Have you heard of immunotherapy and want to understand how it works and if you’re the right candidate? Complete guide in plain language: types of immunotherapy, essential biomarkers (PD-L1, MSI-H, TMB), side effects and how AI helps you navigate these options
Receiving a cancer diagnosis, you may have heard words like “pembrolizumab,” “anti-PD-1,” “CAR-T,” or simply “immunotherapy” for the first time. If these terms have seemed incomprehensible to you, you’ve come to the right place. This guide translates the complex science behind the biggest revolution in modern oncology into words that anyone can understand – without sacrificing medical rigor. You’ll learn what immunotherapy is, how it works, what types exist, who it’s suitable for, and what the practical implications are for your treatment.
1. Why is immunotherapy different from chemotherapy or radiotherapy?
For decades, the standard cancer treatment arsenal has included three pillars: surgery (removal of the tumor), chemotherapy (chemicals that kill rapidly dividing cells), and radiation therapy (rays that destroy the tumor locally). All three attack the tumor directly .
Immunotherapy does something fundamentally different: it doesn’t attack the tumor directly, but rather trains and unleashes your own immune system to recognize and destroy it . It’s essentially the difference between killing the enemy yourself and training your army to do it for you.
This distinction has extremely important practical consequences:
- The duration of the response can be much longer – once the immune system “recognizes” the tumor, it can maintain surveillance for years.
- The side effects are different from chemotherapy – hair loss does not typically occur, but specific autoimmune reactions may occur.
- The response may be slower at onset and not all patients benefit – therefore, the correct selection of candidates is crucial.
2. How does cancer manage to “hide” from the immune system?
The immune system is designed to detect and eliminate abnormal cells, including cancer cells. But cancer is an evolved adversary. Over time, tumor cells develop sophisticated mechanisms for camouflage and survival:
The “immune brake” mechanism (immune checkpoint): On the surface of T cells (the soldier cells of the immune system) there are molecular “switches” – called immune checkpoints – originally intended to prevent autoimmune attacks. Cancer cells have learned to activate these switches , sending a false signal of the type “I’m a normal cell, don’t attack me”. The result? The T cells stop, deactivate and the tumor continues to grow unhindered.
“Cold” tumors vs. “hot” tumors:
- “Hot” tumors are infiltrated by immune cells, have high levels of PD-L1, and display many markers recognized by the immune system. These respond best to immunotherapy .
- ” Cold ” tumors are virtually invisible to the immune system, with little immune infiltrate and no recognizable markers. A major goal of current research is to “warm up” these tumors to make them susceptible to immunotherapy.
3. The main types of immunotherapy approved in oncology
3.1. Immune checkpoint inhibitors – “releasing the brakes” on the immune system
This is the most widely used category today. It works exactly the opposite of what the tumor does: if the tumor “puts the brakes” on the immune system, these monoclonal antibodies remove the brakes , leaving the T cells free to attack.
There are three main types of molecular targets:
Anti-PD-1 (blocks the PD-1 receptor on T cells):
- Pembrolizumab (Keytruda) – the best known, with indications in melanoma, lung cancer, head and neck cancer, bladder cancer, gastric cancer, cervical cancer, triple-negative breast cancer and more. It was the first drug approved by the FDA in a tissue-agnostic manner (regardless of tumor location, based on the MSI-H/dMMR biomarker) in 2017.
- Nivolumab (Opdivo) – approved for melanoma, lung cancer, kidney cancer, liver cancer, Hodgkin lymphoma, mesothelioma and others.
- Cemiplimab (Libtayo) – used in cutaneous squamous cell carcinoma, advanced basal cell carcinoma, and lung cancer with high PD-L1 expression.
- Dostarlimab (Jemperli) – for endometrial cancer with dMMR.
Anti-CTLA-4 (blocks another immune checkpoint):
- Ipilimumab (Yervoy) – the first approved checkpoint inhibitor, used primarily for melanoma, often in combination with nivolumab.
Anti-PD-L1 (blocks the ligand on tumor cells):
- Atezolizumab (Tecentriq) – in lung cancer, triple-negative breast cancer, hepatocellular carcinoma, small cell lung cancer.
- Durvalumab (Imfinzi) – in stage III lung cancer post-chemoradiotherapy and in small cell lung cancer.
- Avelumab (Bavencio) – in Merkel cell carcinoma and urothelial cancer.
