Journal of Clinical Oncology, Vol 18, Issue 2
(January), 2000: 317
© 2000 American Society for Clinical Oncology
European Phase II Study of Rituximab (Chimeric Anti-CD20 Monoclonal Antibody) for Patients With Newly Diagnosed Mantle-Cell Lymphoma and Previously Treated Mantle-Cell Lymphoma, Immunocytoma, and Small B-Cell Lymphocytic Lymphoma
By James M. Foran,
Ama Z. S. Rohatiner,
David Cunningham,
Razvan A. Popescu,
Philippe Solal-Celigny,
Michele Ghielmini,
Bertrand Coiffier,
Peter W. M. Johnson,
Christian Gisselbrecht,
Felix Reyes,
John A. Radford,
Eric M. Bessell,
Bertrand Souleau,
Aziz Benzohra,
T. Andrew Lister
From the Imperial Cancer Research Fund Medical Oncology Unit, St Bartholomew’s Hospital, London; Department of Medicine, Royal Marsden Hospital, Sutton; Imperial Cancer Research Fund Cancer Medicine Unit, St. James’ University Hospital, Leeds; Cancer Research Campaign Department of Medical Oncology, Christie Hospital, Manchester; and Department of Clinical Oncology, Nottingham City Hospital, Nottingham, United Kingdom; Centre Jean Bernard, Le Mans; Department of Hematology, Centre Hospitalier Lyon Sud, Lyon; Department of Hematology, Hopital St Louis, Paris; Department of Hematology, Hopital Henri Mondor, Creteil; Service d’Hematologie, Hopital d’Instructions des Armees Percy, Clamart; and Roche Pharmaceuticals, Neuilly, France; and Servizio Oncologico, Ospedale San Giovanni, Bellinzona, Switzerland.
Address reprint requests to James M. Foran, MD, ICRF Medical Oncology Unit, St Bartholomew’s Hospital, 45 Little Britain, London EC1A 7BE United Kingdom; email foran{at}icrf.icnet.uk
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ABSTRACT
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PURPOSE: Mantle-cell lymphoma (MCL), immunocytoma (IMC), and small B-cell lymphocytic lymphoma (SLL) are B-cell malignancies that express CD20 and are incurable with standard therapy. A multicenter phase II study was conducted to assess the toxicity and the overall response rates (RR) and complete response (CR) rates to rituximab (chimeric anti-CD20 monoclonal antibody).
PATIENTS AND METHODS: Between January 1997 and January 1998, 131 patients with newly diagnosed MCL (MCL1; n = 34) and previously treated MCL (MCL2; n = 40), IMC (n = 28), and SLL (n = 29) received rituximab 375 mg/m2/wk for 4 weeks via intravenous infusion. Restaging studies were performed 1 and 2 months after treatment. An analysis of the duration of response was conducted in December 1998.
RESULTS: Eleven patients were unassessable, including one who died of splenic rupture after the first infusion. The RR among the 120 assessable patients was 30% (36 of 120 patients). The RR by histology was as follows: MCL1, 38%; MCL2, 37%; IMC, 28%; and SLL, 14%. Ten patients, all with MCL, achieved CR. The median duration of response in MCL was 1.2 years. Immediate side effects were common and usually responded to adjustments in the infusion rate. There were 31 episodes of infection after treatment; most cases were mild. Cardiac arrhythmia and ophthalmologic side effects occurred in 10 and nine patients, respectively, including one case of severe loss of visual acuity.
CONCLUSION: Single-agent rituximab has moderate activity in MCL and IMC but only limited activity in SLL. The duration of response in MCL was similar to that previously reported in follicular lymphoma. Its use in combination with cytotoxic chemotherapy to increase the CR rate is warranted in MCL and IMC.
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INTRODUCTION
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ANTIBODY-BASED immunotherapy is a long-established concept.1 However, it was not until 1975, when Köhler and Milstein2 reported the fusion of a mouse myeloma cell with a mouse splenocyte from an immunized donor with production of monoclonal antibody of predefined specificity (the so-called ‘hybridoma’), that passive immunotherapy of malignancy, or ‘serotherapy,’ became a practicable possibility. Although the therapeutic potential of such monoclonal antibody (MoAb) therapy was recognized immediately, the associated allergic toxicity, the development of human antimouse antibodies, and the inability of some murine MoAbs to induce a cellular response in humans made the clinical reality more disappointing (see review in Grossbard et al3). The more recent development of humanized MoAbs, either engineered with human constant (Fc) regions4 or complementarity-determining region (CDR) grafted,5 has renewed interest in treatment with unconjugated MoAbs.
