Below is a broad, patient-friendly overview of immunotherapies used in blood cancers (and, in some cases, solid tumors as well). Immunotherapies harness the power of the body’s immune system to target, recognize, and destroy cancer cells. This list is extensive but not exhaustive, and treatments vary based on factors like specific diagnosis, genetic mutations, and patient health. As always, this information is for educational purposes only and does not replace professional medical advice.


1. Monoclonal Antibodies (mAbs)

Monoclonal antibodies are lab-made proteins designed to recognize specific targets (antigens) on cancer cells. Once they bind, they can flag cancer cells for destruction by the immune system or deliver cytotoxic agents directly to tumor cells.

  1. Rituximab (Rituxan)
    • Target: CD20 on B-cells
    • Common Uses: Non-Hodgkin lymphoma (NHL), Chronic Lymphocytic Leukemia (CLL)
    • How It Works: Tags CD20+ cancerous B-cells so immune cells can eliminate them.
  2. Obinutuzumab (Gazyva) / Ofatumumab
    • Target: Also CD20 on B-cells, with slight design differences from rituximab
    • Common Uses: Follicular lymphoma, CLL
    • How It Works: Similar to rituximab but engineered to potentially trigger stronger immune responses in some patients.
  3. Blinatumomab (Blincyto)
    • Type: Bispecific T-cell engager (BiTE)
    • Targets: CD19 on B-cells and CD3 on T-cells
    • Common Uses: Acute Lymphoblastic Leukemia (ALL)
    • How It Works: Brings T-cells in direct contact with leukemia cells, facilitating targeted killing.
  4. Inotuzumab Ozogamicin
    • Type: Antibody-drug conjugate (ADC)
    • Target: CD22 on B-cells
    • Common Uses: Relapsed or refractory B-cell ALL
    • How It Works: Delivers a potent cytotoxic “payload” directly into cancer cells, minimizing damage to healthy cells.
  5. Gemtuzumab Ozogamicin (Mylotarg)
    • Type: ADC
    • Target: CD33 on myeloid cells
    • Common Uses: Acute Myeloid Leukemia (AML)
    • How It Works: Similar mechanism—an antibody linked to a toxin that’s internalized by AML cells.
  6. Brentuximab Vedotin (Adcetris)
    • Type: ADC
    • Target: CD30
    • Common Uses: Hodgkin lymphoma, some T-cell lymphomas
    • How It Works: Once bound to CD30+ cells, it releases a chemotherapy agent inside the tumor cell.
  7. Polatuzumab Vedotin
    • Type: ADC
    • Target: CD79b on B-cells
    • Common Uses: Certain types of relapsed/refractory diffuse large B-cell lymphoma (DLBCL)
    • How It Works: Delivers a toxin to B-cells when internalized, sparing many normal cells.
  8. Daratumumab (Darzalex) / Isatuximab
    • Target: CD38 on plasma cells
    • Common Uses: Multiple Myeloma
    • How It Works: Flags myeloma cells for immune destruction, can also directly induce tumor cell death.
  9. Elotuzumab (Empliciti)
    • Target: SLAMF7 on myeloma cells and NK cells
    • Common Uses: Multiple Myeloma (often combined with other agents like lenalidomide)
    • How It Works: Increases NK cell activity to kill myeloma cells, which also express SLAMF7.

2. Checkpoint Inhibitors

These drugs block proteins (checkpoints) used by cancer cells to avoid being attacked by T-cells. By removing the “brakes” on the immune system, T-cells can recognize and eliminate cancer more effectively.

  1. Nivolumab (Opdivo) / Pembrolizumab (Keytruda)
    • Target: PD-1 on T-cells
    • Common Uses: Hodgkin lymphoma (especially the relapsed or refractory type), some cases of Non-Hodgkin lymphoma, and various solid tumors
    • How It Works: Prevents PD-1 from binding to PD-L1/PD-L2 (on tumor cells or other immune cells), freeing T-cells to attack cancer.
  2. Atezolizumab (Tecentriq) / Durvalumab (Imfinzi)
    • Target: PD-L1 (on tumor or immune cells)
    • Common Uses: More common in solid tumors, but research is expanding into some blood cancers.
    • How It Works: Similar concept—blocks the PD-L1/PD-1 interaction so T-cells stay active against cancer.

