Lymphdx: A Custom Microarray for Molecular Diagnosis and Prognosis in Non-Hodgkin Lymphoma.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 701-701 ◽  
Author(s):  
Sandeep S. Dave ◽  
G. Wright ◽  
B. Tan ◽  
A. Rosenwald ◽  
W. C. Chan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Molecular Diagnosis ◽  
Cell Lymphoma ◽  
Diagnostic Algorithm ◽  
B Cell Lymphoma ◽  
Response To Therapy ◽  
Non Hodgkin Lymphoma

Abstract Clinical management differs significantly for the various types of non-Hodgkin lymphoma (NHL), and the diagnosis of these lymphomas can be challenging in some cases. Further, existing NHL categories include subgroups that can differ substantially in gene expression, response to therapy and overall survival. We have created a custom oligonucleotide microarray, named LymphDx, which could prove clinically useful for molecular diagnosis and outcome prediction in NHL. Biopsy specimens were obtained from 559 patients with a variety of lymphomas and lymphoproliferative conditions. Gene expression profiles of these samples were obtained using Affymetrix U133 A and B microarrays. The 2653 genes on LymphDx were chosen to include:(1)Genes most differentially expressed among NHL types based on Affymetrix U133 or Lymphochip microarrays (2)Genes predicting length of survival in diffuse large B cell lymphoma(DLBCL), follicular lymphoma(FL) and mantle cell lymphoma(MCL) (3)Genes encoded in the EBV and HHV-8 viral genomes (4)Genes encoding all known surface markers, kinases, cytokines and their receptors, as well as oncogenes, tumor suppressors, and other genes relevant to lymphoma. The LymphDx microarray was used to profile gene expression in 434 biopsy samples. These data were used to create a diagnostic algorithm that can distinguish various NHL types and benign follicular hyperplasia(FH) based on gene expression. The algorithm classifies a sample into one of the following categories: Burkitt’s lymphoma(BL), DLBCL, FL, MCL, small lymphocytic lymphoma(SLL) or FH. The algorithm further distinguishes the 3 recognized DLBCL subgroups: germinal center B cell-like, activated B cell-like or primary mediastinal lymphoma. Using a leave one out, cross validation strategy, the algorithm was found to agree well with the pathology diagnosis (see Figure). Some samples were deemed unclassified when their gene expression did not adequately match with that of any of the NHL categories. For a few samples, the gene expression-based diagnosis and the pathology diagnosis were discordant. Pathology review showed that two NHL types coexisted (eg FL and DLBCL) in many of these cases, potentially explaining the results of the diagnostic algorithm. LymphDx could also reliably predict the overall survival of patients with DLBCL, FL and MCL. Prospective evaluation of the LymphDx microarray is warranted since it could be used to provide objective molecular diagnostic, and prognostic information for patients with NHL. Figure Figure

Lymphomas

2017 ◽  
Author(s):  
Kieron Dunleavy ◽  
Wyndham H Wilson
Keyword(s):  
Gene Expression ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Group Performance ◽  
Cell Lymphoma ◽  
International Prognostic Index ◽  
Prognostic Index ◽  
B Cell Lymphoma ◽  
Non Hodgkin Lymphoma

Lymphoma is the fifth most common type of cancer in the United States, with 74,490 new cases estimated in 2009. Approximately 15% of patients with lymphoma have Hodgkin lymphoma; the remainder have one of the non-Hodgkin lymphomas. The incidence of non-Hodgkin lymphoma has increased steadily over recent decades. This chapter reviews the epidemiology, classification, clinical features, pathology, diagnostic evaluation, staging and prognosis, and treatment of Hodgkin and non-Hodgkin lymphoma. Other topics discussed include the acute and chronic effects of therapy for Hodgkin disease, as well as the subtypes of non-Hodgkin lymphomas, including indolent B cell lymphoma, follicular lymphoma, small lymphocytic lymphoma, mantle cell lymphoma, marginal-zone lymphoma, diffuse large B cell lymphoma (DLBCL), primary central nervous system lymphoma (PCNSL), Burkitt lymphoma, and HIV-related non-Hodgkin lymphoma. Figures illustrate the cellular appearance of Hodgkin lymphoma subtypes and DLBCL, diagnosis of DLBCL subtypes by gene expression, computed tomography and plain chest film in primary mediastinal cell lymphoma, MRI of the brain in PCNSL, and gene expression and gene expression predictors of survival among patients with DLBCL treated with rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine [Oncovin], and prednisone (R-CHOP). Tables describe the Ann Arbor classification and the Cotswold modification for staging of lymphoma; the International Prognostic Score for advanced Hodgkin lymphoma; the World Health Organization classification of hematopoietic neoplasms; chromosomal translocations in non-Hodgkin lymphoma; the Eastern Cooperative Oncology Group performance scale; the International Prognostic Index for aggressive non-Hodgkin lymphoma; and the Follicular Lymphoma International Prognostic Index. This chapter has 185 references. This review contains 9 tables, 7 figures and 185 references