💡 Remember: Checkpoint inhibitors are the drugs you hear about most often in oncology today. They can be administered alone or in combination – either with each other (e.g. nivolumab + ipilimumab), or with chemotherapy or targeted therapies.
3.2. CAR-T therapy – genetically reprogrammed immune cells
This is one of the most spectacular innovations of the last decade. The process involves several steps:
- T cells are harvested from the patient’s blood (leukapheresis).
- The cells are sent to the laboratory, where they are genetically modified to express an artificial receptor (CAR – Chimeric Antigen Receptor) that recognizes a specific tumor antigen.
- The modified cells are multiplied in the laboratory, obtaining millions of cells “programmed” to attack the tumor.
- The patient receives conditioning chemotherapy (to prepare space in the immune system), followed by reinfusion of CAR-T cells .
CAR-T therapies approved today:
- Tisagenlecleucel (Kymriah) – for acute lymphoblastic leukemia (ALL) in young people up to 25 years of age and for diffuse large B-cell lymphoma (DLBCL) in adults.
- Axicabtagene ciloleucel (Yescarta) – for several types of aggressive B-cell lymphomas and relapsed/refractory follicular lymphoma.
- Idecabtagene vicleucel (Abecma) – for relapsed/refractory multiple myeloma, now approved after only 2 prior lines of treatment (versus 4, previously).
- Ciltacabtagene autoleucel (Carvykti) – multiple myeloma, with studies showing a 59% reduction in the risk of progression or death compared to standard treatment.
⚠️ Important: CAR-T therapy is currently available mainly for hematological cancers (leukemias, lymphomas, multiple myeloma). Research into its extension to solid tumors is intense, but there are no definitive approvals in this area yet.
3.3. Tumor Infiltrating Lymphocyte (TIL) Therapy – historic approval in 2024
In February 2024 , the FDA approved lifileucel (Amtagvi) , marking a historic moment: the first cell therapy approved for a solid tumor . It represents the culmination of 30+ years of research.
How it works: Lymphocytes that have naturally infiltrated the tumor tissue (TILs – Tumor-Infiltrating Lymphocytes) are extracted from the patient’s tumor. These cells are multiplied in the laboratory and reinfused in high doses.
Clinical results: An objective response rate of 31.4% in patients with advanced melanoma, with a median duration of response of 36.5 months.
Current indication: metastatic or unresectable melanoma, in patients previously treated with an anti-PD-1 antibody.
3.4. Therapeutic anti-cancer vaccines
Unlike classic preventive vaccines, therapeutic vaccines are administered after diagnosis, with the aim of stimulating the immune system to attack the existing tumor.
- Sipuleucel-T (Provenge) – approved for metastatic castration-resistant prostate cancer, demonstrated an improvement in overall survival of 4.1 months over placebo (25.8 vs. 21.7 months).
- Intravesical BCG – used in non-muscle invasive bladder cancer (NMIBC), with response rates for carcinoma in situ of 75.6%.
- Talimogene laherparepvec (T-VEC / Imlygic) – an oncolytic virus (modified from the herpes simplex virus) injected directly into melanoma lesions, which kills tumor cells and stimulates a systemic immune response. Durable response rate: 16% vs. 2% for the control group.
3.5. Bispecific antibodies – the molecular bridge
These are antibodies designed to bind to two different targets simultaneously – usually a protein on the tumor cell and one on the T cell. Basically, they “bring” the immune cell near the cancer cell.
- Blinatumomab (Blincyto) – approved for B-cell acute lymphoblastic leukemia, with a median overall survival of 7.7 months compared to 4 months with standard chemotherapy.
- Tarlatamab (Imdelltra) – approved in 2025 for small cell lung cancer, with a 40% reduction in the risk of death compared to chemotherapy.
3.6. Cytokines – the “classic” immune stimulants
Cytokines such as Interleukin-2 (IL-2) and Interferon alpha-2b were the first forms of oncology immunotherapy, approved several decades ago. Although less commonly used today due to high toxicity, they remain options for selected cases:
- IL-2 (Aldesleukin) – for metastatic melanoma and metastatic renal cancer, with durable complete response rates of ~10 years in 6-7% of patients.
- Interferon alfa-2b – for hairy cell leukemia, adjuvant melanoma, and other indications.
