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 Table of Contents  
Year : 2021  |  Volume : 17  |  Issue : 6  |  Page : 1297-1306

Pulmonary anaplastic large-cell lymphoma: A case-based systematic review of world literature

1 Department of Pathology and Laboratory Medicine, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
2 Department of Pulmonary Medicine, Critical Care, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
3 Department of Medical Oncology/Hematology, Critical Care, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
4 Department of Biostatistics, Kalinga Institute of Medical Sciences, Bhubaneswar, Odisha, India
5 Department of Pathology and Laboratory Medicine, All India Institute of Medical Sciences, Bhubaneswar; Department of Oncopathology, Acharya Harihar Regional Cancer Institute, Cuttack, Odisha, India

Date of Submission07-Dec-2019
Date of Decision26-May-2020
Date of Acceptance11-Jun-2020
Date of Web Publication14-Dec-2021

Correspondence Address:
Sonali Mohapatra
Department of Medical Oncology/Hematology, All India Institute of Medical Sciences, Bhubaneswar, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcrt.JCRT_1089_19

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 > Abstract 

We describe a case of ALK1 negative (–) pulmonary anaplastic large-cell lymphoma (pALCL) in an adult female with an unfavorable outcome following combination chemotherapy and present a systematic review of 39 such sporadic cases reported over the past 28 years (1990–2018). pALCL occurred in 26 males and 13 females (median age, 43 years [5–81]) and 13/39 (33.33%) were ≤18 years. The lesions were endobronchial in 21 (53.85%) and parenchymal in 18 (46.15%) cases. Twenty-six cases were ALK1-; 13 were ALK1+ (positive); and 27/34 cases had a T cell phenotype (where tested). ALK- cases were characterized by higher age (P = 0.012) at presentation, more B symptoms (P = 0.002), and more parenchymal than endobronchial lesions (P = 0.039). The median survival (N = 29/39) was 60 months; pediatric group had a better survival than adult/elderly group (log-rank, P = 0.026). pALCL is rare and may have a distinct biological behavior.

Keywords: Histopathology, outcome, pulmonary lymphoma

How to cite this article:
Padhi S, Panigrahi MK, Mohapatra S, Mishra P, Patra S, Sable MN, Thakur B, Nayak M, Panigrahi A. Pulmonary anaplastic large-cell lymphoma: A case-based systematic review of world literature. J Can Res Ther 2021;17:1297-306

How to cite this URL:
Padhi S, Panigrahi MK, Mohapatra S, Mishra P, Patra S, Sable MN, Thakur B, Nayak M, Panigrahi A. Pulmonary anaplastic large-cell lymphoma: A case-based systematic review of world literature. J Can Res Ther [serial online] 2021 [cited 2022 Jan 20];17:1297-306. Available from: https://www.cancerjournal.net/text.asp?2021/17/6/1297/332368

 > Introduction Top

Primary pulmonary lymphoma is a rare heterogeneous group of neoplasms which constitute 0.4% of all lymphomas and roughly 4% of all non-Hodgkin lymphomas and is characterized by indolent clinical course with tendency to relapse; nonspecific clinical and radiological characteristics masquerading common infective/inflammatory lesions, pseudo lymphomas, as well as primary neoplasms; poor or inferior diagnostic yield by conventional approaches leading to delayed diagnosis; and overall good clinical outcome, especially in those amenable to surgical resection.[1],[2] Dominant or primary bronchopulmonary involvement in anaplastic large-cell lymphoma (pulmonary ALCL) (pALCL) is extremely rare with nearly fifty cases reported in the world literature over the last three decades.[3],[4],[5] In this manuscript, we describe a case of pALCL in an adult female with a systematic review of literature pertaining to clinicoradiological characteristics, diagnostic pitfalls and pathology, and clinical outcome following therapy.

