6 subset, 8-yr PFS was 87% vs 82% (HR=0.58; 95% CI=0.32–1.05) and OS was 96% vs 94% (HR=0.65; 95% CI=0.25–1.72). Among those with CR/CRu after 2 cycles of ABVD, 8-yr PFS was 87% vs 95% (HR=2.8; 95% CI=0.64–12.5) and OS was 96% vs 100%. Among those without CR/CRu after 2 cycles of ABVD, 8-yr PFS was 88% vs 74% (HR=0.35; 95% CI=0.16–0.79) and OS was 95% vs 91% (HR=0.42; 95% CI=0.12–1.44). In the HD11/HD.6 subset, 8-yr PFS was 91% vs 91% (HR=1.15; 95% CI=0.45–2.97) and OS was 95% vs 97% (HR=2.03; 95% CI=0.53–7.79). Among 406 HD10/11 patients, there have been 19 deaths; 7 were attributed to HL or immediate treatment toxicity and 12 to other causes. Among 182 HD.6 patients, there have been 10 deaths; 5 were attributed to HL or immediate treatment toxicity and 5 to other causes. Conclusions: In this non-randomized cohort comparison, TTP was superior and PFS trended to being superior in patients treated with CMT on HD10/11. No differences in OS are evident; longer follow-up is needed to assess trade-offs between disease control and risks of late treatment effects. The role of IFRT in attaining long-term disease control appears to be especially important in those who do not attain CR/CRu status after 2 cycles of ABVD. As outcomes of those eligible for HD10/HD.6 and treated with 4–6 cycles of ABVD alone were excellent if CR/CRu was attained after 2 cycles of ABVD, these data support more recent strategies evaluating response-adapted approaches for use of IFRT. Disclosures: Borchmann:Millenium The Takeda Oncology Company: Research Funding; Takeda Pharma GmbH: Travel Grants, Travel Grants Other. Horning:Genentech: Employment; Roche: Equity Ownership. Engert:Millenium The Takeda Oncology Company: Honoraria. Meyer:Lilly: Honoraria, Research Funding; Celgene: Honoraria, Research Funding; Amgen Canada: Research Funding; Ariad Pharma: Research Funding; Astex Therapeutics: Research Funding; AstraZeneca: Research Funding; Bristol-Myers Squibb: Research Funding; GlaxoSmithKline: Research Funding; Janssen Ortho: Research Funding; Novartis: Research Funding; Oncothyreon: Research Funding; Pfizer: Research Funding; Roche: Research Funding; Sanofi-Aventis: Research Funding; Schering Canada: Research Funding.
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treatment of stage i ii a non bulky hodgkin s lymphoma hl an individual patient data comparison of german hodgkin study group ghsg hd10 and hd11 combined modality therapy cmt and ncic clinical trials group ncic ctg hd 6 abvd alone
Blood, 2012Co-Authors: Annette E Hay, Beate Klimm, Bingshu E Chen, Helen Goergen, Lois E Shepherd, Michael Fuchs, Mary K Gospodarowicz, Peter Borchmann, Joseph M Connors, Jana MarkovaAbstract:Abstract Abstract 548 Background: Excellent results are seen in HL patients with stage I-IIA disease treated with CMT that includes involved field radiation therapy (IFRT), as per GHSG HD10 [Engert NEJM 2010] and HD11 [Eich JCO 2010] or with ABVD alone, as per NCIC CTG/ECOG HD.6 [Meyer NEJM 2012]. Comparing these reports is complicated by differences in eligibility, staging, endpoints and follow-up duration. Our objectives were to use individual patient data from these 3 trials to compare outcomes after standardizing patient eligibility. Methods: Potentially eligible patients were those treated with 2 cycles of ABVD/20 Gy IFRT on GHSG HD10, 4 cycles of ABVD/30 Gy IFRT on GHSG HD11 and 4–6 cycles of ABVD alone on NCIC CTG HD.6. To be included in analysis, patients were required to be eligible for GHSG HD10 or HD11 and NCIC CTG HD.6. Eligibility of HD10/11 patients for HD.6 was determined by the GHSG by applying HD.6 protocol criteria. Anonymized individual patient data of eligible patients was forwarded to NCIC CTG along with reasons for ineligibility of other patients. Eligibility of HD.6 patients for HD10/11 was determined by NCIC CTG by applying HD10/11 protocol criteria