4. Who is immunotherapy suitable for? Biomarkers that make the difference
This is probably the most important question you can ask your oncologist. Not all patients benefit from immunotherapy , and biomarker testing before starting treatment is essential. Here’s what these tests involve:
4.1. PD-L1 – The tumor’s “camouflage shield”
What is it? PD-L1 is a protein expressed on the surface of tumor cells (and immune cells in the tumor microenvironment). When a T cell tries to attack the tumor, PD-L1 binds to the PD-1 receptor on the T cell and sends it a “stop” signal. The more PD-L1 a tumor expresses, the better it is at “fooling” the immune system.
Why does it matter? Anti-PD-1/PD-L1 inhibitors work by blocking this interaction. Studies show that patients with high PD-L1 expression respond better to these treatments.
How is it measured?
- TPS (Tumor Proportion Score): proportion of tumor cells with PD-L1 positive. TPS ≥ 50% = high expression.
- CPS (Combined Positive Score): also includes immune cells expressing PD-L1 in the tumor microenvironment.
💡 Practical example: Pembrolizumab is approved as first-line in lung cancer without EGFR/ALK mutations if TPS ≥ 50% – without associated chemotherapy. With TPS ≥ 1%, it can be combined with chemotherapy.
4.2. MSI-H / dMMR – “Defective DNA Repair System”
What is it? Our cells have molecular “correction” systems that repair errors that occur when copying DNA. When these systems (MMR – Mismatch Repair) are deficient (dMMR) , a large number of genetic errors accumulate, leading to high microsatellite instability (MSI-H) .
Why does it matter for immunotherapy? Tumors with dMMR/MSI-H have an extraordinarily high number of mutations, generating abnormal proteins ( neoantigens ) that the immune system recognizes as “foreign.” These tumors are extremely sensitive to checkpoint inhibitors .
What does the clinical data say?
- Pembrolizumab achieved an objective response rate of 40% in patients with dMMR colorectal cancer, compared to 0% in patients without this mutation.
- Since May 2017, pembrolizumab has tissue-agnostic approval for any MSI-H/dMMR solid tumor – that is, regardless of the organ of origin.
- Nivolumab + ipilimumab received first-line approval for MSI-H/dMMR metastatic colorectal cancer in April 2025 .
✅ Practical conclusion: If your biopsy or molecular profile report mentions “dMMR” or “MSI-H”, urgently discuss your eligibility for immunotherapy with your oncologist – regardless of your cancer type!
4.3. TMB – Tumor Mutational Burden
What is it? TMB measures the number of non-synonymous mutations (i.e., genetic errors that produce altered proteins) per megabase of DNA. Tumors with TMB ≥ 10 mut/Mb are considered TMB-high (TMB-H) .
Logic: The more mutations the tumor has, the more abnormal proteins it produces, the better it is recognized by the immune system and, consequently, the better it can respond to immunotherapy.
Clinical approval: In 2020, the FDA approved pembrolizumab for any metastatic solid tumor with TMB-H (≥10 mut/Mb) that has progressed after prior treatments.
Biomarker limitations: Not all tumors with elevated TMB respond – some have other mechanisms of immune evasion. Current research is exploring predictive models that combine TMB with other factors.
4.4. Integrated predictive models – the future of patient selection
Recent research (2024) has shown that no single biomarker is sufficient to accurately predict response to immunotherapy. The LORIS model (2024), for example, combines 6 factors: TMB, treatment history, serum albumin, neutrophil/lymphocyte ratio, age, and cancer type – achieving a predictive power superior to any individual biomarker.