 > Case Presentation Top

In June 2016, a 47-year-old female presented to an outside hospital with complaints of fever, cough, and loss of weight and appetite for the last 6 months. She was a newly diagnosed case of type 2 diabetes mellitus well controlled with oral medications. Chest non enhanced computerized tomogram (NECT) scan and positron emission tomography (PET) scan performed 6 weeks prior to the visit at our center showed a hypermetabolic right upper lobe mass with irregular spiculated outline adherent to mediastinum along with mild pleural effusion on the right side [Figure 1]a. She was a never smoker and had not suffered from any lung disease in the past. Chest examination revealed diminished breath sound with dull note on the base of the right lung. Examination of other systems was unremarkable; there were no palpable lymphadenopathy and hepatosplenomegaly. A posteroanterior chest radiograph done at presentation reiterated the previous NECT scan finding [Figure 1]b. Hemogram showed hemoglobin; 84 g/L (reference: 120–140 g/L), total white cell count; 4.2 × 109/L (reference: 4–11 × 109/L) with differential count of neutrophil 90%, lymphocyte 9%, eosinophil 1%; and total platelet count; 294 × 109/L (reference: 150–450 × 109/L). Her liver function test showed hypoproteinemia (total protein: 5.5 g/dl, albumin: 2 g/dl) with normal enzymes. Serology for tropical fever like malaria and dengue was negative. Flexible bronchoscopy showed thick, pale yellow mucus plugging occluding the apical and posterior segment of the right upper lobe. Considering the possibility of infective (both bacterial and invasive fungal) etiologies in a diabetic background, she was put on empirical antibiotic levofloxacin and liposomal amphotericin; latter only to be withdrawn due to poor compliance and infusion related toxicities. Endobronchial biopsy demonstrated squamous metaplasia with moderate dysplasia with negative immunostaining for TTF1; and no evidence of invasive fungal disease was noted. Bronchial wash culture for bacterial and fungal organism was noncontributory. Blood and pleural fluid culture for bacteria and fungus were negative. Repeat bronchoscopy after 2 weeks showed similar feature and endobronchial biopsy demonstrated only squamous metaplasia. Bronchial wash staining and nucleic acid amplification for acid-fast bacilli were negative on both occasions. Constitutional symptoms including fever subsided with antibiotic therapy; however, the lung mass appeared increased in size with development of pleural effusion on the left side. Repeat NECT scan of the chest confirmed the increased size of the mass that was more rounded in appearance and extended peripherally abutting pleura. There was bilateral pleural effusion. Aspiration of the left pleural space yielded hemorrhagic fluid, which on cytological examination showed markedly increased cellularity with the presence of numerous large atypical mononuclear cells arranged discretely. These cells showed moderate cytoplasm, few of them showing cytoplasmic vacuoles, irregular nuclear contour, and coarse clumped chromatin. Cellbloric immunohistochemistry showed the mononuclear cells to be strongly and diffusely positive for leukocyte common antigen (LCA), CD3, CD30 (prominent Golgi zone positivity), and epithelial membrane antigen (EMA) (membranous), but negative for anaplastic lymphoma kinase (ALK-1), CD 20, pancytokeratin, WT1, and calretinin. This cytomorphology was consistent with the diagnosis of ALCL (ALK negative, T cell type) involving the pleural space [Figure 2]a, [Figure 2]b, [Figure 2]c, [Figure 2]d. NECT-guided biopsy of the right lung mass did not show any evidence of abnormal lymphoid cells. The patient continued to have worsening cough and increasing dyspnea. Echocardiogram showed significant pericardial effusion with features of early tamponade. Pericardiocentesis was performed emergently and empirically prednisolone was started. Subsequently, the patient underwent staging PET scan, which revealed increased 18F FDG uptake in bilateral supraclavicular lymph nodes (SUVmax 14.7), multiple mediastinal nodes (SUVmax 6.1), multiple abdominal nodes (SUVmax 18.3), right lung mass (SUVmax 14.3), pleural nodule (SUVmax 5.2), diffuse asymmetric wall thickening involving the distal body and antrum of stomach (SUVmax 8.1), and mild uptake in bone marrow. Left supraclavicular lymph node biopsy further confirmed the diagnosis of ALCL (CD30+, EMA+, ALK1-, proliferation index 80%, T cell phenotype) completely effacing the lymph node architecture. She received 6 cycles of combination chemotherapy comprising cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP). Follow-up chest radiograph 5 months after initiation of CHOP showed complete resolution of the lung mass. One month later (8 months post diagnosis), she had a local relapse, but did not opt for further management. Finally, she succumbed to the disease-related complications and the next of kin of the patient did not give consent to perform full body autopsy. The verbal informed consent was obtained from the next of the kin of the patient in accordance with Declaration of Helsinki.
Figure 1: (a) Thoracic non enhanced computerized tomogram scan performed 3 months prior to present hospital admission depicting a solid homogeneous mass occupying the apical segment of right-side lung and abutting pleura. There was no evidence of mediastinal and or abdominal/retroperitoneal lymphadenopathy at that time. (b) Posterior anterior chest X-ray at the time of present admission demonstrating a solid homogeneous mass in the apex of the right-side lung and pleural effusion on the left side

