Medication Summary
The goals of pharmacotherapy are to induce remission, reduce morbidity, and prevent complications.
Hematopoietic Growth Factors
Class Summary
These agents can induce an increase in reticulocyte counts, with a subsequent increase in hematocrit and hemoglobin levels.
Pegfilgrastim (Neulasta)
Pegfilgrastim is a long-acting filgrastim created by the covalent conjugate of recombinant granulocyte colony-stimulating factor (ie, filgrastim) and monomethoxypolyethylene glycol. As with filgrastim, it acts on hematopoietic cells by binding to specific cell surface receptors, thereby activating and stimulating the production, maturation, migration, and cytotoxicity of neutrophils.
Epoetin alfa (Epogen, Procrit)
This agent is a purified glycoprotein produced from mammalian cells modified with gene coding for human erythropoietin (EPO). Its amino acid sequence is identical to that of endogenous EPO. The biological activity of epoetin alfa mimics human urinary EPO, which stimulates division and differentiation of committed erythroid progenitor cells and induces the release of reticulocytes from bone marrow into the blood stream.
Monoclonal Antibodies
Class Summary
The agents in this class target specific antigens in carcinoma cells and induce cytotoxicity.
Ibritumomab tiuxetan (Zevalin Y-90)
A murine monoclonal antibody that targets the CD20 antigen, ibritumomab tiuxetan is chelated to the radioisotopes indium-111 or yttrium-90. It is used in conjunction with rituximab to treat B-cell NHL or rituximab-refractory follicular NHL. The regimen consists of two low doses of rituximab, an imaging dose, two-three whole-body scans, and a therapeutic dose, all of which are delivered in an outpatient setting over 8 days.
Ofatumumab (Arzerra)
Ofatumumab is an anti-CD20 human monoclonal antibody that inhibits B-cell activation in early stages. It is indicated for chronic lymphocytic leukemia refractory to fludarabine and alemtuzumab.
Alemtuzumab (Lemtrada, Campath)
Alemtuzumab is a monoclonal antibody against CD52, an antigen found on B cells, T cells, and almost all chronic lymphocytic leukemia cells. It binds to the CD52 receptor of the lymphocytes, which slows the proliferation of leukocytes.
Rituximab (Rituxan)
Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an immunoglobulin G1 (IgG1) kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences.
Polatuzumab vedotin (Polatuzumab vedotin-piiq, Polivy)
Polatuzumab is a CD79b-directed antibody-drug conjugate with activity against dividing B cells. MMAE is an antimitotic agent covalently attached to the antibody via a cleavable linker. The monoclonal antibody binds to CD79b, where polatuzumab is internalized and linker is cleaved by lysosomal proteases to enable intracellular delivery of MMAE. MMAE binds to microtubules and kills dividing cells by inhibiting cell division and inducing apoptosis. It is indicated, in combination with bendamustine and a rituximab product is indicated for relapsed or refractory DLBCL, not otherwise specified, after at least 2 prior therapies.
Corticosteroids
Class Summary
These drugs have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Dexamethasone (Decadron, Dexamethasone intensol)
A component of the m-BACOD (methotrexate, bleomycin, doxorubicin [Adriamycin], cyclophosphamide, Oncovin, and dexamethasone) regimen, dexamethasone is a glucocorticoid that acts as an immunosuppressant by stimulating the synthesis of enzymes needed to decrease the inflammatory response. It also acts as an anti-inflammatory agent by inhibiting the recruitment of leukocytes and monocyte-macrophages into affected areas via inhibition of chemotactic factors and factors that increase capillary permeability.
Dexamethasone is readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Most of the adverse effects of corticosteroids are dose dependent or duration dependent.
Prednisone (Prednisone Intensol, Rayos, Deltasone)
A component of several regimens, such as CHOP, prednisone is a glucocorticoid that acts as an immunosuppressant by stimulating the synthesis of enzymes needed to decrease the inflammatory response. It also acts as an anti-inflammatory agent by inhibiting the recruitment of leukocytes and monocyte-macrophages into affected areas via inhibition of chemotactic factors and factors that increase capillary permeability.
Prednisone is readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Most of the adverse effects of corticosteroids are dose dependent or duration dependent.
