Cancer Immunotherapy: Types, How It Works, Side Effects

Cancer immunotherapy uses the body’s own immune system to recognize and destroy cancer cells — an approach fundamentally different from chemotherapy, which kills rapidly dividing cells indiscriminately, or radiation, which targets tissue locally. The immune system can already detect cancer in its early stages, but advanced tumors develop molecular strategies to evade immune attack. Immunotherapy dismantles those strategies.

The field has been transformed by a sequence of breakthroughs: the first checkpoint inhibitor approval (ipilimumab, 2011), the first tissue-agnostic cancer drug approval in history (pembrolizumab for MSI-H/dMMR any solid tumor, May 2017), the first CAR-T cell therapy (tisagenlecleucel, 2017), the first LAG-3 inhibitor (relatlimab, 2022), and the first personalized mRNA cancer vaccine to demonstrate benefit in a Phase 2 trial (mRNA-4157 + pembrolizumab, KEYNOTE-942, published 2024). Today, cancer immunotherapy spans checkpoint inhibitors, CAR-T cell therapy, bispecific antibodies, cancer vaccines, and TIL therapy. For context on how immunotherapy fits within all cancer treatment modalities, see the cancer treatment guide.

49% 7-year overall survival with nivolumab + ipilimumab for advanced melanoma (CheckMate 067) — vs. 26% with ipilimumab alone

47.5 vs. 29.1 mo Overall survival with durvalumab vs. placebo after chemoradiotherapy for unresectable stage III NSCLC (PACIFIC trial)

ORR 97.9% Response rate with ciltacabtagene autoleucel (CAR-T) in relapsed/refractory multiple myeloma — sCR 78.4% (CARTITUDE-1)

RFS HR 0.561 44% risk reduction Personalized mRNA vaccine mRNA-4157 + pembrolizumab vs. pembrolizumab alone — adjuvant high-risk melanoma (KEYNOTE-942, Phase 2b, NEJM 2024)

How Cancer Evades the Immune System

T cells patrol the body scanning for abnormal peptides (neoantigens) displayed on MHC class I molecules on every cell’s surface. When a T cell receptor matches a neoantigen on a cancerous cell, the T cell activates, proliferates, and kills. Most malignant cells are eliminated before they ever form a detectable tumor — a process called immune surveillance.

Cancers that survive and progress have acquired mechanisms to defeat this surveillance:

PD-L1 Upregulation

Cancer cells express PD-L1, which binds PD-1 on T cells → exhaustion signal. T cells remain physically present but become functionally inert — unable to kill.

CTLA-4 Exploitation

CTLA-4 on T cells suppresses T cell activation in lymph nodes during the priming phase. Tumors benefit from fewer new anti-tumor T cells being generated.

LAG-3 Co-Inhibition

LAG-3 synergizes with PD-1 to drive deep T cell exhaustion in the tumor microenvironment — a third brake that compounds PD-1-mediated suppression.

Immunosuppressive TME

Tumors secrete TGF-β, IL-10, VEGF; recruit immunosuppressive Tregs and M2-polarized macrophages — creating a local environment hostile to immune attack.

Checkpoint Inhibitors

Immune checkpoints (PD-1, CTLA-4, LAG-3) are molecular off-switches on T cells that normally prevent autoimmunity. Cancer exploits them to shut down anti-tumor T cell responses. Checkpoint inhibitor drugs are monoclonal antibodies that block these interactions — freeing T cells to attack the tumor.

CTLA-4 Inhibitors — The First Checkpoint

Ipilimumab (Yervoy) was the first checkpoint inhibitor approved anywhere in the world (FDA March 2011) and the first drug to demonstrate an overall survival benefit in advanced melanoma. It works in the lymph nodes — blocking the CTLA-4 brake during T cell priming — allowing more anti-tumor T cells to be generated. Today ipilimumab is most commonly used in combination with nivolumab. The CheckMate 067 trial reported 7-year OS of 49% with the combination versus 26% with ipilimumab alone — landmark data establishing the feasibility of long-term survival in metastatic melanoma.