The CD20 antigen is an ideal target for treatment with a MoAb. Its expression is restricted to the B-cell lineage, where it is reliably present in almost all B-cell non-Hodgkin’s lymphomas,6,7 it does not modulate, and it is not shed in response to stimulation. Ligation of CD20 by specific MoAb has been shown to inhibit malignant B-cell proliferation in vitro and to induce apoptosis.8
Rituximab (IDEC-C2B8) is a chimeric (mouse/human) anti-CD20 MoAb that comprises human IgG1 and kappa constant regions, with specific murine variable regions.4 Studied initially in patients with follicular lymphoma,9,10 it was well tolerated, and clinically active, with an overall response rate (RR) of approximately 50%.11,12 Few complete responses (CRs) were seen, however.
Mantle-cell lymphoma (MCL), immunocytoma (IMC; including lymphoplasmacytoid lymphoma and Waldenström’s macroglobulinemia in the Kiel classification),13 and small B-cell lymphocytic lymphoma (SLL) are less common B-cell malignancies.13-17 As a group, patients with these diagnoses typically present with advanced-stage disease and at an older age. Despite responsiveness to chemotherapy, the clinical course is characterized by recurrence, and each of these subtypes of lymphoma is demonstrably incurable with standard therapy. The median survival of patients with SLL is approximately 7 years, whereas for patients with IMC, and particularly MCL, it is significantly shorter (approximately 5 and 3 years, respectively).15,18-21
Virtually all cases of MCL, IMC, and SLL express CD20 (with the exception of a minority of IMC with late plasmacytoid differentiation). A phase II study of rituximab as a single agent was undertaken accordingly. The results form the basis for this report.
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PATIENTS AND METHODS
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An open phase II trial was conducted at 19 centers in England, France, and Switzerland from January 1997 through January 1998 (see Appendix for list of participating investigators and centers). The primary aim of the study was to assess the overall RR and CR rate to therapy with rituximab. The secondary aim was to assess the toxicity profile of rituximab in this population. The study protocol was approved by the local hospital ethics committee of each participating institution, and all patients gave informed, written consent before therapy commenced.
Patients
Eligible patients included adults ( 18 years of age) with either newly diagnosed MCL (MCL1), previously treated MCL (MCL2), IMC, or SLL. Histologic diagnosis was assigned at the individual treatment center according to standard Kiel criteria;13 the diagnosis of MCL was made in accordance with the criteria of the Revised European-American Lymphoma (REAL) classification.14 CD20 positivity was confirmed in all patients.
In the Kiel classification,13 IMC includes patients with lymphoplasmacytoid lymphoma (B-cell chronic lymphocytic leukemia [B-CLL] with plasmacytoid differentiation in the REAL classification)14 and lymphoplasmacytic lymphoma (lymphoplasmacytoid IMC in the REAL classification), including those with the clinical entity of Waldenström’s macroglobulinemia (WM). For the purposes of this analysis, all patients with lymphoplasmacytoid or lymphoplasmacytic lymphoma (the former being the most common; n = 21) and those with WM (n = 7) are considered together as IMC.
One hundred thirty-one patients were registered and treated, including 34 patients with MCL1, 40 patients with MCL2, 28 patients with IMC (as defined in the preceding paragraph), and 29 patients with SLL. Clinical characteristics at the time of study entry are listed in Table 1. All patients had a World Health Organization performance status of  2 at study entry; those with evidence of active hepatitis B or C infection, human immunodeficiency virus infection, or CNS disease were excluded. Patients with lymphocytosis were not excluded from treatment. Any prior therapy must have been completed at least 1 month before initiation of treatment with rituximab. On review, two patients who were initially registered as MCL1 had received prior therapy, in one case 1 month before rituximab; both are, therefore, considered as MCL2 in this analysis.
Baseline staging studies were performed within 2 weeks of registration, including computed tomography scan of chest, abdomen, and pelvis, and bone marrow (BM) trephine biopsy and aspirate.