Antineoplastic Agents
Class Summary
These agents inhibit cell growth and proliferation and lead to cell death.
Chlorambucil (Leukeran)
Chlorambucil alkylates and cross-links strands of DNA, inhibiting DNA replication and RNA transcription. It is used mainly to treat indolent lymphomas, particularly chronic lymphocytic leukemia (CLL) and Waldenstrom macroglobulinemia. This agent may be preferable for elderly patients with serious comorbid medical problems who require treatment for lymphoma. It is well absorbed orally.
Cyclophosphamide
Cyclophosphamide is chemically related to nitrogen mustards. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells. This agent can be used alone but is mostly used as a component of multiple combination chemotherapy regimens.
Bendamustine (Bendeka, Treanda)
Bendamustine is an alkylating agent that is a bifunctional mechlorethamine derivative. It forms covalent bonds with electron-rich nucleophilic moieties that can lead to cell death. It is active against both quiescent and dividing cells and is indicated for chronic lymphocytic leukemia (CLL).
Cisplatin
Cisplatin is a platinum-containing compound that exerts its antineoplastic effect by covalently binding to DNA, with preferential binding to the N-7 position of guanine and adenosine. It can react with 2 different sites on DNA to cause cross-links. The platinum complex also can bind to the nucleus and to cytoplasmic protein. A bifunctional alkylating agent, once cisplatin is activated to the aquated form in the cell, it binds to DNA, resulting in interstrand and intrastrand cross-linking and denaturation of the double helix.
Doxorubicin (Adriamycin)
An anthracycline antibiotic that can intercalate with DNA, doxorubicin affects many of the functions of DNA, including synthesis. It forms DNA-cleavable complexes by interaction with topoisomerase II, which is responsible for the cytocidal activity of the drug. Doxorubicin is administered IV and distributes widely into bodily tissues, including the heart, kidneys, lungs, liver, and spleen. It does not cross the blood-brain barrier and is excreted primarily in bile. It forms an important part of multiple chemotherapeutic regimens for lymphomas, including cyclophosphamide, hydroxydaunomycin (doxorubicin), vincristine (Oncovin), and prednisone (CHOP).
Vincristine (Vincasar PFS)
The mechanism of action of vincristine is uncertain. It may involve a decrease in reticuloendothelial cell function or an increase in platelet production; however, neither of these mechanisms fully explains the effect in thrombocytopenic purpura and hemolytic-uremic syndrome. Vincristine is used in hematologic and nonhematologic malignancies. It is a component of CHOP and other regimens for lymphoma.
Fludarabine
Fludarabine is a purine analogue that interferes with DNA synthesis by inhibiting ribonucleotide reductase. It is also incorporated into RNA, causing inhibition of RNA and protein synthesis; however, its primary effect may result from activation of apoptosis.
Nelarabine (Arranon)
Nelarabine is a prodrug of the deoxyguanosine analogue 9-beta-D-arabinofuranosylguanine (ara-G). It is converted to the active 5'-triphosphate, ara-GTP, a T-cell–selective nucleoside analog. Leukemic blast cells accumulate ara-GTP. This allows for incorporation into DNA, leading to inhibition of DNA synthesis and cell death
Cytarabine
Cytarabine is converted intracellularly to the active compound cytarabine-5'-triphosphate, which inhibits DNA polymerase. It is cell cycle S phase specific and it blocks the progression from the G1 to the S phase, in turn killing cells that undergo DNA synthesis in the S phase of the cell proliferation cycle.
Gemcitabine (Gemzar)
Gemcitabine is a cytidine analog. It is metabolized intracellularly to an active nucleotide. It inhibits ribonucleotide reductase and competes with deoxycytidine triphosphate for incorporation into DNA. It is cell-cycle specific for the S phase. Gemcitabine is indicated as first-line treatment for locally advanced (nonresectable stage II or stage III) or metastatic (stage IV) pancreatic adenocarcinoma.
Etoposide (Toposar)
Etoposide is a glycosidic derivative of podophyllotoxin that exerts its cytotoxic effect through stabilization of the normally transient covalent intermediates formed between DNA substrate and topoisomerase II, leading to single- and double-strand DNA breaks. This causes cell proliferation to arrest in the late S or early G2 portion of the cell cycle.
