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  1 / 29065 MEDLINE  
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PMID:29322203
Author:Dada R
Address:Department of Oncology MBC J-64, King Faisal Specialist Hospital and Research Center, P.O. Box 40047, Jeddah, 21499, Kingdom of Saudi Arabia. rdada@kfshrc.edu.sa.
Title:Program death inhibitors in classical Hodgkin's lymphoma: a comprehensive review.
Source:Ann Hematol; 97(4):555-561, 2018 Apr.
ISSN:1432-0584
Country of publication:Germany
Language:eng
Abstract:Cancer cells are able to induce immune system tolerance through different mechanisms. Recent achievements in the understanding of tumor microenvironment, invasion, and metastasizing have contributed to accelerated drug developments and approvals. Hodgkin lymphoma (HL) cells are the minority in a lymphocyte-rich microenvironment of HL tissue. The program death-1 (PD-1)/PD-ligand-1 checkpoint is one of the known effective pathways in classical HL to escape the immune system cells. The approval of PD-1 inhibitors in different cancer types with exciting response rates is truly revolutionizing our treatment armamentarium against cancer in general and classical HL in specific. Although the disease is one of the most curable tumors, we still need better outcome with more gentle treatment, especially for relapsed and refractory (r/r) patients. In this article, we review the current literature on immune checkpoint inhibitors and currently ongoing studies with nivolumab and pembrolizumab in r/r classical HL.
Publication type:JOURNAL ARTICLE; REVIEW
Name of substance:0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 0 (Antineoplastic Agents, Immunological); 0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (Neoplasm Proteins); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 31YO63LBSN (nivolumab); DPT0O3T46P (pembrolizumab)


  2 / 29065 MEDLINE  
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PMID:29157619
Author:Szalat R; Munshi NC
Address:Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, M230 Boston, MA 02215, USA.
Title:Diagnosis of Castleman Disease.
Source:Hematol Oncol Clin North Am; 32(1):53-64, 2018 02.
ISSN:1558-1977
Country of publication:United States
Language:eng
Abstract:Castleman disease (CD) is a rare and heterogenous group of disorders sharing in common an abnormal lymph node pathology. CD comprises distinct subtypes with different prognoses. Unicentric CD and multicentric CD are featured by specific systemic manifestations and may be associated with Kaposi sarcoma, non-Hodgkin and Hodgkin lymphoma, and POEMS syndrome. Multicentric CD is classically associated with systemic symptoms and poorer prognosis. In this article, the authors review how to diagnose the disease, keeping in context the clinical findings, biochemical changes and complications associated with CD.
Publication type:JOURNAL ARTICLE; REVIEW


