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G Pichert

Publications and source records attributed to G Pichert.

At least 19 recordsLinked to original sources
PubMed2003

Evidence-based management options for women at increased breast/ovarian cancer risk.

Recent developments in our ability to predict breast cancer risk necessitates primary care physicians learn to evaluate breast cancer risk and its importance in shaping decisions concerning surveillance and risk reduction measures. This article reviews the current opinion on risk assessment and management of women with an increased risk of breast/ovarian cancer. Management options are given for women at slightly, moderately and highly elevated breast cancer risk, as well as for BRCA1/2 carriers, based on currently available evidence.

Breast Neoplasms↗
PubMed2001

Cancer genetics in oncology practice.

Cancer is a genetic disease caused by the progressive accumulation of mutations in critical genes that control cell growth and differentiation. Completion of the Human Genome Project promises to revolutionize the practice of Medicine, especially Oncology care. The tremendous gains in the knowledge of the structure and function of human genes will surely impact the diagnosis, prognosis and treatment of cancer. Moreover, it will lead to more effective cancer control through the use of genetics to quantify individual cancer risks. This article reviews the current status of genetic testing and counseling for cancer risk assessment and will suggest a framework for integrating such counseling into oncology practice.

Adenomatous Polyposis Coli↗
PubMed2001

Weekly x 4 induction therapy with the anti-CD20 antibody rituximab: effect on circulating t(14;18)(+) follicular lymphoma cells.

Rituximab 375 mg/m(2) weekly x 4 has been reported to induce a 60% response rate in patients with relapsed follicular lymphomas (FL). Our aim was to examine the effect of this rituximab schedule on circulating FL cells in an ongoing multicenter study. One hundred fifty-four patients with FL were examined by nested polymerase chain reaction (PCR) at baseline for the presence of t(14;18) translocation-carrying lymphoma cells in bone marrow and/or blood. Sixty-four patients (42%) had PCR-detectable t(14;18)(+) FL cells. Pretreatment characteristics of these 64 patients were as follows: one had stage I, nine had stage II, 14 had stage III, and 40 had stage IV disease. Thirty-five patients had bulky disease (> or = 5 cm) and 25 patients had an elevated serum lactate dehydrogenase (LDH) level. Bone marrow was morphologically assessed in 64 patients, and 39 of these patients had an infiltration with FL cells. Blood samples from 51 patients were available for PCR analysis between weeks 8-12 after induction therapy, and 28 of these patients (55%) were PCR negative. Paired blood and bone marrow samples were available for PCR analysis from 39 patients between weeks 8-12 after induction therapy with rituximab. Thirteen of these patients (33%) did not have PCR-detectable cells in blood and bone marrow, while 26 patients (67%) still had circulating t(14;18)(+) cells in either bone marrow (eight patients), blood (one patient), or both (17 patients). PCR negativity in blood and bone marrow in 13 patients was statistically significantly associated with partial or complete response after induction therapy with rituximab (P = 0.006). However, clearance of PCR-detectable t(14;18)(+) cells in bone marrow and/or blood could not be associated with any low tumor burden pretreatment characteristics such as stages I/II, absence of morphological bone marrow infiltration or tumor bulk of > or = 5 cm, and normal serum LDH.

Adult↗
PubMed2000

Organizing cancer genetics programs: the Swiss model.

PURPOSE: Inherited predisposition to cancer is a complex issue, and risk assessment, counseling, and management are multidisciplinary tasks. An infrastructure is needed through which clinical services may be delivered and research activities conducted. METHODS: The Swiss Institute for Applied Cancer Research (SIAK) Network for Cancer Predisposition Testing and Counseling was established in 1999. The goals of the Network are to set common standards for clinical services, to coordinate research activities, to address psychosocial and ethical issues concerning genetic counseling and testing, and to translate the knowledge gained into medical practice. RESULTS: An algorithm for genetic testing and counseling of the families studied by the SIAK Network centers has been established in a consensual process. Eight regional centers currently operate according to this algorithm. Furthermore, a proposal has been submitted for the setup of a Swiss databank for the characterization of BRCA1 and BRCA2 mutation patterns and the identification of potentially unique mutations in probands who seek genetic counseling and testing at the respective centers of the SIAK Network. CONCLUSION: Our coordinated effort will ensure state-of-the-art genetic testing and counseling services in Switzerland and will allow us to acquire knowledge for appropriate risk assessment and surveillance/prevention strategies for individuals with an inherited cancer predisposition.