Mitoxantrone
Related to anthracyclines. Mitoxantrone intercalates into DNA. This results in cross-links and strand breaks. Binds to nucleic acids and inhibits DNA and RNA synthesis by template disordering and steric obstruction. Replication is decreased by binding to DNA topoisomerase II. Active through entire cell cycle.
Carboplatin
Carboplatin is an analog of cisplatin. This is a heavy metal coordination complex that exerts its cytotoxic effect by platination of DNA, a mechanism analogous to alkylation, leading to interstrand and intrastrand DNA cross-links and inhibition of DNA replication. It binds to protein and other compounds containing the SH group. Cytotoxicity can occur at any stage of the cell cycle, but the cell is most vulnerable to action of these drugs in the G1 and S phases. It has same efficacy as cisplatin, but with a better toxicity profile. The main advantages over cisplatin include less nephrotoxicity and ototoxicity, the lack of a need for extensive prehydration, and a smaller likelihood of inducing nausea and vomiting; however, it is more likely to induce myelotoxicity.
Bleomycin
This agent is composed of a group of glycopeptides extracted from Streptomyces species. Each molecule has a planar end and an amine end; different glycopeptides of the group differ in their terminal amine moieties. The planar end intercalates with DNA, while the amine end facilitates oxidation of bound ferrous ions to ferric ions, thereby generating free radicals, which subsequently cleave DNA, acting specifically at purine-G-C-pyrimidine sequences.
Vorinostat (Zolinza)
Vorinostat is a histone deacetylase (HDAC) inhibitor. HDAC inhibition results in hypoacetylation of core nucleosomal histones, it condenses the chromatin structure, and it represses gene transcription. It is indicated for the treatment of progressive, persistent, or recurrent cutaneous T-cell lymphoma.
Belinostat (Beleodaq)
Belinostat is a histone deacetylase (HDAC) inhibitor. HDACs catalyze the removal of acetyl groups from the lysine residues of histones and some nonhistone proteins. Inhibiting this action induces cell cycle arrest and/or apoptosis.
Umbralisib (Ukoniq)
Umbralisib is a dual inhibitor of PI3K-delta and casein kinase (CK1) 1-epsilon expressed on malignant B cells. It was granted accelerated approval to umbralisib (Ukoniq) for the treatment of adults with relapsed or refractory marginal zone lymphoma (MZL) who have received at least 1 prior anti-CD20-based regimen and for adults with relapsed or refractory follicular lymphoma (FL) who have received at least 3 prior lines of systemic therapy.
Antineoplastics, Tyrosine Kinase Inhibitor
Class Summary
Ibrutinib received accelerated approval from the FDA for marginal zone lymphoma following analysis of phase 2 data in 63 patients who had a median follow-up of 19.4 months. Of these patients, 3% (n=2) treated with ibrutinib achieved complete responses (CR) and 45% (n=27) achieved partial responses (PR). Overall, 78% of patients experienced tumor reduction. Median progression-free survival was 14.2 months. [37]
Ibrutinib (Imbruvica)
Bruton’s tyrosine kinase (BTK) inhibitor forms a covalent bond with a cysteine residue in the BTK active site, leading to inhibition of BTK enzymatic activity. BTK is a signaling molecule of the B-cell antigen receptor (BCR) and cytokine receptor pathways.
BTK’s role in signaling through the B-cell surface receptors results in activation of pathways necessary for B-cell trafficking, chemotaxis, and adhesion. It is indicated for mantle cell lymphoma in patients who have received at least 1 previous therapy. It also indicated for marginal zone lymphoma (MZL) in patients who require systemic therapy and have received at least 1 prior anti-CD20-based therapy.
Antineoplastics, PI3K Delta Inhibitors
Class Summary
This drug class inhibits one or more of the phosphoinositide 3-kinase enzymes, which are part of the PI3K/AKT/mTOR pathway, an important signalling pathway for many cellular functions such as growth control, metabolism and translation initiation. Within this pathway there are many components, inhibition of which may result in tumor suppression.