  3 / 29065 MEDLINE  
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Clinical Trials Registry
Clinical Trials Registry
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PMID:29224502
Author:Connors JM; Jurczak W; Straus DJ; Ansell SM; Kim WS; Gallamini A; Younes A; Alekseev S; Illés Á; Picardi M; Lech-Maranda E; Oki Y; Feldman T; Smolewski P; Savage KJ; Bartlett NL; Walewski J; Chen R; Ramchandren R; Zinzani PL; Cunningham D; Rosta A; Josephson NC; Song E; Sachs J; Liu R; Jolin HA; Huebner D; Radford J; ECHELON-1 Study Group
Address:From the University of British Columbia and the Department of Medical Oncology, British Columbia Cancer Agency Centre for Lymphoid Cancer, Vancouver, Canada (J.M.C., K.J.S.); the Department of Hematology, Jagiellonian University, Krakow (W.J.), the Department of Hematology, Institute of Hematology a
Title:Brentuximab Vedotin with Chemotherapy for Stage III or IV Hodgkin's Lymphoma.
Source:N Engl J Med; 378(4):331-344, 2018 01 25.
ISSN:1533-4406
Country of publication:United States
Language:eng
Abstract:BACKGROUND: Brentuximab vedotin is an anti-CD30 antibody-drug conjugate that has been approved for relapsed and refractory Hodgkin's lymphoma. METHODS: We conducted an open-label, multicenter, randomized phase 3 trial involving patients with previously untreated stage III or IV classic Hodgkin's lymphoma, in which 664 were assigned to receive brentuximab vedotin, doxorubicin, vinblastine, and dacarbazine (A+AVD) and 670 were assigned to receive doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD). The primary end point was modified progression-free survival (the time to progression, death, or noncomplete response and use of subsequent anticancer therapy) as adjudicated by an independent review committee. The key secondary end point was overall survival. RESULTS: At a median follow-up of 24.6 months, 2-year modified progression-free survival rates in the A+AVD and ABVD groups were 82.1% (95% confidence interval [CI], 78.8 to 85.0) and 77.2% (95% CI, 73.7 to 80.4), respectively, a difference of 4.9 percentage points (hazard ratio for an event of progression, death, or modified progression, 0.77; 95% CI, 0.60 to 0.98; P=0.04). There were 28 deaths with A+AVD and 39 with ABVD (hazard ratio for interim overall survival, 0.73 [95% CI, 0.45 to 1.18]; P=0.20) [corrected]. All secondary efficacy end points trended in favor of A+AVD. Neutropenia occurred in 58% of the patients receiving A+AVD and in 45% of those receiving ABVD; in the A+AVD group, the rate of febrile neutropenia was lower among the 83 patients who received primary prophylaxis with granulocyte colony-stimulating factor than among those who did not (11% vs. 21%). Peripheral neuropathy occurred in 67% of patients in the A+AVD group and in 43% of patients in the ABVD group; 67% of patients in the A+AVD group who had peripheral neuropathy had resolution or improvement at the last follow-up visit. Pulmonary toxicity of grade 3 or higher was reported in less than 1% of patients receiving A+AVD and in 3% of those receiving ABVD. Among the deaths that occurred during treatment, 7 of 9 in the A+AVD group were associated with neutropenia and 11 of 13 in the ABVD group were associated with pulmonary-related toxicity. CONCLUSIONS: A+AVD had superior efficacy to ABVD in the treatment of patients with advanced-stage Hodgkin's lymphoma, with a 4.9 percentage-point lower combined risk of progression, death, or noncomplete response and use of subsequent anticancer therapy at 2 years. (Funded by Millennium Pharmaceuticals and Seattle Genetics; ECHELON-1 ClinicalTrials.gov number, NCT01712490 ; EudraCT number, 2011-005450-60 .).
Publication type:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Immunoconjugates); 0 (Immunologic Factors); 11056-06-7 (Bleomycin); 5V9KLZ54CY (Vinblastine); 7GR28W0FJI (Dacarbazine); 7XL5ISS668 (brentuximab vedotin); 80168379AG (Doxorubicin)


  4 / 29065 MEDLINE  
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PMID:29443738
Author:Qin Y; Lu L; Lu Y; Yang K
Address:Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan.
Title:Hodgkin lymphoma involving the tonsil misdiagnosed as tonsillar carcinoma: A case report and review of the literature.
Source:Medicine (Baltimore); 97(7):e9761, 2018 Feb.
ISSN:1536-5964
Country of publication:United States
Language:eng
Abstract:RATIONALE: Primary Hodgkin lymphoma (HL) involving the tonsil is extremely rare. Only about 20 such cases with verification of biopsy and immunohistochemistry have been reported. Because of its rarity and unremarkable clinical presentation, a timely correct diagnosis is very challenging. PATIENT CONCERNS: A 43-year-old man complained left tonsillar enlargement and painless masses in left neck, with night sweat. The clinical examination found a marked tonsillar asymmetry, with an enlarged left tonsil and ipsilateral cervical lymphadenopathy and a normal right tonsil. DIAGNOSIS: The patient was initially regarded as tonsillar lymphoepithelial carcinoma. INTERVENTIONS: The patient received a resection of left tonsil and left cervical masses and then was definitively diagnosed as HL (IIEB). He was managed by 6 cycles of chemotherapy (adriamycin, bleomycin, vinblastine, and dacarbazine) and radiotherapy to the Waldeyer ring. OUTCOMES: The patient has been disease free for more than 3 years after diagnosis. LESSONS: As the reason of an extreme rare occurrence of HL involving the tonsil, doctors can easily misdiagnose the disease as tonsillar lymphoepithelial carcinoma. This case serves as a reminder important role of biopsy.
Publication type:CASE REPORTS; JOURNAL ARTICLE; REVIEW