Lack of Increased Clinical Efficacy When Interleukin-12 Is Added to Rituximab in B-Cell Lymphoma Patients Is Related to Inadequate Delivery of the Cytokine to the Sites of Lymphoma.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1397-1397
Author(s):  
Stephen M. Ansell ◽  
Deanna M. Grote ◽  
Thomas E. Witzig ◽  
Anne J. Novak
Keyword(s):  
Gene Expression ◽  
Lymph Nodes ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Peripheral Blood ◽  
Phase Ii Study ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Interleukin 12 ◽  
Non Hodgkin Lymphoma

Abstract Rituximab is a chimeric murine/human monoclonal antibody that binds to CD20 on B-lymphocytes. Binding of the Fab domain to B-cells directly induces apoptosis, while the Fc domain recruits immune effector functions to mediate cell lysis. Because rituximab therapy alone does not result in durable responses for all patients, combination therapies have been explored. We have previously shown in a phase I study that interleukin-12 (IL-12), which facilitates cytolytic T-cell responses and enhances the lytic activity of NK cells, can be safely combined with rituximab and that IL-12 significantly upregulated gamma interferon, CXCL10 (inducible protein-10) and NK cell activity in the peripheral blood. To confirm whether IL-12 could augment the immune mediated cell lysis induced by rituximab, a subsequent randomized phase II study of the combination was performed in patients with B-cell lymphoma. While the combination of IL-12 and rituximab was well tolerated with acceptable toxicity, only moderate disease activity was seen and the response rate to the combination was similar to that seen with rituximab alone. Additionally, the sequential administration of IL-12 at the time of disease progression after treatment with rituximab did not result in any clinical responses. This study was therefore performed to determine potential biologic reasons for the lack of increased clinical efficacy when IL-12 was added to rituximab therapy in patients with B-cell non-Hodgkin lymphoma. Of the 52 patients treated on the phase II study, 8 patients had matched tumor biopsies and peripheral blood specimens obtained prior to therapy and again 2 weeks after treatment was started. Six of the patients were receiving IL-12 plus rituximab at the time the specimens were obtained while 2 were receiving rituximab alone. Gene expression array analysis using the Affymetrix U133 plus chip was performed on RNA isolated from cells from involved lymph nodes and from peripheral blood mononuclear cells. Specimens from the peripheral blood of patients who received IL-12 in combination with rituximab showed a greater than 5-fold increase in the expression of multiple genes known to be upregulated by IL-12 signaling including interferon gamma, CXCL10, IFIT2 and 4 (interferon-induced protein with tetratricopeptide repeats 2 and 4), IL-8 and CXCL2 (macrophage inflammatory protein-2). These increases in gene expression were not seen in the peripheral blood of patients who received rituximab alone. Furthermore, the significant changes seen in cells obtained from the peripheral blood were not seen in cells obtained from lymph nodes involved by lymphoma, despite the samples being obtained from the same patient on the same day. In the tumor specimens, the changes in gene expression involved none of the genes downstream of IL-12 signaling. Instead, many of the upregulated genes were associated with cell cycle and spindle checkpoint proteins suggesting ongoing tumor cell proliferation. In conclusion, while IL-12 significantly upregulated gene expression in the peripheral blood, the same changes were not seen in the tumor. This would suggest that systemically administered IL-12 may not be effectively delivered to the site of tumor involvement. This finding may explain the lack of additional clinical benefit when IL-12 was added to rituximab as therapy for patients with non-Hodgkin lymphoma.