PD-1 Inhibitors — The Broadest Reach

Pembrolizumab (Keytruda) is the most broadly approved cancer drug in history with indications across 18+ cancer types. It blocks PD-1 on T cells within the tumor microenvironment — restoring effector function where it matters most. Key results:

KEYNOTE-024 (NSCLC, PD-L1 ≥50%): PFS 10.3 vs. 6.0 months; OS 26.3 vs. 14.2 months vs. platinum chemotherapy → standard 1L monotherapy for high PD-L1 NSCLC
KEYNOTE-189 (non-squamous NSCLC, all PD-L1): OS 22.0 vs. 10.7 months with pembrolizumab added to pemetrexed/carboplatin → standard 1L combination regardless of PD-L1 status (except EGFR/ALK-positive)
KEYNOTE-177 (MSI-H/dMMR mCRC 1L): PFS 16.5 vs. 8.2 months vs. chemotherapy (OS HR 0.74) → 1L standard for MSI-H metastatic CRC
Tissue-agnostic — MSI-H/dMMR (May 2017): First tissue-agnostic cancer drug approval in history — any solid tumor with MSI-H/dMMR, regardless of origin
Tissue-agnostic — TMB-H ≥10 mut/Mb (June 2020): ORR ~29% across tumor types (KEYNOTE-158)

Nivolumab (Opdivo) is approved for melanoma, NSCLC, RCC, esophageal SCC, HCC, CRC (MSI-H), and gastric/GEJ cancer. In metastatic RCC (CheckMate 214), nivolumab + ipilimumab achieved 5-year OS of 47% versus 26.6% with sunitinib in intermediate/poor-risk patients.

PD-L1 Inhibitors

Durvalumab (Imfinzi) produced one of the most practice-defining results in oncology with PACIFIC: consolidation durvalumab after concurrent chemoradiotherapy for unresectable stage III NSCLC extended OS to 47.5 versus 29.1 months — an 18-month survival gain. Durvalumab + gemcitabine/cisplatin is also the first-line standard for biliary tract cancer after TOPAZ-1 (OS HR 0.80).

Atezolizumab (Tecentriq) combined with bevacizumab is the preferred first-line treatment for unresectable HCC (IMbrave150: OS 19.2 vs. 13.4 months vs. sorafenib). Avelumab (Bavencio) is the standard switch-maintenance therapy for urothelial carcinoma after non-progressive platinum chemotherapy (JAVELIN Bladder 100: PFS 3.7 vs. 2.0 months).

LAG-3 — The Third Validated Checkpoint

In March 2022, relatlimab + nivolumab (Opdualag) became the first LAG-3 inhibitor approved. RELATIVITY-047 demonstrated PFS of 10.1 versus 4.6 months (HR 0.75) in advanced melanoma versus nivolumab monotherapy — validating LAG-3 as a meaningful third immune checkpoint target. Crucially, the toxicity profile was substantially better than the nivolumab + ipilimumab combination, offering checkpoint combination benefit without the same irAE burden.

Immunotherapy Biomarkers

Biomarker	Assay Method	Clinical Use	FDA Approval
PD-L1 (TPS/CPS)	IHC (22C3, 28-8, SP263 — assay varies by drug)	Pembrolizumab monotherapy (NSCLC TPS ≥50%); combinations (TPS ≥1%; CPS ≥10 for gastric/TNBC)	By tumor type
MSI-H / dMMR	IHC (MLH1/MSH2/MSH6/PMS2) or PCR/NGS	Pembrolizumab any solid tumor; nivolumab ± ipi CRC (MSI-H)	May 2017 — tissue-agnostic
TMB-H (≥10 mut/Mb)	NGS (FoundationOne CDx or equivalent)	Pembrolizumab any solid tumor (ORR ~29%)	June 2020 — tissue-agnostic

MSI-H/dMMR: The Most Predictive Single Immunotherapy Biomarker

MSI-H/dMMR tumors have defective DNA mismatch repair, generating thousands of frameshift mutations — each a potential neoantigen for immune recognition. Pembrolizumab in MSI-H/dMMR colorectal cancer 1L (KEYNOTE-177: PFS 16.5 vs. 8.2 months) has replaced FOLFOX/FOLFIRI as the first-line treatment for this subgroup. All patients with newly diagnosed metastatic cancer should be tested for MSI-H/dMMR status regardless of tumor type, since the tissue-agnostic approval covers any solid tumor.

CAR-T Cell Therapy

CAR-T cell therapy genetically engineers a patient’s own T cells to express a synthetic chimeric antigen receptor (CAR) that recognizes specific cancer cell surface proteins — bypassing MHC-I, the primary mechanism by which tumors hide from T cells.