Treatment
Rituximab 375 mg/m2 was administered once weekly for 4 weeks as an intravenous (IV) infusion in 1 L of normal saline. Premedication with an antipyretic and an antihistamine (eg, paracetamol and chlorpheniramine) was given routinely to most patients; corticosteroids, which represented a protocol violation, were not given. Patients considered to be at risk of a tumor-lysis syndrome received prophylactic allopurinol and hydration with the first infusion in accordance with practices at the individual centers. Rituximab was administered over several hours, with frequent monitoring of vital signs in accordance with the investigational drug brochure guidelines.22 Briefly, the first infusion was started at 50 mg/m2/h for the first hour and, if well tolerated, was increased by increments of 50 mg/m2/h to a maximum of 300 mg/m2/h. In subsequent weeks, the infusion was started at 100 mg/m2/h and increased in increments of 100 mg/m2/h to a maximum of 400 mg/m2/h. The infusion was stopped for any episode of hypotension (either absolute, or 30 mmHg drop in systolic blood pressure from baseline), bronchospasm, rigors, mucosal congestion or edema, or any other medically significant event. Infusions were restarted at one half of the previous infusion rate as medically appropriate and then accelerated as tolerated on the schedule noted above.
Patients underwent a weekly clinical review before treatment, including physical examination, to assess for toxicity and for evidence of progressive disease (PD). Serum chemistries (electrolytes, urea and creatinine, liver function tests) and full blood counts (hemoglobin, WBC count, and platelet count) were also performed at baseline, weekly before therapy, and at follow-up.
Restaging studies (computed tomography scans of chest, abdomen, and pelvis, BM aspirate, and trephine biopsy) were repeated 1 month after finishing therapy and again 1 month later to assess for late responses. All patients achieving a CR or partial response (PR) to therapy underwent confirmatory restaging studies performed 1 month later; patients with a late response (occurring at 2 months), therefore, underwent confirmatory restaging investigations 3 months after finishing the treatment. All patients with BM infiltration at baseline had repeat BM aspirate and trephine biopsies performed at the 1- and 2-month restaging studies. Flow cytometric analysis of peripheral blood or BM was not routinely performed.
Definitions
Strict response criteria were applied, according to the following definitions: CR, the complete disappearance of all clinically detectable disease (including BM infiltration and nonnmeasurable disease), with no residual lymph nodes greater than 1.0 cm2, as determined by two observations not less than 4 weeks apart; PR, 50% decrease in the sum of bidimensional measurements for all measurable lesions as determined by two observations 1 month apart, and/or an estimated decrease in nonmeasurable disease by 50% (eg, BM infiltration), with no new lesions; stable disease, less than 50% decrease in the sum of bidimensional measurements of all measurable lesions or less than 25% increase in the sum of bidimensional measurements and/or in the estimated size of nonmeasurable disease; PD, 25% increase in the bidimensional size of one or more lesions or the appearance of any new lesions.
Follow-Up
Because of the nature of the underlying disease, patients were free to receive further therapy at the discretion of the treating physician at the end of treatment/response evaluation. Surveillance of patients in remission after rituximab was performed according to the practices at the individual centers. However, a retrospective analysis of remission duration was conducted in December 1998 of the patients with MCL and IMC who achieved a CR or PR to therapy. Six patients with MCL received further therapy as consolidation of remission after rituximab treatment, which was administered before the documented progression of disease; therefore, they are censored at that time in the follow-up analysis (see Statistical Considerations).
Statistical Considerations
RRs (and 95% confidence intervals [95% CI]) were calculated for assessable patients. The duration of response in MCL was calculated according to the method of Kaplan and Meier23; patients were censored in this analysis at last follow-up if they remained in remission, and at the time of further therapy if it was administered before the documentation of PD (ie, if treatment was given to consolidate the response achieved with rituximab; n = 6). Differences in the duration of response between groups with MCL were tested for statistical significance using the log-rank test. Differences in the RR between groups of previously treated patients were tested for statistical significance using Fisher’s exact test (two-tail).
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RESULTS
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Response
Thirty-six patients achieved a PR or CR to rituximab; therefore, the overall RR was 27% (36 of 131 patients). However, treatment was not completed in nine patients because of treatment-related toxicity, including one patient who died of splenic rupture (see Toxicity). One additional patient finished treatment but did not have outcome restaging studies performed because of an intercurrent illness, and another patient withdrew consent to continue treatment before its completion.