Adult↗
PubMed2000

The effect of Rituximab on patients with follicular and mantle-cell lymphoma. Swiss Group for Clinical Cancer Research (SAKK).

BACKGROUND: Clinical activity of the anti CD-20 monoclonal antibody Rituximab has been reported in patients with follicular lymphoma (FL) and mantle-cell lymphoma (MCL). PATIENTS AND METHODS: 120 patients with bi-dimensionally measurable FL or MCL (R.E.A.L. Classification) were treated with Rituximab 375 mg/m2/week for 4 weeks. A central pathology review confirmed the diagnosis of FL in 76 of 78 and of MCL in 39 of 42 cases. The response was evaluated after 8 weeks and confirmed after 12 weeks from the start of treatment. RESULTS: The toxicity of the treatment was, as expected, grade 1-2 fever and rigors during the first infusion and mild asthenia during the treatment period. Serious adverse events, probably or possibly related to the study treatment, included four deaths (3 of cardiac origin, 1 caused by P. carinii pneumonia) and 10 further nonfatal cases, including a permanent agranulocytosis and one case of heart failure. Response rate at week 12 was 52% for FL and 22% for MCL. After treatment, the BCL-2 rearrangement disappeared in 15 of 29 blood but only in 5 of 23 bone marrow samples; BCL-1 disappeared in 5 of 12 blood and 0 of 7 bone marrow specimens, as determined by PCR. CONCLUSIONS: Rituximab is an active agent for the treatment of FL, while its efficacy is modest in MCL. The effect in reducing minimal residual disease is more pronounced on the blood than it is on the bone marrow.

Adult↗
PubMed1999

A prospective study of risk-adapted therapy for large cell non-Hodgkin's lymphoma with VACOP-B followed by high-dose CBV and autologous progenitor cell transplantation for high-risk patients in remission.

Several centres reported a favourable outcome after high-dose chemotherapy with autologous progenitor cell transplantation in selected patients with high-risk large cell non-Hodgkin's lymphoma in first remission. Based on these observations, we wanted to prospectively determine the outcome of a risk-adapted therapy for patients with large cell lymphoma. Patients aged 60 years or less received 12 weeks of VACOP-B chemotherapy. For high-risk patients in remission this was immediately followed by high-dose chemotherapy with cyclophosphamide, carmustine and etoposide and autologous progenitor cell transplantation. High-risk criteria were defined before the establishment of the International Index and included large cell lymphoma stage III or IV or mediastinal large lymphoma with sclerosis stage II or higher, and the presence of bulky tumours and/or an elevated LDH. 89 patients fulfilled the clinical selection criteria and were entered onto this multicentre study. 82 patients were evaluable after confirmation of large cell histology by pathology review. Of these, 51 were considered to be in the low-risk group and 31 in the high-risk group. The 3-year event-free survival for all patients was 68%. The 3-year event-free survival was 76% for the low-risk and 55% for the high-risk group (P = 0.061). Only 22/31 high-risk patients were able to receive the high-dose chemotherapy in first remission as intended. In conclusion, although our study demonstrated that a risk-adapted therapy for large cell lymphoma could be safely administered, the potential impact on outcome of the strategy chosen here is likely to be small.

Adult↗
PubMed1999

Involvement of the CD27-CD70 co-stimulatory pathway in allogeneic T-cell response to follicular lymphoma cells.