The CAR-T Process

Leukapheresis: T cells collected from patient blood (4–6 hours)
Genetic engineering: Viral transduction with CAR construct: extracellular scFv targeting cancer antigen + CD3ζ signaling + co-stimulatory domain (CD28 or 4-1BB)
Expansion: Engineered cells expanded to tens–hundreds of millions over 2–4 weeks
Lymphodepletion: Patient receives fludarabine + cyclophosphamide to create space for CAR-T cells
Infusion → tumor killing: CAR-T cells recognize cancer antigen → cytotoxic killing + cytokine release

Approved CAR-T Products: Key Results

Product	Target	Cancer	Key Trial / Result
Axicabtagene ciloleucel (Yescarta)	CD19	DLBCL, PMBCL, FL	ZUMA-1: ORR 72%, CR 51%, 5-yr OS 42.6%; ZUMA-7: 2L EFS 8.3 vs 2.0 mo
Tisagenlecleucel (Kymriah)	CD19	DLBCL, FL, B-ALL (≤25 yr)	JULIET: ORR 52%, CR 40%; ELARA FL: ORR 86.2%, CR 69.1%
Lisocabtagene maraleucel (Breyanzi)	CD19	DLBCL, FL	TRANSFORM: 2L DLBCL EFS 10.1 vs 2.3 mo
Idecabtagene vicleucel (Abecma)	BCMA	Multiple myeloma	KarMMa: ORR 73%; KarMMa-3: PFS 13.3 vs 4.4 mo
Ciltacabtagene autoleucel (Carvykti)	BCMA (dual-domain)	Multiple myeloma	CARTITUDE-1: ORR 97.9%, sCR 78.4%; CARTITUDE-4: PFS HR 0.26

CAR-T Toxicity: CRS and ICANS — Specialized Center Required

Cytokine release syndrome (CRS): Fever, hypotension, hypoxia from massive cytokine release as CAR-T cells kill cancer cells. Managed with tocilizumab (anti-IL-6R) ± corticosteroids; grade 3–4 in a minority of patients but requires prompt recognition. ICANS (neurotoxicity): Encephalopathy, aphasia, seizures; managed with corticosteroids. CAR-T must be administered at certified treatment centers equipped to manage these toxicities. CD19-targeting CAR-T also destroys normal B cells → permanent hypogammaglobulinemia → lifelong IVIG replacement every 3–4 weeks.

cancer immunotherapy CAR-T cell therapy checkpoint inhibitor immune system — Cancer immunotherapy includes checkpoint inhibitors that remove T cell brakes and CAR-T cells that genetically engineer immune cells to seek and destroy cancer.

Bispecific Antibodies and TIL Therapy

Bispecific T Cell Engagers

Bispecific antibodies bind two targets simultaneously — typically a cancer surface antigen and CD3 on T cells — physically bridging T cell to cancer cell and triggering killing without MHC-I presentation or prior T cell priming. They are off-the-shelf (no manufacturing wait) unlike CAR-T.

Blinatumomab (Blincyto): CD19 × CD3 BiTE; continuous IV infusion. TOWER: R/R B-ALL: OS 7.7 vs. 4.0 months vs. chemo. BLAST: MRD-positive B-ALL — 78% achieved MRD-negative remission.
Teclistamab (Tecvayli): BCMA × CD3; SC injection; R/R myeloma: ORR 63%, CR 39.4% (MajesTEC-1)
Glofitamab (Columvi): CD20 × CD3; R/R DLBCL: ORR 52%, CR 39%; STARGLO: superior to R-GemOx
Epcoritamab (Epkinly): CD20 × CD3; SC; R/R DLBCL: ORR 63.1%, CR 38.9%
Tebentafusp (Kimmtrak): gp100 × CD3 ImmTAC; uveal melanoma (HLA-A*02:01 patients only): OS 21.7 vs. 16.0 months — first drug ever to improve OS in uveal melanoma (IMCgp100-202, NEJM 2021)

TIL Therapy — Lifileucel (Amtagvi)

Lifileucel (Amtagvi, Iovance) received FDA approval in February 2024 as the first TIL therapy. Tumor-infiltrating lymphocytes extracted from the patient’s resected tumor — cells already primed against the patient’s specific tumor neoantigens — are expanded ex vivo to billions and reinfused after lymphodepletion. In the C-144-01 trial, patients with advanced melanoma who had progressed on anti-PD-1 achieved ORR 31.5%, CR 4.5%. Unlike CAR-T, TIL therapy is polyclonal — multiple T cell clones targeting many different neoantigens simultaneously — potentially harder for tumors to escape through antigen loss.