The RR among the 120 assessable patients was, therefore, 30% (36 of 120). Most responses were partial; only 10 patients, all with MCL, achieved a CR. Sixty-one patients had stable disease, and 23 had evidence of PD during therapy or at the 1-month restaging study. Most responses were evident within 1 month after completion of therapy, although there were two late responses (ie, occurring 2 months after finishing therapy), and responses improved from partial to complete at the confirmatory restaging in four other patients with MCL. Two of the 26 patients achieving PR developed early PD at the confirmatory (2-month) restaging studies (as reflected in Duration of Response, below).
The RR according to histology is listed in Table 2. Patients with MCL1 and MCL2 had a similar RR. No CR was seen in patients with IMC or SLL; the overall RR in the latter group was only 14%. Among the previously treated patients, the RR within each histologic subgroup was not statistically significantly higher in those patients who had received only one or two prior treatments when compared with the RR of the more heavily pretreated patients (ie, three previous treatments). A response to rituximab was achieved in two of the 11 patients who had previously undergone high-dose therapy; both patients had MCL.
Duration of Response
Twenty-five patients with MCL achieved a CR or PR to rituximab; eight of 25 patients have subsequently developed progressive MCL. At a median follow-up from treatment of 1.3 years, the projected median duration of response in MCL was 1.2 years (Fig 1). The duration of response was not significantly greater for patients achieving CR versus PR, or for patients with MCL1 versus MCL2.
Seven patients with IMC also achieved a PR (including two patients with WM); four have developed PD (at 3, 3, 11, and 12 months after therapy, respectively). While in remission of lymphoma, one patient died of metastatic gastric carcinoma, and another developed acute myeloid leukemia; both events occurred 10 months after completion of rituximab therapy. The remaining patient remains in unmaintained remission 15+ months after therapy.
Thirty-six patients had lymphocytosis at baseline (ie, peripheral-blood lymphocytes > 5.0 x 109/L), 24 of whom achieved normalization of lymphocytosis; seven of the latter patients achieved a clinical response. Ten of the 36 patients (eight with SLL) had marked lymphocytosis at baseline (ie, > 25.0 x 109/L); none of these 10 patients achieved a response to rituximab. Thirty-three of those with baseline lymphocytosis also had demonstrable BM infiltration; this resolved after treatment with rituximab in only four patients, three of whom achieved a clinical response.
Toxicity
All 131 patients are included in the evaluation of toxicity (Table 3). The infusions were generally well tolerated. Infusional side effects (eg, fever, rigor, nausea, and so on) were relatively common, occurred most frequently with the first treatment, and, in most cases, were managed with adjustments in the infusion rate. The average duration of the first infusion was 5.2 hours (95% CI, 4.7 to 5.7 hours), compared with 3.4 hours (95% CI, 3.2 to 3.6 hours) for subsequent infusions (ie, weeks 2 through 4), which reflects the fact that there were fewer interruptions for adverse reactions, and a more rapid infusion rate in later weeks. No evident excess in infusional toxicity was observed in the 10 patients presenting with a marked lymphocytosis (ie, > 25 x 109/L), although one patient did experience a severe anaphylactic-type reaction with the first infusion, which necessitated its discontinuation. The latter patient was subsequently able to complete treatment without further reaction.
Eight patients did not finish therapy because of adverse events, having been withdrawn because of anaphylaxis/severe allergic reaction (n = 3), atrial fibrillation and congestive heart failure (n = 1), elevation in serum liver function tests (n = 1), syncope (n = 1), syncope and bradycardia (n = 1), and urticaria and hypotension (n = 1). Another patient with underlying diabetes mellitus and extensive chemotherapy-refractory MCL died of splenic rupture several hours after completing the first infusion, which had been complicated by fevers, rigors, and hypoglycemia (cause of death was confirmed on postmortem examination). Four of these nine patients had a baseline lymphocytosis, but none had marked lymphocytosis (ie, > 25 x 109/L).
Thirty-one episodes of infection were noted in follow-up (Table 3). Most were mild or moderate, and the most common site was the respiratory tract. Ten patients had varicella zoster (shingles) or herpes simplex virus infection. There were four episodes of late neutropenia ( 1 month after therapy); in three cases, this was accompanied by fever. All four episodes resolved spontaneously.