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Figure 2: Cytosmears from the centrifuged deposit of pleural fluid (left side) demonstrating markedly increased cellularity comprising of monotonous population of intermediate to large sized atypical cells with increased nuclear to cytoplasmic ratio, nuclei showing irregular membrane contour, dense chromatin and one to two conspicuous nucleoli; consistent with a malignant effusion (a) (May Grunewald Giemsa stain, ×400). On cellblock immunohistochemistry these atypical cells were strongly and diffusely positive for leukocyte common antigen (b), CD 30 (Golgi zone, c), epithelial membrane antigen (d), but negative for anaplastic lymphoma kinase 1(ALK1) consistent with a diagnosis of ALK1 negative anaplastic large-cell lymphoma (Peroxidase-antiperoxidase, ×400). Left supraclavicular lymph node biopsy, 1½ month later, confirmed the present diagnosis (histopathological features not represented)

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 > Review of Literature Top

Study period

January 1990 to December 2018 (28 years).

Search engines

The search engines were PubMed/Medline, PubMed Central, Directory of Open Access Journals, Google Scholar, and Research Gate. The following search items were used for literature search: pulmonary non Hodgkin lymphoma, pulmonary involvement in ALCL, pulmonary involvement in hematolymphoid malignancies, primary pulmonary lymphomas, primary pulmonary ALCL, primary lymphoproliferative disorders in lungs, anaplastic large cell non Hodgkin lymphoma in lungs, pleuropulmonary involvement in systemic ALCL, pleural effusion in ALCL, pleural effusion in malignant lymphomas, secondary pulmonary involvement in ALCL, Endobronchial ALCL, etc.

Inclusion and exclusion criteria

All those cases where pulmonary involvement was described as the first or dominant or only extranodal site of presentation and/or the diagnosis was first made from the samples such as endobronchial/transbronchial/image-guided biopsies, resection specimens, bronchial brushings/washings, bronchoalveolar lavage fluid, or the pleural effusion cytology were included in the study. We followed the guidelines proposed by Piña-Oviedo et al. to define primary pALCL.[2] As per this, primary pALCL was defined as lymphoma confined to the lung and/or bronchi with or without hilar lymph node involvement at the time of diagnosis or up to 3 months thereafter. All cases of primary tracheal ALCLs (including one of 5 cases as described by Rush et al.[6]) and those high-grade B cell lymphomas with anaplastic morphology were excluded from the study. We found 43 papers which described 52 sporadic cases of primary or dominant pulmonary involvement in ALCL. Out of these, four cases with secondary pleuropulmonary involvement in systemic disease were excluded. Among nine of the remainder 48 cases (4 Chinese, 3 Spanish, 1 Bosnian, and 1 Mexican), full-length articles were not available and hence were excluded from the analysis. Finally, 39 cases satisfied the criteria of primary pALCL and thus were included in this study.[3],[4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36],[37] Among 29 of these 39 cases, detailed therapeutic and follow-up information were available and hence were subjected to survival analysis [Flowchart 1].