Cancer Vaccines and mRNA Immunotherapy

Sipuleucel-T (Provenge) — First FDA-Approved Cancer Vaccine

Sipuleucel-T collects patient dendritic cells, activates them ex vivo with prostatic acid phosphatase fused to GM-CSF, and reinfuses them to stimulate a prostate cancer-specific immune response. The IMPACT trial demonstrated OS of 25.8 versus 21.7 months in asymptomatic/minimally symptomatic metastatic CRPC — a statistically significant benefit without PSA or radiographic response. Use has declined with newer mCRPC agents, but sipuleucel-T remains FDA-approved and approved by NCCN for selected patients.

Personalized mRNA Cancer Vaccines — The New Frontier

The most consequential development in cancer vaccines applies mRNA technology to cancer’s greatest vulnerability: each tumor carries hundreds of unique mutations creating tumor-specific neoantigens that no other human’s immune system has ever seen. A personalized mRNA vaccine encodes those unique neoantigens, training the immune system to recognize and attack those exact cancer cells.

mRNA-4157/V940 (Moderna/Merck) is the most advanced. In the KEYNOTE-942 Phase 2b trial (NEJM 2024), mRNA-4157 combined with pembrolizumab as adjuvant treatment for high-risk resected melanoma reduced recurrence-free survival risk by 44% (RFS HR 0.561) and reduced distant metastasis or death by 65% (DMFS HR 0.347) compared to pembrolizumab alone at 3-year follow-up. FDA Breakthrough Therapy designation granted. Phase 3 (KEYNOTE-B26) is now enrolling. This approach — sequencing a patient’s tumor, identifying their unique neoantigens, encoding them in mRNA, and delivering a fully personalized vaccine — represents a new paradigm for cancer treatment detailed further in the upcoming precision medicine cancer article.

Oncolytic Virus — T-VEC (Imlygic)

Talimogene laherparepvec (T-VEC) is an engineered herpes simplex virus-1 that selectively replicates in tumor cells and expresses GM-CSF — promoting dendritic cell recruitment and potentially systemic immune activation. Injected intralesionally into accessible melanoma lesions. OPTiM trial: durable response rate 16.3% vs. 2.1% (GM-CSF alone). FDA-approved 2015 for injectable, unresectable melanoma.

Immune-Related Adverse Events (irAEs)

By releasing immune checkpoints, checkpoint inhibitors can trigger autoimmune-like inflammation in normal tissues. Most irAEs are manageable, but some can be life-threatening — early recognition is critical.

Organ/System	irAE	Management	Notes
Skin	Rash, pruritis, vitiligo	Topical steroids; continue IO for grade 1–2	Vitiligo in melanoma may predict response
GI / Colitis	Diarrhea, bloody stool	Hold IO; prednisone; infliximab if steroid-refractory	Most common severe irAE with ipilimumab
Thyroid	Thyroiditis → hypothyroidism	Levothyroxine (permanent); NO high-dose steroids	Most common endocrine irAE; rarely reverses
Pituitary	Hypophysitis → panhypopituitarism	Physiologic hydrocortisone + other deficient hormones (permanent)	Most common with ipilimumab
Pancreas	Type 1 DM (rare)	Insulin (permanent); check glucose if symptomatic	Can present as DKA; permanent
Lung	Pneumonitis	Hold IO; prednisone 1–2 mg/kg; CT scan	More common with PD-1/PD-L1; potentially fatal
Heart	Myocarditis (rare ~0.1–0.5%)	Immediately discontinue; methylprednisolone 1000 mg/day IV; escalate early	~50% mortality grade 3–4; cardiac MRI + troponin
Liver	Immune hepatitis	Hold IO; prednisone; mycophenolate if refractory	Monitor LFTs every cycle

Endocrine irAEs: Permanent Hormone Replacement — Do NOT Use High-Dose Steroids

Most endocrine irAEs (hypothyroidism, type 1 diabetes, adrenal insufficiency) do not resolve — they require permanent hormone replacement regardless of whether immunotherapy is discontinued. High-dose corticosteroids are NOT appropriate for hypothyroidism or type 1 DM (they treat the inflammation of hypophysitis but not the resulting hormone deficiencies). Adrenal insufficiency requires physiologic hydrocortisone (20 mg AM / 10 mg PM), not immunosuppressive doses. All patients on checkpoint inhibitors need regular thyroid function tests and should be counseled to report new fatigue, constipation, weight changes, or excessive thirst immediately.