Ten patients developed an arrhythmia with treatment, including bradycardia (n = 3), atrial fibrillation (n = 2), and nonspecified arrhythmia or tachyarrhythmia (n = 5). One other patient had palpitations, and another was noted to have premature ventricular complexes. In most cases, these were noted with the infusions or immediately afterwards. Ophthalmologic toxicity (mostly mild) was seen in nine patients, including conjunctivitis (n = 4), transient ocular edema (n = 2), a burning sensation in the eyes (n = 1), and transient visual changes (n = 1). The remaining patient, who had MCL2 and underlying well-controlled glaucoma, developed a permanent and severe loss of visual acuity 1 month after rituximab, for which no etiology was established.
With the exception of the patient withdrawn for grade 3 elevation of serum ALT (according to the National Cancer Institute common toxicity criteria) (above), significant abnormalities in serum chemistries were rare. No other patient developed a greater than grade 2 elevation in serum creatinine, ALT, or AST, and only two patients developed grade 3 elevation in total bilirubin (both had grade 2 bilirubin elevation at baseline). Hematologic abnormalities, however, were relatively common (Table 4); in most cases, these abnormalities normalized after therapy. It must be noted that many patients did not have a normal complete blood count at baseline, and in most cases, hematologic toxicity represented an increase from baseline by a grade of only 1 or 2. In only nine cases of lymphocytopenia that reached grade 3 or 4 toxicity, and in only three cases of leukopenia, did the patient have a normal complete blood count at baseline. Persistent lymphocytopenia (ie, at 1 month after therapy) was noted in 16 patients, and persistent leukopenia, anemia, and thrombocytopenia were present after rituximab therapy in 11, nine, and five patients, respectively.
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DISCUSSION
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Standard therapy with alkylating agents alone (with or without corticosteroids) offers substantial palliation but no cure to patients with MCL, IMC, and SLL. CRs are rare, and treatment ultimately fails in almost all who present with advanced-stage disease. More intensive therapy, with the inclusion of an anthracycline (eg, doxorubicin), has been shown to increase the RR, particularly in MCL,24,25 but it has not been shown to affect the overall survival. Consolidation of complete remission with high-dose therapy and hematopoietic stem-cell support has not yet been demonstrated to influence the natural history of these diseases.20,26-28 New treatments are needed.
Rituximab has been shown to induce responses (mostly partial) in approximately 50% of patients with follicular lymphoma, which is the most common of the less aggressive lymphomas.12 It also has some activity in diffuse large B-cell lymphoma.29 This is the first study to assess its efficacy at this dose and schedule in patients with MCL, IMC, and SLL. Although the RR (CR and PR) was only 30%, the results remain encouraging. Rituximab represents a new treatment, with a novel mode of action, which is administered over a short period of time. Furthermore, it can induce remissions in heavily pretreated patients with MCL and IMC, albeit in a minority.
The activity in MCL, including 10 CRs, was particularly encouraging and was similar to that reported in a smaller number of patients (n = 13) treated with 8 weeks of therapy (RR, 33%), some of whom received 500 mg/m2/wk.29 There is no evident advantage, therefore, to a higher dose or a longer course of therapy. The RR and the duration of response were the same for both newly diagnosed and previously treated patients in this study. The reason for this is not clear, although it suggests that prior treatment with chemotherapy does not diminish the activity of rituximab in patients with MCL. The projected duration of response (median, 1.2 years) was similar to that previously reported in patients with follicular lymphoma.12
IMC is an uncommon illness, considered predominantly in the REAL classification as a subclass of B-CLL (with the exception of lymphoplasmacytic IMC, which is recognized as a distinct entity in the REAL classification).13,14 Despite some activity, the overall RR seen in this study was not better than that expected with standard alkylating agent–based treatment regimens.16-18,20,21 Furthermore, no patient entered complete remission, which is again consistent with the low CR rates observed with other treatments for this disease. Rituximab alone, therefore, is not likely to add significantly to the ability to cure these patients but instead may offer palliation in selected patients.