Non-activated follicular lymphoma (FL) cells do not function as effective antigen-presenting cells in vivo. CD40 activation of FL cells up-regulates critical adhesion and co-stimulatory molecules, thereby inducing lymphoma-specific cytotoxic T cells in vitro. However, other evidence suggests that CD70 is another important co-stimulatory molecule involved in antigen dependent T-cell activation. Here, we showed that freshly isolated FL cells from eight diagnostic biopsies expressed intermediate to high levels of CD27, whereas only insignificant levels of CD70 were detected on their cell surface. Together with the low to intermediate expression of B7, these findings help to explain the poor antigen-presenting capacity of non-activated FL cells. Activation of FL cells by CD27 and CD40 induced a significantly higher alloantigen T-cell response than CD40 alone, whereas CD27 activation induced only a mostly insignificant T-cell proliferation. Both CD40 and CD27 + CD40 activation resulted in a high up-regulation of CD70 and B7 molecules, whereas CD27 activation up-regulated CD70 but not B7 expression on the surface of FL cells. Thus, expression of both CD70 and B7 co-stimulatory molecules appears to be essential for an efficient T-cell-mediated immune response. However, the molecules responsible for the significantly higher alloantigen T-cell response to FL cells activated through CD27 and CD40 remain to be identified. In summary, we conclude that CD27+CD70 represents another co-stimulatory pathway involved in T-cell-mediated immune responses to FL cells. Our findings suggest that several co-stimulatory pathways exist and should be taken into consideration to optimize antigen presentation for the generation of lymphoma-directed cytotoxic T cells for adoptive immunotherapy.

Antigens, CD↗
PubMed1998

Selection and immunomagnetic purging of peripheral blood CD34+ cells for autologous transplantation in B-cell non-Hodgkin's lymphomas.

BACKGROUND: Clonogenic tumor cells in the hematopoietic progenitor cell harvest may contribute to relapse after high dose therapy for B-cell malignancies. Purging of the HPC harvest requires large amounts of anti-B-cell antibodies, whereas CD34-selection enriches self renewing HPC's but malignant cells are still detectable in many CD34+ fractions. PATIENTS AND METHODS: We examined the feasibility and safety of a CD34-selection followed by purging with anti B-cell antibodies in 11 patients with B-cell non-Hodgkin's lymphomas undergoing high-dose therapy with cyclophosphamide, BCNU and etoposide with retransfusion of autologous HPC's. RESULTS: A mean number of 340 x 10(8) mononuclear cells was used for CD34-selection and immunomagnetic purging. CD34+ cells were enriched from a mean of 1.7% (range 0.2%-4.5%) to a mean of 68% (range 49%-87%) with a mean recovery of 27% (range 15%-43%). The mean number of retransfused CD34+ cells was 1.2 x 10(6)/kg (range 0.6-2.2 x 10(6)/kg) body weight with a median of 11 days (range 10-13 days) to neutrophil recovery of 0.5 x 10(9)/l and 17 days (range 13-25 days) to platelet recovery of 50 x 10(9)/l. Mean number of intravenous antibodies and inpatient days were 8 (range 0-14) and 22 (range 19-26) respectively. Major toxicity consisted in four septicemias. CONCLUSIONS: CD34-selected and purged HPC's are safe and mediate rapid hematological recovery after high dose therapy for B-cell non-Hodgkin's lymphomas.

Antibodies, Monoclonal↗
PubMed1997

T-cell derived cytokines co-stimulate proliferation of CD40-activated germinal centre as well as follicular lymphoma cells.