Frequently Asked Questions

What is cancer immunotherapy?

Cancer immunotherapy is a broad category of treatments that use or enhance the body’s immune system to fight cancer. Rather than directly damaging cancer cells with chemotherapy or radiation, immunotherapy either removes the molecular brakes that prevent immune cells from attacking tumors (checkpoint inhibitors: anti-PD-1, anti-CTLA-4, anti-LAG-3), engineers immune cells to directly recognize cancer cell surface markers (CAR-T cell therapy, bispecific T cell engagers), or trains the immune system to recognize cancer-specific mutations (personalized mRNA cancer vaccines, sipuleucel-T). The field has transformed outcomes in advanced melanoma, NSCLC, lymphoma, leukemia, and multiple myeloma — in some cases converting previously fatal diagnoses into long-term remissions. According to the National Cancer Institute, immunotherapy categories include checkpoint inhibitors, CAR-T cells, cancer vaccines, monoclonal antibodies, and cytokines.

How do checkpoint inhibitors work?

Immune checkpoints (PD-1, CTLA-4, LAG-3) are proteins that act as “off switches” on T cells, normally preventing autoimmunity by limiting immune responses. Cancer cells exploit these checkpoints — expressing PD-L1 to exhaust PD-1-expressing T cells, benefiting from CTLA-4-mediated suppression of new T cell activation, and co-activating LAG-3 to compound T cell exhaustion. Checkpoint inhibitor drugs are monoclonal antibodies that block these interactions: anti-CTLA-4 (ipilimumab) works in lymph nodes to allow new anti-tumor T cells to be generated; anti-PD-1 (pembrolizumab, nivolumab) and anti-PD-L1 (durvalumab, atezolizumab) restore activity of exhausted T cells already within the tumor. Anti-LAG-3 (relatlimab, approved with nivolumab March 2022) adds a third layer of checkpoint blockade. Combining anti-CTLA-4 + anti-PD-1 (CheckMate 067, melanoma: 7-yr OS 49%) is more effective than either alone because they target different immune brakes at different anatomical sites.

What is CAR-T cell therapy and who is it for?

CAR-T cell therapy genetically engineers a patient’s own T cells to express a chimeric antigen receptor (CAR) that binds a cancer cell surface protein — CD19 on B cell malignancies, BCMA on plasma cell myeloma — and triggers cytotoxic killing without needing MHC-I antigen presentation (bypassing the mechanism cancer uses to hide). The process takes 3–5 weeks: leukapheresis to collect T cells, viral transduction with the CAR gene, ex vivo expansion, a course of lymphodepleting chemotherapy, then infusion. CAR-T is FDA-approved for: relapsed/refractory large B cell lymphoma (DLBCL) from the 2nd-line setting onward; follicular lymphoma after ≥2 prior lines; B cell ALL in patients up to 25 years; and multiple myeloma after 2–4 prior lines. The CARTITUDE-1 trial reported ORR of 97.9% with ciltacabtagene autoleucel in heavily pretreated myeloma — response rates unprecedented in that disease. CAR-T requires specialized certified centers due to the risk of cytokine release syndrome (CRS) and ICANS. More information on CAR-T eligibility from the Cancer Research Institute.

What are the side effects of cancer immunotherapy?

Side effects of cancer immunotherapy are immune-mediated, not dose-toxic — they can affect any organ where the unleashed immune system attacks normal tissue. Checkpoint inhibitors cause immune-related adverse events (irAEs): most commonly skin (rash, vitiligo), GI (colitis — managed with corticosteroids + infliximab if severe), endocrine (hypothyroidism, hypophysitis, type 1 diabetes — typically permanent and requiring lifelong hormone replacement), liver inflammation, and pneumonitis. Rare but severe irAEs include myocarditis (~50% mortality for grade 3–4 — requires immediate high-dose steroids and ICU) and neurological toxicities (Guillain-Barré syndrome, encephalitis). Most irAEs are manageable: grade 1 continues therapy; grade 2 holds therapy with oral steroids; grade 3–4 usually permanently discontinues with IV methylprednisolone. CAR-T causes CRS (fever/hypotension/hypoxia — managed with tocilizumab) and ICANS (neurological toxicity — managed with corticosteroids). For a checklist of questions to ask your oncologist before starting immunotherapy, see the cancer diagnosis questions guide.