Expression of BLyS and its receptors in B-cell non-Hodgkin lymphoma: correlation with disease activity and patient outcome

Blood ◽  
2004 ◽  
Vol 104 (8) ◽  
pp. 2247-2253 ◽  
Author(s):  
Anne J. Novak ◽  
Deanna M. Grote ◽  
Mary Stenson ◽  
Steven C. Ziesmer ◽  
Thomas E. Witzig ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
De Novo ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Lactic Dehydrogenase ◽  
Response To Therapy ◽  
Non Hodgkin Lymphoma ◽  
Important Therapeutic Target

Abstract BLyS, recently shown to be critical for survival of normal B cells, has been found to be elevated in a number of immune disease models. A role for BLyS in the survival of malignant B cells has also been revealed and we therefore sought to identify a role for BLyS and its receptors in non-Hodgkin lymphoma (NHL). We found that tumor cells from all NHL histologic subtypes expressed one or more of 3 known receptors (BCMA, TACI, and BAFF-R) for BLyS; however, the pattern of expression was variable. We provide evidence that BLyS is expressed in tumors from patients with NHL and that BLyS levels increase as tumors transform to a more aggressive phenotype. Additionally, we provide evidence that serum BLyS levels are elevated in a subgroup of patients with NHL. In patients with de novo large B-cell lymphoma, a high BLyS level correlated with a poorer median overall survival, the presence of constitutional symptoms, and elevated values of lactic dehydrogenase. When BLyS levels were correlated with response to therapy in all patients, responding patients had a significantly lower BLyS level than those with progressive disease. In summary, we found that BLyS and its receptors represent a potentially important therapeutic target in B-cell lymphoma.

Lymphomas

2018 ◽  
Author(s):  
Kieron Dunleavy ◽  
Wyndham H Wilson
Keyword(s):  
Gene Expression ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Group Performance ◽  
Cell Lymphoma ◽  
International Prognostic Index ◽  
Prognostic Index ◽  
B Cell Lymphoma ◽  
Non Hodgkin Lymphoma

Lymphoma is the fifth most common type of cancer in the United States, with 74,490 new cases estimated in 2009. Approximately 15% of patients with lymphoma have Hodgkin lymphoma; the remainder have one of the non-Hodgkin lymphomas. The incidence of non-Hodgkin lymphoma has increased steadily over recent decades. This chapter reviews the epidemiology, classification, clinical features, pathology, diagnostic evaluation, staging and prognosis, and treatment of Hodgkin and non-Hodgkin lymphoma. Other topics discussed include the acute and chronic effects of therapy for Hodgkin disease, as well as the subtypes of non-Hodgkin lymphomas, including indolent B cell lymphoma, follicular lymphoma, small lymphocytic lymphoma, mantle cell lymphoma, marginal-zone lymphoma, diffuse large B cell lymphoma (DLBCL), primary central nervous system lymphoma (PCNSL), Burkitt lymphoma, and HIV-related non-Hodgkin lymphoma. Figures illustrate the cellular appearance of Hodgkin lymphoma subtypes and DLBCL, diagnosis of DLBCL subtypes by gene expression, computed tomography and plain chest film in primary mediastinal cell lymphoma, MRI of the brain in PCNSL, and gene expression and gene expression predictors of survival among patients with DLBCL treated with rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine [Oncovin], and prednisone (R-CHOP). Tables describe the Ann Arbor classification and the Cotswold modification for staging of lymphoma; the International Prognostic Score for advanced Hodgkin lymphoma; the World Health Organization classification of hematopoietic neoplasms; chromosomal translocations in non-Hodgkin lymphoma; the Eastern Cooperative Oncology Group performance scale; the International Prognostic Index for aggressive non-Hodgkin lymphoma; and the Follicular Lymphoma International Prognostic Index. This chapter has 185 references.

scholarly journals Is Absolute Lymphocyte Count at Time of Diagnosis a Predictor of Overall Survival in Non-Hodgkin Lymphoma Patients?