Follicular lymphomas, the malignant counterparts of normal germinal centre (GC) B-cells, grow in vivo in close association with polyclonal T-cells, predominantly from the T-helper cell type. T-cell-derived growth factors are involved in the development of GC B-cells. However, their role in the pathogenesis of follicular lymphomas has not been clearly defined. We investigated the co-stimulatory activity of 14 cytokines (interleukin-1 to -8, IL-10, IL-13, INF-alpha, TNF-alpha, GM-CSF and SCF) on the proliferation of CD40-activated follicular lymphoma cells in comparison to tonsillar GC B-cells. Tonsillar GC B-cells (n = 4), malignant cells from diagnostic lymph node biopsies of patients with follicular (n = 4) or transformed (n = 4) lymphomas were grown on irradiated CD40-ligand transfectants, with and without cytokines. [3H]-thymidine uptake was measured at day 7. IL-10 and IL-4 proved to be the most potent co-stimulators of proliferation of tonsillar GC B-cells, whereas proliferation of follicular lymphoma cells was co-stimulated by IL-4. The fact that IL-4 is a T-cell derived cytokine, suggests that lymphoma infiltrating T-cells play a role in the growth of these malignancies. Moreover, proliferation of both non-neoplastic tonsillar GC B-cells and follicular lymphomas is co-stimulated by T-cell derived cytokines, indicating that responsiveness to paracrine factors may not be a characteristic of the malignant phenotype.

3T3 Cells↗
PubMed1996

Fate of contaminating t(14; 18)+ lymphoma cells during ex vivo expansion of CD34-selected hematopoietic progenitor cells.

The use of ex vivo expanded CD34-selected hematopoietic progenitor cells (HPCs) for autologous stem cell support or gene therapy is a major area of research and is likely to increase in the future. At present, little is known about the fate of contaminating malignant cells during ex vivo expansion of CD34-selected HPCs. We established a competitive polymerase chain reaction (PCR) titration assay to determine the number of residual lymphoma cells before and after selection and ex vivo expansion of CD34-selected HPCs in patients with t(14; 18) translocation carrying non-Hodgkin's lymphoma. Seven bone marrow (BM) and 2 mobilized peripheral blood progenitor cell samples from 8 patients without histologic BM involvement at the time of the harvest were analyzed by competitive PCR titration assay and determined to contain between < or = 10 and 4,000 lymphoma cells/ 10(6) mononuclear cells (MNCs). Immunoadsorption enriched CD34+ cells from a mean of 5% (range, 1% to 9%) to a mean of 88% (range, 76% to 94%) of MNCs and resulted in a 1 to 4 log depletion of contaminating tumor cells. Two HPC samples became PCR negative after CD34 selection, whereas 7 samples still contained < or = 10 to 200 residual lymphoma cells/10(5) MNCs. CD34-selected cells were consecutively expanded in suspension culture in the presence of stem cell factor, interleukin-1 beta (IL-1 beta), IL-3, and IL-6. The mean increase of cells was 13-fold (range, 4- to 22-fold) at day 7 and 65-fold (range, 43- to 110-fold) at day 14 of culture. Expansion resulted predominantly in myelomonocytic differentiation, whereas B-cell antigen-expressing cells became undetectable. Six of the seven PCR-positive CD34-selected samples became PCR-negative for the t(14; 18) translocation at day 7 and/or 14 of expansion. One PCR-positive and one PCR-negative CD34-selected sample were PCR-positive after ex vivo expansion, but the number of residual lymphoma cells remained at the limit of detection. We conclude that CD34-selection does not eliminate contaminating lymphoma cells in the majority of t(14; 18)+ HPC harvests. However, during ex vivo expansion of CD34-selected HPCs, residual t(14; 18)+ lymphoma cells do not proliferate and become undetectable by PCR in the majority of cases.

Antigens, CD34↗
PubMed1995

Distinct patterns of minimal residual disease associated with graft-versus-host disease after allogeneic bone marrow transplantation for chronic myelogenous leukemia.