Which cancers respond best to immunotherapy?

Checkpoint inhibitors work best in “hot” tumors with high mutational burden, high PD-L1 expression, MSI-H/dMMR mismatch repair deficiency, or abundant tumor-infiltrating lymphocytes. Cancer types with outstanding single-agent checkpoint inhibitor responses include: melanoma (7-yr OS 49% nivo+ipi), Merkel cell carcinoma (ORR 50–60%), Hodgkin lymphoma (ORR 85–90%), MSI-H/dMMR tumors of any type (tissue-agnostic; ORR ~40%), and NSCLC with PD-L1 ≥50%. CAR-T has been transformative in relapsed/refractory DLBCL (5-yr OS 42.6% from a disease with historically poor prognosis), follicular lymphoma, and multiple myeloma. “Cold” tumors — microsatellite-stable colorectal cancer, most pancreatic cancers, and prostate cancer — have low response rates to checkpoint inhibitors as single agents and require combination strategies. The targeted therapy cancer guide covers biomarker-driven approaches that complement immunotherapy selection.

What biomarkers predict immunotherapy response?

Three FDA-approved biomarkers guide checkpoint inhibitor prescribing: (1) PD-L1 expression (IHC; TPS ≥50% selects for pembrolizumab monotherapy in NSCLC; CPS ≥10 for gastric, TNBC, cervical cancers — measured by assay specific to each drug); (2) MSI-H/dMMR (IHC for mismatch repair proteins or PCR/NGS for microsatellite instability; tissue-agnostic pembrolizumab approval for any solid tumor — the most predictive single biomarker available); (3) TMB-H ≥10 mut/Mb (NGS panel; tissue-agnostic pembrolizumab approval; ORR ~29%). Beyond these validated biomarkers, tumor microenvironment “temperature” (inflamed vs. immune-desert), STK11 co-mutation (negative predictor in KRAS-mutated NSCLC), and circulating immune signatures are under active investigation. No biomarker is perfectly predictive — some PD-L1-low tumors respond well, and some TMB-high tumors do not. MSI-H/dMMR testing should be performed in all patients with newly diagnosed metastatic cancer since pembrolizumab is approved for any MSI-H solid tumor. More on biomarker testing in the upcoming precision medicine cancer article. The ASCO patient resource on immunotherapy explains biomarker testing in patient-friendly language.

Wolchok JD et al. — CheckMate 067 7-yr OS (nivo+ipi melanoma); NEJM Evidence 2022
Reck M et al. — KEYNOTE-024 (pembro vs chemo PD-L1 ≥50% NSCLC); NEJM 2016; updated OS 2019
Gandhi L et al. — KEYNOTE-189 (pembro + chemo non-sq NSCLC); NEJM 2018
André T et al. — KEYNOTE-177 (pembro vs chemo MSI-H mCRC); NEJM 2020
Spigel DR et al. — PACIFIC 5-yr (durvalumab stage III NSCLC); JCO 2022
Tawbi HA et al. — RELATIVITY-047 (relatlimab + nivo melanoma); NEJM 2022
Locke FL et al. — ZUMA-1 5-yr OS (axi-cel DLBCL); Lancet Oncol 2022
Westin JR et al. — ZUMA-7 (axi-cel 2L DLBCL); NEJM 2022
Fowler NH et al. — ELARA (tisa-cel FL); Nature Med 2022
San-Miguel J et al. — CARTITUDE-1 (cilta-cel myeloma); NEJM 2023
Munshi NC et al. — KarMMa (ide-cel myeloma); NEJM 2021
Kantarjian H et al. — TOWER (blinatumomab R/R ALL); NEJM 2017
Weber JS et al. — KEYNOTE-942 (mRNA-4157 + pembro melanoma); NEJM 2024
Nathan P et al. — IMCgp100-202 (tebentafusp uveal melanoma); NEJM 2021
Kantoff PW et al. — IMPACT (sipuleucel-T mCRPC); NEJM 2010
National Cancer Institute — Immunotherapy to Treat Cancer
Cancer Research Institute — What Is Cancer Immunotherapy?
ASCO — What Is Immunotherapy?

This article is for educational purposes only and does not constitute medical advice. Discuss all cancer treatment decisions with your oncology care team.