3. CAR T-Cell Therapy

Chimeric Antigen Receptor (CAR) T-cell therapy is a form of adoptive cell transfer. A patient’s T-cells are collected, genetically engineered to produce special receptors that bind cancer-specific antigens, then expanded in a lab and infused back into the patient.

  1. CD19-Targeted CAR T-Cells
    • Examples: Tisagenlecleucel (Kymriah), Axicabtagene Ciloleucel (Yescarta), Lisocabtagene Maraleucel (Breyanzi)
    • Common Uses: Relapsed/refractory B-cell ALL (Kymriah), large B-cell lymphoma (Yescarta, Breyanzi), and other CD19+ lymphomas
    • How It Works: Engineered T-cells home in on CD19+ cancer cells and initiate a strong immune attack.
  2. BCMA-Targeted CAR T-Cells
    • Examples: Idecabtagene Vicleucel (Abecma), Ciltacabtagene Autoleucel (Carvykti)
    • Common Uses: Relapsed/refractory multiple myeloma (targeting BCMA on myeloma cells)
    • How It Works: T-cells gain a receptor that recognizes BCMA, a protein found primarily on plasma cells.
  3. New Targets (e.g., CD22, CD30)
    • CAR T research is rapidly expanding to target various antigens in different blood cancers, such as AML, T-cell lymphomas, and more.
    • Combining CAR T with checkpoint inhibitors or other immunotherapies is an active area of study.

4. Immunomodulatory Drugs (IMiDs)

IMiDs aren’t traditional “immunotherapies” in the sense of antibodies or CAR T-cells, but they enhance immune function and directly curb cancer cell growth.

  1. Thalidomide / Lenalidomide (Revlimid) / Pomalidomide (Pomalyst)
    • Uses: Multiple myeloma, sometimes certain lymphomas (e.g., mantle cell lymphoma with lenalidomide)
    • How They Work: They strengthen T-cell and NK cell activity, decrease tumor-supporting blood vessels, and degrade proteins vital to myeloma cells.
  2. Mechanisms:
    • Anti-Angiogenesis: Reduces formation of new blood vessels needed by tumors.
    • Immune Activation: Boosts cytokine release and immune cell effectiveness.

5. Cytokines & Growth Factors

While not always termed “immunotherapy,” cytokines and growth factors can enhance the immune response or support blood cell recovery.

  1. Interleukin-2 (IL-2)
    • Historically used in some leukemias and lymphomas (as well as melanoma, renal cell carcinoma).
    • Stimulates growth of T-cells and NK cells, though side effects can be significant.
  2. Interferons (IFN-α)
    • Have been used in chronic myelogenous leukemia (CML), hairy cell leukemia, and some lymphomas.
    • Can slow cancer cell division and boost immune activity.
  3. Colony-Stimulating Factors (G-CSF, GM-CSF)
    • Often used supportively to rebuild white cell counts after chemotherapy, reducing infection risks.
    • Some therapies are researching ways to combine these with vaccines or immunostimulants for better anti-tumor responses.

6. Cancer Vaccines & Oncolytic Viruses

Still in development or used in specific settings, these approaches aim to prime the immune system or directly infect and kill tumor cells, spurring an immune response.

  1. Therapeutic Vaccines
    • Designed to stimulate immune cells against specific cancer antigens.
    • Used in certain trials for lymphomas or myeloma, though not widely standard yet.
  2. Oncolytic Viruses
    • Viruses engineered to replicate inside tumor cells, causing them to burst.
    • Can also release tumor antigens, boosting T-cell responses.

Key Points About Immunotherapies

  1. Target Specificity: Many immunotherapies hone in on markers unique to cancer cells, sparing normal tissues.
  2. Side Effects: While often less toxic than chemotherapy, immunotherapies can cause immune-related effects—like cytokine release syndrome (CRS) with CAR T or checkpoint inhibitors, or infusion reactions with mAbs.
  3. Personalized Approach: Biomarker testing (e.g., CD19, PD-L1 levels, BCMA) helps match the right therapy to each patient.
  4. Combination Potential: Immunotherapies are frequently used alongside chemo, targeted therapies, or radiation to enhance outcomes.
  5. Rapidly Evolving Field: New immunotherapy agents and combinations are constantly in clinical trials, expanding options for patients.

Disclaimer

This extensive list of immunotherapies is provided for general educational purposes and does not replace individualized medical advice. Specific treatment choices depend on factors like cancer subtype, genetic markers, patient health, and the latest clinical research. Always consult a qualified oncologist or hematologist for personalized guidance.