  5 / 29065 MEDLINE  
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PMID:29228840
Author:Chang A; Schlafer D; Flowers CR; Allen PB
Address:a Department of Hematology and Medical Oncology , Winship Cancer Institute, Emory University School of Medicine , Atlanta , GA , USA.
Title:Investigational PD-1 inhibitors in HL and NHL and biomarkers for predictors of response and outcome.
Source:Expert Opin Investig Drugs; 27(1):55-70, 2018 Jan.
ISSN:1744-7658
Country of publication:England
Language:eng
Abstract:INTRODUCTION: Inhibitors against the PD-1/PD-L1 pathway are revolutionizing the treatment and management of malignancies. Areas covered: We summarize our current understanding of the function of PD-1, its role in immune evasion, the clinical data available that support the use of PD-1 antagonist in Hodgkin and non-Hodgkin lymphomas, and potential predictors of response. Expert opinion: We anticipate that in the next 10 years, agents that modulate the immune system such as PD-1 antagonists will be increasingly used in favor over traditional cytotoxic chemotherapeutic agents. PD-1 antagonists will be combined with future immunotherapies or used as adjuncts to cellular therapy to boost tumor-specific immune responses.
Publication type:JOURNAL ARTICLE; REVIEW
Name of substance:0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (Drugs, Investigational); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor)


  6 / 29065 MEDLINE  
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PMID:29271057
Author:Reddy JP; Hernandez M; Gunther JR; Dabaja BS; Martin GV; Jiang W; Akhtari M; Allen PK; Atkinson BJ; Smith GL; Pinnix CC; Milgrom SA; Abou Yehia Z; Osborne EM; Oki Y; Lee H; Hagemeister F; Fanale MA
Address:Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Title:Pre-treatment neutrophil/lymphocyte ratio and platelet/lymphocyte ratio are prognostic of progression in early stage classical Hodgkin lymphoma.
Source:Br J Haematol; 180(4):545-549, 2018 02.
ISSN:1365-2141
Country of publication:England
Language:eng
Abstract:To determine whether pre-treatment neutrophil/lymphocyte (NLR) or platelet/lymphocyte ratios (PLR) are predictive for progression in early-stage classical Hodgkin lymphoma (cHL), we derived NLR and PLR values for 338 stage I/II cHL patients and appropriate cut-off point values to define progression. Two-year freedom from progression (FFP) for patients with NLR ≥6·4 was 82·2% vs. 95·7% with NLR <6·4 (P < 0·001). Similarly, 2-year FFP was 84·3% for patients with PLR ≥266·2 vs. 96·1% with PLR <266·2 (P = 0·003). On univariate analysis, both NLR and PLR were significantly associated with worse FFP (P = 0·001). On multivariate analysis, PLR remained a significant, independent prognostic factor (P < 0·001).
Publication type:JOURNAL ARTICLE