with listing of reasons for ineligibility. Eligibility questions were resolved through consensus. Patients meeting mutually inclusive eligibility criteria were stratified by a propensity score (PSc) based on age, gender, stage, ESR and number of disease sites. Outcomes were based on Revised Response Criteria for Malignant Lymphoma [Cheson JCO 2007]; no trial incorporated PET scanning. The primary outcome measure was progression-free survival (PFS), which includes disease progression and death from any cause as events. Secondary outcomes included overall survival (OS) and time to progression (TTP), which includes disease progression and death from HL as events. A priori subsets for analysis included eligibility for HD10 vs. HD11 and CR/CRu status after 2 cycles of ABVD among those eligible for both HD10 and HD.6. Cox models stratified by PSc were used to obtain hazard ratios (HR) for PFS, OS and TTP; HRs are expressed as GHSG HD10/11 relative to NCIC CTG HD.6. Results: Of 655 patients eligible for selected arms of HD10/HD11, 406 were eligible when applying the inclusion criteria for HD.6 (HD10 = 254; HD11 = 152). Most common reasons for ineligibility were B symptoms (n=127) and large mediastinal mass (n=80). Of 196 HD.6 patients, 182 were eligible for HD10 (n=110) or HD11 (n=71; 1 patient not assignable). Median follow-up for both HD10 and HD11 was 91 months and for HD.6 was 134 months. Results that include all eligible patients are shown in table; TTP was superior in GHSG trials. Endpoint GHSG HD10/11 NCIC CTG HD.6 HR 95% CI 8-yr PFS 89% 86% 0.71 0.42-1.18 8-yr OS 95% 95% 1.09 0.49-2.40 8-yr TTP 93% 87% 0.44 0.24-0.78 In the HD10/HD.6 subset, 8-yr PFS was 87% vs 82% (HR=0.58; 95% CI=0.32–1.05) and OS was 96% vs 94% (HR=0.65; 95% CI=0.25–1.72). Among those with CR/CRu after 2 cycles of ABVD, 8-yr PFS was 87% vs 95% (HR=2.8; 95% CI=0.64–12.5) and OS was 96% vs 100%. Among those without CR/CRu after 2 cycles of ABVD, 8-yr PFS was 88% vs 74% (HR=0.35; 95% CI=0.16–0.79) and OS was 95% vs 91% (HR=0.42; 95% CI=0.12–1.44). In the HD11/HD.6 subset, 8-yr PFS was 91% vs 91% (HR=1.15; 95% CI=0.45–2.97) and OS was 95% vs 97% (HR=2.03; 95% CI=0.53–7.79). Among 406 HD10/11 patients, there have been 19 deaths; 7 were attributed to HL or immediate treatment toxicity and 12 to other causes. Among 182 HD.6 patients, there have been 10 deaths; 5 were attributed to HL or immediate treatment toxicity and 5 to other causes. Conclusions: In this non-randomized cohort comparison, TTP was superior and PFS trended to being superior in patients treated with CMT on HD10/11. No differences in OS are evident; longer follow-up is needed to assess trade-offs between disease control and risks of late treatment effects. The role of IFRT in attaining long-term disease control appears to be especially important in those who do not attain CR/CRu status after 2 cycles of ABVD. As outcomes of those eligible for HD10/HD.6 and treated with 4–6 cycles of ABVD alone were excellent if CR/CRu was attained after 2 cycles of ABVD, these data support more recent strategies evaluating response-adapted approaches for use of IFRT. Disclosures: Borchmann: Millenium The Takeda Oncology Company: Research Funding; Takeda Pharma GmbH: Travel Grants, Travel Grants Other. Horning: Genentech: Employment; Roche: Equity Ownership. Engert: Millenium The Takeda Oncology Company: Honoraria. Meyer: Lilly: Honoraria, Research Funding; Celgene: Honoraria, Research Funding; Amgen Canada: Research Funding; Ariad Pharma: Research Funding; Astex Therapeutics: Research Funding; AstraZeneca: Research Funding; Bristol-Myers Squibb: Research Funding; GlaxoSmithKline: Research Funding; Janssen Ortho: Research Funding; Novartis: Research Funding; Oncothyreon: Research Funding; Pfizer: Research Funding; Roche: Research Funding; Sanofi-Aventis: Research Funding; Schering Canada: Research Funding.