PURPOSE: Allogeneic bone marrow transplantation (BMT) has been shown to provide effective therapy for chronic myelogenous leukemia (CML), but previous reports have also demonstrated the persistence of bcr-abl-positive cells for months to years after BMT in the majority of patients. To evaluate the biologic significance of persistent bcr-abl-positive cells, we examined the relationship between clinical parameters known to affect the risk of relapse and the ability to detect bcr-abl-positive cells post-BMT. PATIENTS AND METHODS: We analyzed 480 samples from 92 patients at two transplant centers for the presence of bcr-abl-positive cells by polymerase chain reaction (PCR). Two different BMT preparative regimens and protocols for prevention of graft-versus-host disease (GVHD) were used. One center used cyclophosphamide plus total-body irradiation (CY/TBI) and T-cell-depleted marrow; the second center used busulfan plus cyclophosphamide (Bu/CY) and untreated marrow with cyclosporine and methotrexate (Csp/MTX) as GVHD prophylaxis. RESULTS: We first determined the percent of patients at each center with > or = one PCR-positive (PCR+) result at defined intervals post-BMT. Between 0 and 6 months post-BMT, the majority of patients (80% to 83%) in both populations had PCR-detectable bcr-abl-positive cells. Between 6 and 24 months post-BMT, 80% to 88% of patients who received T-cell-depleted marrow remained PCR+, as compared with 26% to 30% of patients who received unmodified marrow. After 24 months post-BMT, the percentage of PCR+ patients was not significantly different in the two populations. This pattern of detection of bcr-abl-positive cells post-BMT followed the development of chronic GVHD in patients who received unmodified marrow. All patients were also divided into three groups based on post-BMT PCR results as follows: (1) persistent PCR+ (n = 29), (2) intermittent PCR-negative ([PCR-] n = 40), and (3) persistent PCR- (n = 23). These three groups were found to have a low, intermediate, and high probability of maintaining remission and disease-free survival, respectively (P = .0001). Intermittent or persistent PCR- results, which reflect levels of minimal residual disease < or = the limit of detection by PCR, were clearly associated with both acute (P = .004) and chronic (P = .000005) GVHD. Nevertheless, 44% of patients without GVHD also had intermittent or persistent PCR- assays. CONCLUSION: The persistence of PCR-detectable bcr-abl-positive cells early post-BMT in more than 80% of patients suggests that neither BMT preparative regimen effectively eradicates CML cells in most patients. Subsequently, acute and/or chronic GVHD are associated with a decreased ability to detect residual bcr-abl-positive cells, which suggests that immunologic mechanisms mediated by donor cells are important for inducing long-term remissions after BMT. The demonstration that 44% of patients without GVHD had either low or undetectable levels of residual leukemia suggests the presence of mechanisms capable of suppression or eradication of CML independent of GVHD.

Acute Disease↗
PubMed1995

Functional consequences of APO-1/Fas (CD95) antigen expression by normal and neoplastic hematopoietic cells.