  7 / 29065 MEDLINE  
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PMID:29248133
Author:Mikkilineni L; Whitaker-Menezes D; Domingo-Vidal M; Sprandio J; Avena P; Cotzia P; Dulau-Florea A; Gong J; Uppal G; Zhan T; Leiby B; Lin Z; Pro B; Sotgia F; Lisanti MP; Martinez-Outschoorn U
Address:Department of Medical Oncology, National Cancer Institute, Bethesda, MD.
Title:Hodgkin lymphoma: A complex metabolic ecosystem with glycolytic reprogramming of the tumor microenvironment.
Source:Semin Oncol; 44(3):218-225, 2017 06.
ISSN:1532-8708
Country of publication:United States
Language:eng
Abstract:BACKGROUND: Twenty percent of patients with classical Hodgkin Lymphoma (cHL) have aggressive disease defined as relapsed or refractory disease to initial therapy. At present we cannot identify these patients pre-treatment. The microenvironment is very important in cHL because non-cancer cells constitute the majority of the cells in these tumors. Non-cancer intra-tumoral cells, such as tumor-associated macrophages (TAMs) have been shown to promote tumor growth in cHL via crosstalk with the cancer cells. Metabolic heterogeneity is defined as high mitochondrial metabolism in some tumor cells and glycolysis in others. We hypothesized that there are metabolic differences between cancer cells and non-cancer tumor cells, such as TAMs and tumor-infiltrating lymphocytes in cHL and that greater metabolic differences between cancer cells and TAMs are associated with poor outcomes. METHODS: A case-control study was conducted with 22 tissue samples of cHL at diagnosis from a single institution. The case samples were from 11 patients with aggressive cHL who had relapsed after standard treatment with adriamycin, bleomycin, vinblastine, and dacarbazine (ABVD) or were refractory to this treatment. The control samples were from 11 patients with cHL who achieved a remission and never relapsed after ABVD. Reactive non-cancerous lymph nodes from four subjects served as additional controls. Samples were stained by immunohistochemistry for three metabolic markers: translocase of the outer mitochondrial membrane 20 (TOMM20), monocarboxylate transporter 1 (MCT1), and monocarboxylate transporter 4 (MCT4). TOMM20 is a marker of mitochondrial oxidative phosphorylation (OXPHOS) metabolism. Monocarboxylate transporter 1 (MCT1) is the main importer of lactate into cells and is a marker of OXPHOS. Monocarboxylate transporter 4 (MCT4) is the main lactate exporter out of cells and is a marker of glycolysis. The immunoreactivity for TOMM20, MCT1, and MCT4 was scored based on staining intensity and percentage of positive cells, as follows: 0 for no detectable staining in > 50% of cells; 1+ for faint to moderate staining in > 50% of cells, and 2+ for high or strong staining in > 50% of cells. RESULTS: TOMM20, MCT1, and MCT4 expression was significantly different in Hodgkin and Reed Sternberg (HRS) cells, which are the cancerous cells in cHL compared with TAMs and tumor-associated lymphocytes. HRS have high expression of TOMM20 and MCT1, while TAMs have absent expression of TOMM20 and MCT1 in all but two cases. Tumor-infiltrating lymphocytes have low TOMM20 expression and absent MCT1 expression. Conversely, high MCT4 expression was found in TAMs, but absent in HRS cells in all but one case. Tumor-infiltrating lymphocytes had absent MCT4 expression. Reactive lymph nodes in contrast to cHL tumors had low TOMM20, MCT1, and MCT4 expression in lymphocytes and macrophages. High TOMM20 and MCT1 expression in cancer cells with high MCT4 expression in TAMs is a signature of high metabolic heterogeneity between cancer cells and the tumor microenvironment. A high metabolic heterogeneity signature was associated with relapsed or refractory cHL with a hazard ratio of 5.87 (1.16-29.71; two-sided P < .05) compared with the low metabolic heterogeneity signature. CONCLUSION: Aggressive cHL exhibits features of metabolic heterogeneity with high mitochondrial metabolism in cancer cells and high glycolysis in TAMs, which is not seen in reactive lymph nodes. Future studies will need to confirm the value of these markers as prognostic and predictive biomarkers in clinical practice. Treatment intensity may be tailored in the future to the metabolic profile of the tumor microenvironment and drugs that target metabolic heterogeneity may be valuable in this disease.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
Name of substance:0 (Membrane Transport Proteins); 0 (Monocarboxylic Acid Transporters); 0 (Muscle Proteins); 0 (Receptors, Cell Surface); 0 (SLC16A4 protein, human); 0 (Symporters); 0 (TOMM20 protein, human); 0 (monocarboxylate transport protein 1); 11056-06-7 (Bleomycin); 5V9KLZ54CY (Vinblastine); 7GR28W0FJI (Dacarbazine); 80168379AG (Doxorubicin)