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 32-32
Author(s):  
Mallak Zatreh ◽  
Anahat Kaur ◽  
Anas Albawaliz ◽  
Sheetal Bulchandani ◽  
Ghazal Khan
Keyword(s):  
Overall Survival ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Lymphocyte Count ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Absolute Lymphocyte Count ◽  
Histopathological Diagnosis ◽  
Non Hodgkin Lymphoma

Introduction:The prognostic significance of absolute lymphocyte count (ALC) has been an area of debate in non-Hodgkin-lymphoma (NHL). Several studies have reported that lymphocyte count during and after chemotherapy independently predict outcome in patients with acute myelocytic lymphoma (AML), follicular lymphoma and diffuse large B-cell lymphoma (DLBCL). Furthermore, lymphocytopenia is a poor prognostic marker in initial staging of NHL and in relapsed DLBCL. Therefore, we aimed to investigate whether ALC at time of diagnosis is an independent predictor of overall survival (OS) in NHL. Methods:We retrospectively reviewed patients with aggressive NHL who were seen at hospitals affiliated with Saint Luke's Health System from January 2000 to December 2017 with at least 2 year longitudinal follow up after diagnosis. We retrieved 447 patients with histopathological diagnosis of DLBCL, Burkitt's Lymphoma, Follicular Lymphoma Grade IIIB, primary Effusion Lymphoma, B-cell Lymphoma unclassifiable, and high-grade B cell lymphoma. Through chart review we determined pathological and clinical characteristics of these patients, calculated the ALC at time of diagnosis, studied the treatment patterns, response to therapy and survival in our center. ALC at time of diagnosis was obtained on 358 patients based on data availability. Results:A multivariate analysis was conducted to see if ALC at time of diagnosis is a predictor of OS by correcting for age at diagnosis, gender, race, stage at diagnosis, international prognostic index (IPI), central nervous system involvement, histopathological diagnosis and type of chemotherapy. ALC at diagnosis after controlling all variables was not a significant predictor of OS (P: 0.7126). Conclusion:We found that ALC at time of diagnosis did not have a statistically significant effect on OS. We believe that prospective large-scale studies are needed to determine whether ALC at time of diagnosis affects OS in NHL patients. Table Disclosures No relevant conflicts of interest to declare.

Lymphomas

2017 ◽  
Author(s):  
Kieron Dunleavy ◽  
Wyndham H Wilson
Keyword(s):  
Gene Expression ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Group Performance ◽  
Cell Lymphoma ◽  
International Prognostic Index ◽  
Prognostic Index ◽  
B Cell Lymphoma ◽  
Non Hodgkin Lymphoma

Lymphoma is the fifth most common type of cancer in the United States, with 74,490 new cases estimated in 2009. Approximately 15% of patients with lymphoma have Hodgkin lymphoma; the remainder have one of the non-Hodgkin lymphomas. The incidence of non-Hodgkin lymphoma has increased steadily over recent decades. This chapter reviews the epidemiology, classification, clinical features, pathology, diagnostic evaluation, staging and prognosis, and treatment of Hodgkin and non-Hodgkin lymphoma. Other topics discussed include the acute and chronic effects of therapy for Hodgkin disease, as well as the subtypes of non-Hodgkin lymphomas, including indolent B cell lymphoma, follicular lymphoma, small lymphocytic lymphoma, mantle cell lymphoma, marginal-zone lymphoma, diffuse large B cell lymphoma (DLBCL), primary central nervous system lymphoma (PCNSL), Burkitt lymphoma, and HIV-related non-Hodgkin lymphoma. Figures illustrate the cellular appearance of Hodgkin lymphoma subtypes and DLBCL, diagnosis of DLBCL subtypes by gene expression, computed tomography and plain chest film in primary mediastinal cell lymphoma, MRI of the brain in PCNSL, and gene expression and gene expression predictors of survival among patients with DLBCL treated with rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine [Oncovin], and prednisone (R-CHOP). Tables describe the Ann Arbor classification and the Cotswold modification for staging of lymphoma; the International Prognostic Score for advanced Hodgkin lymphoma; the World Health Organization classification of hematopoietic neoplasms; chromosomal translocations in non-Hodgkin lymphoma; the Eastern Cooperative Oncology Group performance scale; the International Prognostic Index for aggressive non-Hodgkin lymphoma; and the Follicular Lymphoma International Prognostic Index. This chapter has 185 references.

scholarly journals Molecular Diagnosis of Primary Mediastinal B Cell Lymphoma Identifies a Clinically Favorable Subgroup of Diffuse Large B Cell Lymphoma Related to Hodgkin Lymphoma