Murine monoclonal antibody (mAb) 7C11 binds to the same cell surface epitope as anti-APO-1 and anti-Fas and reacts specifically with cells transfected with a cDNA encoding the human Fas antigen. Furthermore, incubation with 7C11 causes death of hematopoietic cell lines that express APO-1/Fas but not APO-1/Fas-negative cell lines. 7C11 therefore recognizes the human APO-1/Fas (CD95) antigen, a 40 to 50 kDa cell surface glycoprotein that can trigger apoptosis or programmed cell death. Expression of APO-1/Fas antigen by normal and neoplastic hematopoietic cells was determined by flow cytometry using 7C11. APO-1/Fas is expressed by approximately 30 to 40% of resting peripheral blood T cells, B cells, and monocytes and by approximately 5% of resting NK cells and thymocytes. It was not detected on granulocytes, erythrocytes, or platelets. Approximately 80 to 90% of activated T cells, B cells, and thymocytes express APO-1/Fas, as do the majority of activated NK cells. Perturbation of APO-1/Fas by 7C11 does not affect the viability of resting lymphocytes or monocytes. In contrast, activated T cells and NK cells undergo apoptosis within 3 hours of exposure to 7C11. Other mAb that stimulate T cells or NK cells do not cause rapid induction of programmed cell death. APO-1/Fas antigen is expressed by many cell lines of lymphoid and myeloid lineage. However, this antigen was detected on neoplastic cells from only one of 69 patients with acute myeloid leukemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, chronic lymphocytic leukemia, or multiple myeloma. Only 3 out of 25 tumor samples from patients with non-Hodgkin's lymphoma were found to express APO-1/Fas. All three of these lymphomas harbored the bcl-2-Ig fusion gene associated with the chromosomal translocation t (14;18). Conversely, only 27% of lymphomas that possessed the bcl-2-Ig gene were found to express the APO-1/Fas antigen. Like normal activated lymphocytes, leukemia and lymphoma cells that expressed APO-1/Fas antigen were found to undergo apoptosis in vitro after incubation with 7C11. The APO-1/Fas antigen appears to regulate the growth of normal hematopoietic cells, and the marked upregulation of this antigen on activated normal lymphocytes contrasts sharply with the absence of APO-1/Fas on neoplastic cells of hematopoietic lineage. Defects in the apoptotic signal delivered through this antigen might contribute to the pathogenesis of hematopoietic neoplasms. Thus, the gene encoding APO-1/Fas can be considered a novel type of tumor suppressor gene, just as bcl-2 can be considered a cellular proto-oncogene.

Animals↗
PubMed1994

Persistence of myeloid progenitor cells expressing BCR-ABL mRNA after allogeneic bone marrow transplantation for chronic myelogenous leukemia.

Previous studies have shown that tumor-specific bcr-abl mRNA can often be detected by polymerase chain reaction. (PCR) for months to years after allogeneic bone marrow transplantation (BMT) for chronic myelocytic leukemia (CML). Nevertheless, the presence of bcr-abl mRNA by itself does not invariably predict for clinical relapse post-BMT. This has led to the hypothesis that bcr-abl mRNA might be expressed in cells that have lost either proliferative or myeloid differentiation potential. To directly characterize the cells detected by PCR in patients with CML after allogeneic BMT, we first identified five individuals in whom PCR-positive cells could be detected at multiple times post-BMT. Bone marrow samples from these individuals were cultured in vitro and single erythroid, granulocytic, and macrophage colonies, each containing 50 to 100 cells, were examined for the presence of bcr-abl mRNA by PCR. PCR-positive myeloid colonies could be detected in four of five individuals in marrow samples obtained 5 to 56 months post-BMT. Overall, 7 of 135 progenitor cell colonies (5.2%) were found to be PCR-positive. The expression of bcr-abl mRNA appeared to be equally distributed among committed erythroid, macrophage, and granulocyte progenitors. These patients have now been followed-up for an additional 20 to 33 months from the time of progenitor cell PCR analysis but only one of these individuals has been found to have cytogenetic evidence of recurrent Ph+ cells. These results show that long-term persistence of PCR-detectable bcr-abl mRNA after allogeneic BMT can be caused by the persistence of CML-derived clonogenic myeloid precursors that have survived the BMT preparative regimen. These cells continue to have both proliferative and myeloid differentiation capacity in vitro. Nevertheless, these PCR-positive cells do not appear to either expand or differentiate in vivo for prolonged periods, suggesting the presence of mechanisms for suppression of residual clonogenic leukemia cells in vivo.

Adult↗
PubMed1994

Randomized study of recombinant human granulocyte colony-stimulating factor after high-dose chemotherapy and autologous bone marrow transplantation for high-risk lymphoid malignancies.