Collection of data

Data were collected into an Excel sheet with regard to the following: age (in years); gender; symptom with duration; smoking history; underlying immune status (retroviral status, prolonged steroid or any other immunosuppressive therapy); presence or absence of B symptoms (fever, night sweats, and weight loss); imaging modalities used and their lesional characteristics; localization of pulmonary lesion; presence or absence of collapse/atelectasis/pleural effusion; extrathoracic/extrapulmonary sites of involvement (if any) at the time of diagnosis; pathology, immunophenotyping, and molecular characteristics (if any); treatment given; and described outcome from the time of diagnosis.

Statistical analysis

Baseline characteristics were described using mean (±standard deviation) for continuous variables and count (percentage) for nominal variables. Comparison between two subgroups was done using Pearson's Chi-square and Fisher's exact test. The Kaplan–Meier method was used to determine survival patterns for variables identified as having a significant effect on survival. Differences between survival curves were evaluated using log-rank tests. All statistical tests were two-sided; P < 0.05 was considered statistically significant. Analyses were performed using IBM SPSS statistics (version 20.0) (Armonk, NY, USA).

 > Results and Discussion Top

The detailed clinicoravidogical, pathological, managent, an follow up data are presented in [Table 1] and [Table 2]; are a comparison between petiatric on adult population is presentation [Table 3].
Table 1: Primary pulmonary anaplastic large-cell lymphoma: A comprehensive review (January 1990-December 2018) (n=39/48)*

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Table 2: Baseline characteristics of all cases of primary pulmonary anaplastic large-cell lymphoma (n=39)

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Table 3: Comparison between pediatric and adult cases of pulmonary anaplastic large-cell lymphoma

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Clinicoradiological characteristics

There were 26 males (66.67%) and 13 females (33.33%) with a male-to-female ratio of 2:1. The median age at presentation was 43 years (range: 5–81 years); 13 (33.33%) cases were under the age of 18 years. Thirty-five (89.74%) cases had no evidence of underlying immunosuppression; 6 (15.39%) were past or present smokers; and 23 (59%) had associated B symptoms (more so in adults than pediatric; 17/26 vs. 6/13 cases, respectively, P = 0.014). Symptom duration ranged from days to months prior to diagnosis. Fever, cough with or without sputum production, and breathlessness/dyspnea were the three most common presentations; 7 had worsening dyspnea/respiratory failure; 3 had hemoptysis; one had asthma like presentation; and two were asymptomatic.

Computerized tomogram (CT) scans with or without contrast and plain chest radiographs were used most commonly to characterize the lesions. The lesions were characteristically described as fleshy or polypoidal “endobronchial” lesions in 21 cases (53.85%) and “parenchymal” in 18 (46.15%) cases. A higher proportion (22/39, 56.41% vs. 12/39, 30.76%) of these tumors occurred in the right side, whereas 5 (12.82%) had bilateral lesions. Fifteen of 21 (71.42%) cases with endobronchial lesions presented with evidence of partial or complete collapse. Almost half of all cases (10/21; 47.61%) with endobronchial lesions occurred in the pediatric age group (≤18 years). On imaging, the lesions had a varied appearance mimicking infective, autoimmune/inflammatory, or even primary lung malignancies. These were described as follows: mass or mass like in 25 (64.10%); nodular infiltrates in 11 (28.20%); consolidation, cavity, and ground-glass opacities in 1 case each (02.56%); associated collapse/atelectasis in 15 (38.36%); effusion in 6 (15.38%); and hilar and/or mediastinal adenopathy in 3 cases (7.70%). The spectrum of radiological features in pulmonary lymphoproliferative lesions (reactive and neoplastic) have been reported to be varied and nonspecific, ranging from solitary nodule to lymphangitic parenchymal involvement. Features such as nodules, mass-like consolidation, cavitation, air bronchograms, perivascular and/or peribronchial interstitial thickening mimicking lymphangitis carcinomatosa, and mediastinal adenopathy were more commonly reported in malignant lesions.[38] Von Ende et al. described an unusual radiological finding of the left upper lobe atelectasis seen on chest radiographs in the form of the “luftsichel sign” in a case of pALCL, a sign which is almost always indicative of central primary lung cancer.[5]