2003 ◽  
Vol 198 (6) ◽  
pp. 851-862 ◽  
Author(s):  
Andreas Rosenwald ◽  
George Wright ◽  
Karen Leroy ◽  
Xin Yu ◽  
Philippe Gaulard ◽  
...  
Keyword(s):  
Gene Expression ◽  
B Cell ◽  
Gene Expression Profiling ◽  
Hodgkin Lymphoma ◽  
Molecular Diagnosis ◽  
Expression Profiling ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Using current diagnostic criteria, primary mediastinal B cell lymphoma (PMBL) cannot be distinguished from other types of diffuse large B cell lymphoma (DLBCL) reliably. We used gene expression profiling to develop a more precise molecular diagnosis of PMBL. PMBL patients were considerably younger than other DLBCL patients, and their lymphomas frequently involved other thoracic structures but not extrathoracic sites typical of other DLBCLs. PMBL patients had a relatively favorable clinical outcome, with a 5-yr survival rate of 64% compared with 46% for other DLBCL patients. Gene expression profiling strongly supported a relationship between PMBL and Hodgkin lymphoma: over one third of the genes that were more highly expressed in PMBL than in other DLBCLs were also characteristically expressed in Hodgkin lymphoma cells. PDL2, which encodes a regulator of T cell activation, was the gene that best discriminated PMBL from other DLBCLs and was also highly expressed in Hodgkin lymphoma cells. The genomic loci for PDL2 and several neighboring genes were amplified in over half of the PMBLs and in Hodgkin lymphoma cell lines. The molecular diagnosis of PMBL should significantly aid in the development of therapies tailored to this clinically and pathogenetically distinctive subgroup of DLBCL.

scholarly journals Clinical significance of metabolism-related biomarkers in non-Hodgkin lymphoma – MCT1 as potential target in diffuse large B cell lymphoma

2019 ◽  
Vol 42 (3) ◽  
pp. 303-318 ◽  
Author(s):  
Julieta Afonso ◽  
Tatiana Pinto ◽  
Susana Simões-Sousa ◽  
Fernando Schmitt ◽  
Adhemar Longatto-Filho ◽  
...  
Keyword(s):  
B Cell ◽  
Hodgkin Lymphoma ◽  
Clinical Significance ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Potential Target ◽  
Non Hodgkin Lymphoma ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Familial risk for non-Hodgkin lymphoma and other lymphoproliferative malignancies by histopathologic subtype: the Swedish Family-Cancer Database

Blood ◽  
2005 ◽  
Vol 106 (2) ◽  
pp. 668-672 ◽  
Author(s):  
Andrea Altieri ◽  
Justo Lorenzo Bermejo ◽  
Kari Hemminki
Keyword(s):  
B Cell ◽  
Hodgkin Lymphoma ◽  
Cell Lymphoma ◽  
Familial Risk ◽  
B Cell Lymphoma ◽  
Non Hodgkin Lymphoma ◽  
Large B Cell Lymphoma ◽  
Swedish Family ◽  
History Of ◽  
Large B Cell

Abstract Non-Hodgkin lymphoma (NHL) consists of a heterogeneous group of tumors. Population-based data on the familial risk for specific histopathologic subtypes have not been established. Such data are useful for clinical counseling and for searching tumor subtypes sharing common genetic pathways. We used the Swedish Family-Cancer Database to calculate standardized incidence ratios (SIRs) for histopathology-specific subtypes of NHL in 4455 offspring with NHL whose parents or siblings were affected with different types of lymphoproliferative malignancies. A familial history of NHL significantly increased the risk for NHL (SIRparent = 1.8; SIRsibling = 1.9) and for diffuse large B-cell lymphoma (SIRparent = 2.3), follicular lymphoma (SIRsibling = 2.3), and B-cell lymphoma not otherwise specified (NOS) (SIRsibling = 3.4). For a parental history of histopathology-specific concordant cancer, the risks were significantly increased for diffuse large B-cell lymphoma (SIR = 11.8), follicular NHL (SIR = 6.1), plasma cell myeloma (SIR = 2.5), and chronic lymphocytic leukemia (SIR = 5.9). Familial clusters for NHL seemed stronger in females and in siblings. Our study provides the first quantification of the familial risks for NHL by histopathology. The present findings give evidence for a strong familial association of NHL, with little differences in the magnitude of risks for various histopathologic subtypes. The patterns of risks in parents and siblings support the hypothesis of an autosomal-dominant component for diffuse large B-cell NHL and a recessive one for follicular NHL. (Blood. 2005;106:668-672)

A Phase II Clinical Study of Rituximab and High-Dose Biweekly THP-COP (Pirarubicin, Cyclophosphamide, Vincristine and Predonisolone) with G-CSF for Non-Hodgkin Lymphoma: Results of a Multicentric Study of NMLSG (Niigata Malignant Lymphoma Study Group).