PURPOSE: The aim of this prospective randomized trial was to examine the efficacy and safety of filgrastim after high-dose chemotherapy and autologous bone marrow transplantation (ABMT). PATIENTS AND METHODS: Patients with poor-risk non-Hodgkin's lymphoma or relapsed Hodgkin's disease were treated in a randomized, open-label trial to study the use of filgrastim as an adjunct to high-dose chemotherapy and ABMT. Of 43 assessable patients, 19 were randomized to receive filgrastim by continuous subcutaneous infusion at a dose of 10 micrograms/kg/d, 10 to filgrastim 20 micrograms/kg/d, and 14 to a parallel control group that received no filgrastim after ABMT. RESULTS: For all filgrastim-treated patients analyzed together, the median time to neutrophil recovery > or = 0.5 x 10(9)/L after the day of ABMT was significantly accelerated to 10 days compared with 18 days in control patients (P = .0001). The median number of platelet transfusions was identical in both groups. Clinical parameters, including the median number of days with fever (1 v 4, P = .0418) and neutropenic fever (5 v 13.5, P = .0001) were significantly shorter in the filgrastim than in the control group. The number of days on intravenous antibiotics and duration of hospitalization were also shorter in the treated groups; however, the differences did not reach statistical significance. For patients treated with the two different dose levels of filgrastim, the neutrophil recovery and clinical results were similar. Filgrastim-associated toxicity appeared to be minimal, with five adverse events considered at least possibly related to filgrastim: two in the higher-dose group and three in the lower-dose group. All of these were rated moderate, except one case of severe bone pain that did not preclude continued filgrastim treatment at a lower dose. Survival and relapse-free survival were similar for control and filgrastim-treated patients. CONCLUSION: Taken together, the results of this first randomized study support the role of filgrastim given as an adjunct to ABMT in accelerating neutrophil recovery, as well as in reducing treatment-related morbidity and overall duration of the treatment procedure.

Adolescent↗
PubMed1993

[5 years of dosage intensification and autologous bone marrow or peripheral stem cell transfusion in malignant lymphoma with a high risk of recurrence].

Clinical results of the treatment of malignant lymphomas with a high risk of relapse by dose intensification and autologous bone marrow transplantation are reported. Since 1988, 68 patients with a median age of 34 years (range 16 to 56 years) received dose intensification, including 25 non-Hodgkin's lymphomas in first remission (12 lymphoblastic or Burkitt's lymphomas and 13 large cell lymphomas with risk factors), 20 aggressive non-Hodgkin's lymphomas in chemosensitive relapse, and 23 Hodgkin's lymphomas in chemosensitive relapse. The calculated 3-year overall survival and relapse-free survival was 72% (CI: 57-82%) and 61% (CI: 47-73%) respectively. Treatment related deaths were seen in 4.4%. The median duration of hospitalization was 30 days (range 19-51 days). The relapse-free 3-year survival for the separate treatment groups was 80% for lymphoblastic and Burkitt's lymphomas in first remission, 77% for large cell lymphomas with clinical risk factors in first remission, 39% for aggressive non-Hodgkin's lymphomas in chemosensitive relapse, and 59% for Hodgkin's lymphomas in chemosensitive relapse. These excellent results were obtained with acceptable toxicity and justify the use of dose intensification for a group of young patients with high risk lymphomas.

Adolescent↗
PubMed1993

Clinical significance of bcr-abl gene rearrangement detected by the polymerase chain reaction after allogeneic bone marrow transplantation in chronic myelogenous leukemia.

Although serial detection of bcr-abl positive cells by PCR appears able to identify distinct patient groups with different risks of relapse following BMT, there remain many unanswered questions regarding the clinical utility and biological significance of PCR detectable cells in this disease. Many of the studies summarized have conflicting results and the influence of various clinical parameters which are known to affect the risk of relapse post-BMT has not yet been consistently associated with the ability to detect bcr-abl positive cells by PCR. These clinical parameters include GVHD, T-cell depletion and intensity of immunosuppression following BMT. Prospective studies with larger patient numbers will be necessary to define the impact of these factors in PCR status and relapse. The answers to all these questions will increase our understanding of the biology of chronic myelogenous leukemia and help provide more effective therapies for the future.

Bone Marrow Transplantation↗