Copanlisib (Aliqopa)
Pan class I phosphatidylinositol-3-kinase (PI3K) inhibitor with predominant inhibitory activity against PI3K-alpha and PI3K-delta isoforms expressed in malignant B cells. By inhibiting several key cell-signaling pathways may induce apoptosis and inhibition of proliferation of premalignant B cells and in turn cause tumor cell death. It is indicated for relapsed follicular lymphoma (FL) in patients who have received at least 2 prior systemic therapies.
Idelalisib (Zydelig)
Idelalisib induces apoptosis and inhibits proliferation in cell lines derived from malignant B cells and in primary tumor cells; also inhibits several cell- signaling pathways, including B cell receptor (BCR) signaling and the CXCR4 and CXCR5 signaling, which are involved in trafficking and homing of B cells to the lymph nodes and bone marrow. It gained accelerated approval by the FDA (ie, confirmatory clinical trials in progress) in July 2014 for relapsed follicular B-cell non-Hodgkin lymphoma (FL) and relapsed small lymphocytic lymphoma (SLL) in patients who have received at least 2 prior systemic therapies.
Duvelisib (Copiktra)
Duvelisib is a selective oral small molecule inhibitor of PI3K-delta and PI3K-gamma. Inhibiting PI3K induces growth inhibition and reduces viability in cell lines derived from malignant B cells. It is indicated for adults with relapsed/refractory follicular cell lymphoma after at least 2 prior systemic therapies.
Antineoplastics, Angiogenesis inhibitor
Class Summary
These agents antagonize or inhibit the development of new blood vessels.
Lenalidomide (Revlimid)
Thalidomide analogue; inhibits TNF-alpha production, stimulates T cells, reduces serum levels of the cytokines vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), and inhibits angiogenesis. This agent also promotes G1 cell cycle arrest and apoptosis of malignant cells. Indicated for in combination with rituximab product for the treatment of previously treated follicular lymphoma or marginal zone lymphoma.
PD-1/PD-L1 Inhibitors
Class Summary
Monoclonal antibodies that bind the programmed cell death-1 protein (PD-1) ligands, PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibits T cell proliferation and cytokine production.
Pembrolizumab (Keytruda)
Indicated for the treatment of adult and pediatric patients with refractory primary mediastinal large B-cell lymphoma (PMBCL), or who have relapsed after 2 or more prior lines of therapy.
Antineoplastics, Anti-CD19 Monoclonal Antibodies
Class Summary
The monoclonal antibody binds to human CD19, a transmembrane protein expressed on surface of cells of B-lineage origin.
Loncastuximab tesirine (Zynlonta)
Indicated for adults with relapsed/refractory large-B-cell lymphoma following 2 or more lines of systemic therapy. Indication includes diffuse large B-cell lymphoma (DLBCL) not otherwise specified, DLBCL arising from low-grade lymphoma, and high-grade lymphoma.
Tafasitamab (Monjuvi)
Tafasitamab is a humanized Fc-modified cytolytic CD19 targeting monoclonal antibody. It is indicated, in combination with lenalidomide, for the treatment of adults with relapsed or refractory DLBCL not otherwise specified, including DLBCL arising from low- grade lymphoma, and who are ineligible for autologous stem cell transplant (ASCT).
CAR T-cell Therapy
Class Summary
Chimeric antigen receptor (CAR) T cell therapy is a form of adoptive T-cell therapy in which T cells are genetically engineered to express a CAR. CAR T cells preparation begins with obtaining a blood sample from the patient. The CAR molecule is introduced into the patient’s T cells through viral or nonviral approaches. The cells undergo a brief round of expansion in the laboratory and are then infused back into the patient. T cells become activated when they recognize the target antigen on the surface of the tumor, in this case, CD19. When T cells are activated, they undergo massive expansion in the body. The cells start to produce multiple different cytokines and proliferate. These cytokines improve the T cells’ function, help them traffic to the tumor site, and start killing the tumor cells by expressing cytotoxic molecules (eg, granzymes and perforins).