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4734-4734
Author(s):  
Jun Takizawa ◽  
Sadao Aoki ◽  
Kazue Takai ◽  
Tohri Kurasaki ◽  
Keiichiro Honma ◽  
...  
Keyword(s):  
Clinical Study ◽  
T Cell ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Phase Ii ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
High Dose ◽  
Histological Subtypes ◽  
Non Hodgkin Lymphoma

Abstract Introduction CHOP chemotherapy has been accepted as the standard treatment for patients with non-Hodgkin lymphoma (NHL), but in some histological or clinical subtypes the results are not satisfactory. We have shown the efficacy and safety of high-dose biweekly THP-COP with G-CSF support (HDBW-TCOP(G)) for NHL. In this regimen, we choose pirarubicin in stead of doxorubicin because it was proven high efficacy against NHL and the lower toxicity than doxorubicin. Recently, the combination of rituximab and standard CHOP has been shown to have a synergistic effect for NHL. We performed a phase II multicentric clinical study to assessed the feasibility and toxicity of the combination chemotherapy of rituximab and HDBW-TCOP(G) (HDBW-R-TCOP(G)) compared with those of HDBW-TCOP(G). Patients and methods Between August 1998 and December 2004, Forty-one Japanese patients with previously untreated NHL from whom informed consent was obtained were included in this study. Median age was 45 (range 19–63) years. There were 19 males and 22 females. According to WHO-classification diagnoses, histological subtypes included follicular lymphoma (FL) 15(37%); nodal marginal zone B-cell lymphoma (NMZBCL) 2(5%); mantle cell lymphoma (MCL) 3(7%); anaplastic large cell lymphoma (ALCL) 1(2%), diffuse large B-cell lymphoma (DLBCL) 18(44%); peripheral T-cell lymphoma (PTCL) 1(2%), angioimmunoblastic T-cell lymphoma (AILT) 1(2%). Of 41 patients, one patient was stage 1, stage 2, 11 stage 3 and 16 stage 4. International prognostic index (IPI) included L 6; LI 22; HI 7; H 6. HDBW-TCOP(G) consisted of pirarubicin 70 mg/m2 on day 1; cyclophosphamide 1000 mg/m2 on day 1; vincristine 1.4 mg/m2 on day 1; predonisolone 50 mg/m2 orally from day 1 to 5; lenograstim 2.0 μg/kg/day from day 3. Fifteen patients who enrolled after rituximab was approved in Japan received therapy combined HDBW-TCOP(G) with rituximab 375mg/ m2 on day -2 (HDBW-R-TCOP(G)). Six cycles were administered at intervals of two weeks. Results Of the 41 patients treated, 32 (78.0%) achieved a complete remission (CR) and nine (22.0%) achieved a partial remission (PR), for an overall response rate of 100%. After median follow-up of 36 months (range 2.9– 81.8), progression free survival (PFS) and overall survival (OS) were 68.2% and 97.5%, respectively. PFS was 90.9% for HDBW-R-TCOP(G), and 69.5% for HDBW-TCOP(G), but no significant differences was found among two regimen. There was no significant difference in the PFS and OS between aggressive and indolent histological subtypes. 76% of patients developed Grade4 leukopenia (according to NCI criteria) but no patients experienced febrile neutropenia. 15% of patients developed G4 anemia and 17% of patients G4 thrombocytopenia. Other adverse effects were minimal. Conclusion Both HDBW-TCOP(G) and HDBW-R-TCOP(G) are feasible for NHL with acceptable toxicity. The excellent result suggests they are effective for aggressive NHL patients with poor prognostic factors and advanced stage indolent NHL.

Sign in / Sign up

Export Citation Format

Share Document