Pathology and immunohistochemical characteristics

ALCL is a type of T cell neoplasm, which exhibits diverse histomorphological patterns, which is characterized by the presence of variably sized, Reed Sternberg like giant cells with pleomorphic, often horseshoe shaped/embryo like/wreath like nuclei and moderate to abundant cytoplasm (so called “hallmark cells”) (classical/common variant, type I).[39] At times, the classical histomorphology of ALCL may be obscured by prominent necroinflammatory background (inflammatory type, type II) rich in lymphocytes and histiocytes (lymphohistiocytic [LH] variant), histiocytic/epithelioid cell rich (granuloma like), neutrophils and/or eosinophils rich; prominent vascularity (granulation tissue like); or even associated fibroblastic proliferation. Sporadic reports of tumor cells exhibiting monotonous population of small round cells (small cell [SC] variant, type III) or pleomorphic spindle cell pattern (sarcomatoid variant, type IV) masquerading a spindle cell sarcoma or even malignant fibrous histiocytoma (MFH) are also not uncommon. Rarely, ALCLs with histomorphological features not attributed to the above said categories are segregated into ALCL not otherwise specified (ALCL-NOS, type V) category.[39] Previous studies have reported the SC/LH variant to have an aggressive clinical outcome with the former reported to be notorious for leukemic transformation, followed by ALCL-NOS behaving much aggressively compared to the classical variant.[39],[40],[41] As per this, majority of pALCLs belonged to type I category (18/39, 45%); 8/39 (20.5%) were of type II category; 5/39 (12.8%) were of type III category; 2/39 (5.12%) were of type IV category; and remainder 6/39 (15.38%) were categorized as of type V phenotype.

On immunohistochemistry (IHC), the lesional cells of pALCL typically exhibited strong membranous and Golgi zone positivity for CD30 and variably positivity for EMA, granzyme B, TIA1, LCA, CD56, MUM1, and Vimentin. ALK1 expression was noted (positive; +) in 21/37 cases (where it was tested); and the remainder 26 cases were reported as ALK1 negative (−). Twenty-seven (69.23%) cases were categorized as T cell type, whereas seven cases (17.94%) were of null phenotype. Molecular study (performed in nine cases) demonstrated T cell receptor rearrangement in five cases, t (2; 5) translocation in three cases, and DUSP22/IRF4 amplification in one case. A higher proportion (11/13; 84.61%) of pediatric subjects expressed ALK1 compared to 10/26 (38.46%) adults, both by IHC and at molecular level (P = 0.000). The mean age at presentation and/or diagnosis of ALK1 + pALCL was 30.83 ± 24.5 years compared to that of ALK1 phenotype (47.6 ± 16.9 years) (P = 0.012). B symptoms were more commonly associated with the latter (76.47% vs. 23.53%, respectively, P = 0.002), whereas endobronchial localization of lesions with associated collapse/atelectasis was more associated with ALK1 + phenotype (75.0% vs. 25.0%, respectively, P = 0.039) [Table 3].