Axicabtagene ciloleucel (Yescarta)
CD19-directed genetically modified autologous T cell immunotherapy, binds to CD19-expressing cancer cells and normal B cells. Studies demonstrated that following the binding anti-CD19 CAR T cells with target cells, the CD28 and CD3-zeta co-stimulatory domains activate downstream signaling cascades which eventually leads to killing of CD19-expressing cells. It is indicated for relapsed or refractory large B-cell lymphoma after two or more lines of systemic therapy, including diffuse large B-cell lymphoma (DLBCL) not otherwise specified, primary mediastinal large B-cell lymphoma, high grade B-cell lymphoma, and DLBCL arising from follicular lymphoma.
Tisagenlecleucel (Kymriah)
CD19-directed genetically modified autologous T-cell immunotherapy that involves reprogramming a patient’s own T cells with a transgene encoding a chimeric antigen receptor (CAR) to identify and eliminate CD19-expressing malignant and normal cells. It is indicated in adults with relapsed or refractory large B-cell lymphoma (r/rDLBCL) including DLBCL not otherwise specified, high grade B-cell lymphoma, and DLBCL arising from follicular lymphoma after ≥2 lines of systemic therapy.
Lisocabtagene maraleucel (Breyanzi)
CD19-directed CAR T-cell therapy genetically modified autologous cell immunotherapy is administered as a defined composition to reduce variability in CD8-positive and CD4-positive T cell dose. CAR binding to CD19 expressed on tumor and normal B cells induces activation and proliferation of CAR T cells, release of pro-inflammatory cytokines, and cytotoxic killing of target cells. It is indicated for adults with R/R large B-cell lymphoma (LBCL) after two or more lines of systemic therapy, including DLBCL not otherwise specified (including DLBCL arising from indolent lymphoma), high-grade B-cell lymphoma, primary mediastinal large B-cell lymphoma, and follicular lymphoma grade 3B. It is not indicated for h primary CNS lymphoma.
-
Neoplastic follicles comprising cleaved cells (centrocytes) and larger cells with vesicular nuclei and prominent 2-3 nucleoli (centroblasts).
-
Mantle cell lymphoma. Small lymphoid cells with oval to slightly irregular nuclei and clumped chromatin and rare admixed pink histiocytes.
-
Diffuse large B-cell non-Hodgkin lymphoma. Large cells with abundant cytoplasm and large round-ovoid nuclei with thick nuclear membrane and multiple prominent nucleoli.
-
Burkitt lymphoma. Normal architecture is entirely replaced by lymphoma cells and evenly dispersed macrophages, starry sky (250×).
-
Burkitt lymphoma cells with round noncleaved nuclei and strongly basophilic cytoplasm (1000×).
-
Compartmentalizing fibrosis and infiltrate of medium-sized to large lymphoid cells.
-
Lymphoma cells show strong membranous positivity with CD20 indicative of B-cell origin.
Tables
- Table 1. Chromosomal Abnormalities in B-Cell Non-Hodgkin Lymphoma
- Table 2. Characteristic Immunophenotypes of Major Subtypes of Lymphoma
- Table 3. Lugano Modification of the Ann Arbor Staging System.
- Table 4. Non-Hodgkin lymphoma staging.