The low RR and absence of CRs in SLL was particularly disappointing. Although the reasons for this are not clear, it has been noted that serum antibody concentrations are lower among patients with this disease12; this factor has been correlated with a lower RR.30 This may simply result from a greater tumor burden in SLL. Furthermore, it has been demonstrated that in B-CLL (the leukemic counterpart of SLL), the malignant cells express a lower density of the CD20 antigen on the cell surface, which might partially account for the low RR.31 The experience in this study, as in previous reports,12 suggests little role for rituximab in SLL at this dose and schedule. It must be noted that, in one report, a higher RR was seen in patients with SLL who were treated with a longer course of therapy (8-week schedule).32 It is of interest that the RR in this study was superficially higher in patients with IMC than in those with SLL, as these diseases have considerable clinical similarity and overlap.13-18,20 It seems that patients with lymphocytic lymphoma who have a greater morphologic degree of plasma cell differentiation may be more likely to respond to rituximab.
Therapy was generally well tolerated, with most toxicity being directly related to the infusion (most commonly the first infusion). This is consistent with previous reports. One patient with MCL died of splenic rupture soon after finishing the first infusion; this may have been related to rituximab, although a mechanism is difficult to postulate. Spontaneous splenic rupture has been reported to be a very rare complication of MCL.33
The cardiac and ophthalmologic toxicity are of concern. Arrhythmia that occurs in association with treatment may be secondary to the release of cytokines in response to cell lysis (eg, interleukin-6 and tumor necrosis factor alpha)34 or may simply relate to the advanced median age and heavy pretreatment of this patient group. Ophthalmologic side effects have not been previously reported. Extranodal lymphoma is a well-known phenomenon in these diseases, although none of the patients who experienced ophthalmologic sequelae in this study were known to have direct ocular involvement. CD20 is not known to be present in either the eye or the myocardium.
The hematologic toxicity is similar to that reported previously. Rituximab has previously been associated with anemia and a degree of reversible dyserythropoiesis on BM examination that is similar to that seen after some cytotoxic chemotherapy, possibly on an "innocent bystander" basis (eg, the proximity of immune-mediated cytolysis in the BM).35 T-lymphocyte subsets and immunoglobulins were not routinely assessed in this trial, but in previous reports these were not significantly altered.12 Clinical immunosuppression after rituximab is also apparent. The incidence of infection, which was mostly mild and bacterial and most commonly involved the respiratory tract, was similar to that reported previously. There were no deaths from infection on this study.
In this population, single-agent rituximab did not offer a higher RR or CR rate than alkylating agents.16-21 Therefore, its indication as monotherapy must be restricted to selected patients with depleted BM reserve for whom most other options have failed. However, its novel mechanism of action and its activity, particularly in MCL, suggest that its inclusion in combination chemotherapy may enhance the RR, with little additional toxicity, as demonstrated in a pilot study of patients with follicular lymphoma.36 Ongoing trials in MCL will test that hypothesis.
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APPENDIX
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Principal investigators and participating centers include the following: T.A. Lister, St. Bartholomew’s Hospital, London, UK; D. Cunningham, Royal Marsden Hospital, Sutton, UK; P. Solal-Celigny, Centre Jean Bernard, Le Mans, France; F. Cavalli, Ospedale San Giovanni, Bellinzona, Switzerland; B. Coiffier, Centre Hospitalier Lyon Sud, Lyon, France; P. Johnson, St. James’ Hospital, Leeds, UK; C. Gisselbrecht; Hôpital St. Louis, Paris, France; F. Reyes; Hopital Henri Mondor, Creteil, France; J.A. Radford, Christie Hospital, Manchester, UK; E. Bessell; Nottingham City Hospital, Nottingham, UK; G. Nedellec, Hopital d’Instructions des Armees Percy, Clamart, France; N. Milpied, Hotel Dieu, Nantes, France; J-F. Rossi, Hopital Lapeyronie, Montpellier, France; J. Sweetenham; Royal South Hants. Hospital, Southampton, UK; B. Varet, Hopital Necker, Paris, France; A. Delmer, Hotel Dieu, Paris, France; R. Pettengell, St. George’s Hospital, London, UK; P. Colombat, Hopital Bretonneau, Tours, France; and A.H. Goldstone, University College Hospital, London, UK.
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ACKNOWLEDGMENTS
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We gratefully acknowledge the patients who took part in this study and the physicians who referred them for treatment. We are indebted to the medical and nursing staff who helped care for the patients, the help of pharmacists at the participating centers, and, in particular, the help of the radiologists who patiently measured many lymph nodes in two dimensions.
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accepted August 5, 1999.
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TOP
ABSTRACT
INTRODUCTION