Diagnostic pitfalls

Bronchoscopy is known to have a low diagnostic yield in patients with pulmonary lymphoma and therefore video-assisted thoracoscopic surgery (VATS) or open lung biopsy is recommended.[1] Yang et al. in their review of 11 cases of pALCL found that none other than one case had a positive diagnostic yield on bronchoscopic biopsy.[27] In another retrospective study by Kim et al. on 24 cases of primary pulmonary lymphomas, the diagnostic yield from bronchoscopic biopsy (performed in 80% cases) was reported to be 30%, while a significantly higher proportion (66.7%) needed surgical approaches (open thoracotomy or VATS) for definite diagnosis.[36] In accordance with published literature, the lesions of pALCL were obscured by prominent necroinflammatory, granulation tissue like, or even sarcoma like fibroblastic proliferation, leading to misdiagnosis and re-biopsies. At times, prominent regenerating atypia in adjacent bronchial epithelial surfaces led to a misdiagnosis of bronchogenic carcinomas (as was also in our case), poorly differentiated high-grade malignancy suggestive of a neuroendocrine neoplasm; or rarely high-grade undifferentiated sarcoma reminiscent of so-called inflammatory MFH. Prominent peritumoral inflammatory infiltrate-related systemic symptoms dominated the clinical picture, especially in ALK cases. These all lead to delayed diagnosis; surgical approaches such as endobronchial resections, lobectomy, pneumonectomy, or open lung biopsy were performed, both as a part of management of life-threatening respiratory failure and for better diagnostic yield [Table 4].
Table 4: Histopathology, immunohistochemical characteristics, and diagnostic pitfalls in primary pulmonary anaplastic large-cell lymphoma

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Management and outcome

Of the 31/39 cases where data pertaining to therapeutic and follow-up duration were available, 20 cases received combination chemotherapy (CT) in the form of CHOP, CHVbP, DCDVE, DVMP, DDEVP, or hyper CVAD-A regimens [Table 1]); 8 cases received combination of CT, surgery, and/or radiotherapy; and the remainder 3 cases received supportive care. Twenty-four cases had complete response with no evidence of disease; seven had partial response with 3/7 died due to refractory disease. The median duration of survival was 60 months; the pediatric group had a significantly better survival compared to adults (log-rank, P = 0.026) [Figure 3]a and [Figure 3]b. This was possibly because of the fact that this group harbored favorable ALK1+ phenotype, more endobronchial localization which might have led to earlier presentation, as well as endobronchial resection and biopsy (both for diagnosis and part of management). There was no statistically significant survival difference between ALK1 + and ALK1- group (log-rank, P = 0.692); T or null phenotype (log-rank, P = 0.432); presence or absence of collapse/atelectasis (log-rank, P = 0.628); and presence or absence of effusion (log-rank, P = 0.171) [Figure 3]c, [Figure 3]d, [Figure 3]e. However, all these outcomes need to be interpreted with caution due to less number of cases with null phenotype (n = 7) and effusion (n = 6). A recent large study on 102 systemic ALCL patients has reported that ALK1 expression did not affect the overall survival (OAS) and disease-free survival; rather, the Ann Arbor stage, performance status, international prognostic index, histological subtype, and the degree of the background inflammatory infiltrate were found to impact the OAS significantly. Histological subtypes such as inflammatory/LH (type II) and SC (type III) had worst prognosis followed by ALCL-NOS (type V), whereas the classical variant (type I) had the best prognosis. Cases with dense inflammatory background had inferior OAS compared to those with absent or sparse inflammatory infiltrate.[40],[41],[42]
Figure 3: Kaplan Meier survival analysis in pulmonary anaplastic large-cell lymphoma using log-rank test (n = 29). The median overall survival was 60 months (a) which was significantly higher among pediatric population (≤18 years) compared to adults (>18 years) (log-rank, P = 0.026) (b). There was no statistical significance in survival when correlated with ALK1 status [c], blue line; ALK1+ (, red line; ALK-), presence or absence of collapse/atelectasis (d); or effusion (e) (log-rank, P > 0.05)

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 > Conclusion Top

pALCL is a distinctly rare histological subtype of non-Hodgkin lymphoma with a favorable outcome. Histomorphology may be misleading which can lead to delayed/misdiagnosis for which surgical intervention may be necessary, both for diagnosis and a part of multimodality management.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3], [Table 4]


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