  8 / 29065 MEDLINE  
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PMID:29178401
Author:Nakata K; Ito Y; Magadi W; Bonaventure A; Stiller CA; Katanoda K; Matsuda T; Miyashiro I; Pritchard-Jones K; Rachet B
Address:Cancer Control Center, Osaka International Cancer Institute, Osaka, Japan.
Title:Childhood cancer incidence and survival in Japan and England: A population-based study (1993-2010).
Source:Cancer Sci; 109(2):422-434, 2018 Feb.
ISSN:1349-7006
Country of publication:England
Language:eng
Abstract:The present study aimed to compare cancer incidence and trends in survival for children diagnosed in Japan and England, using population-based cancer registry data. The analysis was based on 5192 children with cancer (age 0-14 years) from 6 prefectural cancer registries in Japan and 21 295 children diagnosed in England during 1993-2010. Differences in incidence rates between the 2 countries were measured with Poisson regression models. Overall survival was estimated using the Kaplan-Meier method. Incidence rates for Hodgkin lymphoma, renal tumors and Ewing sarcomas in England were more than twice as high as those in Japan. Incidence of germ cell tumors, hepatic tumors, neuroblastoma and acute myeloid leukemia (AML) was higher in Japan than in England. Incidence of all cancers combined decreased in Japan throughout the period 1993 to 2010, which was mainly explained by a decrease in registration of neuroblastoma in infants. For many cancers, 5-year survival improved in both countries. The improvement in survival in chronic myeloid leukemia (CML) was particularly dramatic in both countries. However, 5-year survival remained less than 80% in 2005-2008 in both countries for AML, brain tumors, soft tissue sarcomas, malignant bone tumors and neuroblastoma (age 1-14 years). There were significant differences in incidence of several cancers between countries, suggesting variation in genetic susceptibility and possibly environmental factors. The decrease in incidence for all cancers combined in Japan was related to the cessation of the national screening program for neuroblastoma. The large improvement in survival in CML coincided with the introduction of effective therapy (imatinib).
Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE


  9 / 29065 MEDLINE  
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PMID:29289336
Author:Turpin A; Michot JM; Kempf E; Mazeron R; Dartigues P; Terroir M; Boros A; Bonnetier S; Castilla-Llorente C; Coman T; Danu A; Ghez D; Pilorge S; Arfi-Rouche J; Dercle L; Soria JC; Carde P; Ribrag V; Fermé C; Lazarovici J
Address:Cancer campus Grand-Paris, Gustave-Roussy cancer comprehensive center, département des innovation thérapeutiques et essais précoces, 114, rue Édouard-Vaillant, 94805 Villejuif, France; Cancer campus Grand-Paris, Gustave-Roussy cancer comprehensive center, département d'hématologie, 114, rue Édouard-
Title:Le lymphome de Hodgkin : stratégies thérapeutiques actuelles et futures. [Hodgkin lymphoma: Current and future therapeutic strategies].
Source:Bull Cancer; 105(1):81-98, 2018 Jan.
ISSN:1769-6917
Country of publication:France
Language:fre
Abstract:Hodgkin lymphoma (HL) is a cancer that mostly affects young people, in which modern therapeutic strategies using chemotherapy and radiotherapy result in a cure rate exceeding 80%. Survivors are exposed to long-term consequences of treatments, such as secondary malignancies and cardiovascular diseases, whose mortality exceeds the one of the disease itself, with long-term follow-up. The current therapeutic strategy in HL, based on the assessment of initial risk factors, is the result of large clinical trials led by the main international cooperating groups. More recently, several groups have tried to develop treatment strategies adapted to the response to chemotherapy, evaluated by interim PET/CT scan. However to date, the combined treatment with chemotherapy followed by radiation therapy remains a standard in most of the above-diaphragmatic localized forms. Immune checkpoint inhibitors, and especially anti-PD1 antibodies, have shown dramatic results in some serious forms of relapsed or refractory HL, with limited toxicity, and may contribute in the future to reduce the toxicities of treatments.
Publication type:JOURNAL ARTICLE; REVIEW
Name of substance:0 (Antineoplastic Agents); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor)


  10 / 29065 MEDLINE  
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PMID:29224505
Author:Longo DL; DeVita VT
Address:From the Yale Cancer Center, New Haven, CT (V.T.D.).
Title:Progress in the Treatment of Hodgkin's Lymphoma.
Source:N Engl J Med; 378(4):392-394, 2018 01 25.
ISSN:1533-4406
Country of publication:United States
Language:eng
Publication type:LETTER; COMMENT



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