- Table 3. International Society for Cutaneous Lymphoma/European Organization for Research and Treatment of Cancer tumor-node-metastasis classification for cutaneous B-cell lymphoma
Cytogenetic Abnormality |
Histology |
Antigen Rearrangement |
Oncogene Expression |
t(14;18)(q32;q21) |
Follicular, diffuse large cell |
IgH* |
bcl- 2 |
t(11;14)(q13;q32) |
Mantle cell |
IgH |
cyclin-D1/bcl-1 |
t(1;14)(p22;q32) |
MALT lymphoma |
IgH |
bcl- 10 |
t(11;18)(q21;q21) |
MALT lymphoma |
IgH |
Unknown |
t(9;14)(p13;q32) |
Lymphoplasmacytic lymphoma |
IgH |
PAX-5 |
8q24 translocations t(8;14)(q24;q32) t(2;8)(p11-12;q24) t(8;22)(q24;q11) |
Burkitt lymphoma |
IgH Ig-8 Ig-6 |
c-myc |
Trisomy 12, deletion 11q22-23, 17p13, and 6q21 |
CLL |
… |
… |
*Immunoglobulin H (IgH) MALT = Mucosa-associated lymphoid tissue. |
|||
Lymphoma |
Immunophenotype |
Follicular |
CD20+, CD3-, CD10+, CD5-, BCL2+, CD23-/+, CD43-, cyclinD-1-, BCL6+ |
Small lymphocytic |
CD 20+, CD3-, CD10-, CD5+, CD23+, |
MALT |
CD20+, CD3-, CD 10-, CD5-, CD23-/+, BCL2+ |
Marginal zone |
CD20+, CD3-, CD 10-, CD5-, CD23-/+, CD43-/+, cyclinD-1-, BCL2 |
Mantle cell |
CD20+, CD23-/+, CD10-/+, CD5+, CD43-/+, cyclinD-1+ |
Mediastinal large B-cell |
CD20+, CD30+, MUM-1+ |
Burkitt |
slg+,CD20+, Tdt-, CD10+, BCL2--, BCL6+, Ki-67+ (≥95%) |
B-lymphoblastic |
slg-, CD19+, CD10-/+, CD20-/+, TdT+ |
MALT = mucosa-associated lymphoid tissue. |
|
Stage |
Area of Involvement |
Extranodal (E) Status |
|
I |
Single node or adjacent group of nodes |
Single extranodal lesions without nodal involvement |
|
II |
Multiple lymph node groups on same side of diaphragm |
Stage I or II by nodal extent with limited contiguous extranodal involvement |
|
II bulky* |
Multiple lymph node groups on same side of diaphragm with “bulky disease”. |
N/A |
|
III |
Multiple lymph node groups on both sides of diaphragm; nodes above the diaphragm with spleen involvement |
N/A |
|
IV |
Multiple noncontiguous extranodal sites |
N/A |
|
*Stage II bulky disease considered limited or advanced as determined by histology and a number of prognostic factors. Suffixes A and B are not required X for bulky disease replaced with documenting of largest tumor diameter Definition of “Bulky” disease varies depending on lymphoma histology. |
|||
Stage |
Area of Involvement |
Extranodal (E) Status |
|
I |
Single node or adjacent group of nodes |
Single extranodal lesions without nodal involvement |
|
II |
Multiple lymph node groups on same side of diaphragm |
Stage I or II by nodal extent with limited contiguous extranodal involvement |
|
II bulky* |
Multiple lymph node groups on same side of diaphragm with “bulky disease” |
N/A |
|
III |
Multiple lymph node groups on both sides of diaphragm; nodes above the diaphragm with spleen involvement |
N/A |
|
IV |
Multiple noncontiguous extranodal sites |
N/A |
|
Tumor |
Involvement |
Node |
Involvement |
Metastatic Spread |
Involvement |
T1 |
Solitary skin involvement T1a: ≤5 cm diameter T1b: >5 cm diameter |
N0 |
No lymph node involvement |
M0 |
No evidence of extracutaneous non-lymph node disease |
T2 |
Multiple lesions limited to one body region or two contiguous body regions T2a: all-disease in a < 15-cm diameter T2b: all-disease in a >15- and < 30-cm diameter T2c: all-disease in a >30-cm diameter |
N1 |
Involvement of one peripheral lymph node region |
M1 |
Evidence of extracutaneous non-lymph node disease |
T3 |
Generalized skin involvement T3a: multiple lesions involving two noncontiguous body regions T3b: multiple lesions involving three body regions |
N2 |
Involvement of two or more peripheral lymph node regions or involvement of any lymph node region that does not drain an area of current or prior skin involvement |
||
N3 |
Central lymph nodes involvement |
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- Overview
- Presentation
- DDx
- Workup
- Treatment
- Guidelines
- Medication
- Medication Summary
- Hematopoietic Growth Factors
- Monoclonal Antibodies
- Corticosteroids
- Antineoplastic Agents
- Antineoplastics, Tyrosine Kinase Inhibitor
- Antineoplastics, PI3K Delta Inhibitors
- Antineoplastics, Angiogenesis inhibitor
- PD-1/PD-L1 Inhibitors
- Antineoplastics, Anti-CD19 Monoclonal Antibodies
- CAR T-cell Therapy
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- Media Gallery
- Tables
- References