5. What types of cancer benefit from immunotherapy today?
The list of approved indications has expanded dramatically. Here is an overview:
| Type of cancer | Immunotherapy used |
| Melanoma (advanced or adjuvant stage) | Pembrolizumab, nivolumab, ipilimumab, nivolumab + ipilimumab, lifileucel (TIL) |
| Non-small cell lung cancer (NSCLC) | Pembrolizumab, nivolumab, atezolizumab, durvalumab, cemiplimab |
| Small cell lung cancer (SCLC) | Atezolizumab, durvalumab, tarlatamab |
| Kidney cancer (RCC) | Nivolumab, pembrolizumab + axitinib, avelumab + axitinib, nivolumab + ipilimumab |
| Bladder cancer (urothelial) | Pembrolizumab, nivolumab, atezolizumab, avelumab (maintenance) |
| Colorectal cancer MSI-H/dMMR | Pembrolizumab, nivolumab + ipilimumab |
| Gastric/esophageal cancer | Nivolumab + chemotherapy, pembrolizumab + chemotherapy |
| Hepatocellular carcinoma (HCC) | Atezolizumab + bevacizumab, nivolumab + ipilimumab |
| Triple-negative breast cancer | Pembrolizumab + chemotherapy, atezolizumab |
| Classical Hodgkin lymphoma | Nivolumab, pembrolizumab |
| Multiple myeloma | CAR-T (Abecma, Carvykti) |
| Acute lymphoblastic leukemia (B-ALL) | CAR-T (Kymriah), blinatumomab |
| Aggressive B-cell lymphomas (DLBCL, etc.) | CAR-T (Yescarta, Breyanzi, Kymriah) |
| Cervical cancer | Pembrolizumab |
| Endometrial cancer dMMR | Dostarlimab, pembrolizumab |
| Any MSI-H or TMB-H solid tumor | Pembrolizumab (tissue-agnostic approval) |
| Merkel cell carcinoma | Avelumab, pembrolizumab |
| Cutaneous squamous cell carcinoma | Cemiplimab |
This list is not exhaustive. The indications are frequently updated based on new clinical studies.
6. How is immunotherapy administered and how long does the treatment last?
Immune checkpoint inhibitors are usually administered intravenously (infusion) , at regular intervals:
- Every 3 weeks (Q3W) or 6 weeks (Q6W) – most common.
- Some inhibitors now have a subcutaneous formulation (injection under the skin), approved in 2024-2025: subcutaneous pembrolizumab and subcutaneous nivolumab, which represents a major added convenience for patients.
The duration of treatment varies depending on:
- The type of cancer and the stage of the disease.
- Response to treatment (is the tumor shrinking? Is it stabilizing?).
- Side effects that occurred.
In some adjuvant indications (after surgery), treatment lasts for 1 year . In metastatic disease, it can continue as long as there is clinical benefit and tolerance .
7. Side effects of immunotherapy – what you need to know
Unlike chemotherapy, immunotherapy does not destroy healthy cells that divide rapidly (cells in hair follicles, digestive mucosa, etc.). Therefore, hair loss, severe nausea, and a marked decrease in white blood cells are not typical effects.
However, by activating the immune system, autoimmune reactions called irAEs (immune-related Adverse Events) can occur – that is, immunologically mediated side effects. Basically, an overactivated immune system can sometimes attack healthy tissues.
The most common irAEs include :
- Colitis (intestinal inflammation) – diarrhea, abdominal cramps.
- Pneumonitis (lung inflammation) – cough, shortness of breath. Warning: can be severe if not recognized quickly!
- Hepatitis – increased liver enzymes.
- Endocrinopathies – hypothyroidism (most common), hyperthyroidism, type 1 diabetes, adrenal insufficiency.
- Skin problems – rashes, itching.
- Nephritis (kidney inflammation).
- Rare neurological disorders – myasthenia gravis, Guillain-Barré syndrome.
How are irAEs managed?
- Mild-moderate forms: temporary cessation of treatment, corticosteroids (prednisone).
- Severe forms: permanent cessation of treatment, high-dose corticosteroids, sometimes additional immunosuppressive medication (infliximab).
⚠️ Important message: Report any new symptoms that occur during immunotherapy to your doctor immediately – from persistent diarrhea to shortness of breath. Early recognition and treatment of irAEs is essential!
8. The phenomenon of “pseudoprogression” – why can a tumor appear to grow before it shrinks?
This is a crucial concept that any patient receiving immunotherapy should be aware of .
Unlike chemotherapy, where tumor shrinkage occurs rapidly if the treatment works, immunotherapy acts indirectly – it first activates immune cells, and they migrate into the tumor. In 2-10% of patients , this immune infiltration can cause an apparent tumor growth or the appearance of new lesions on imaging (CT or MRI) – not because the tumor is growing, but because it fills with immune cells and edema occurs.
The phenomenon is called pseudoprogression and is followed by actual tumor regression on subsequent scans.
What does this mean practically?
- If the tumor appears larger at the first imaging reevaluation, the decision to stop treatment is not automatically made .
- confirmatory scan is performed at ~4 weeks to differentiate pseudoprogression from true progression.
- The decision to continue or stop is always made together with the oncologist, taking into account the patient’s clinical condition.
9. Perioperative immunotherapy – a major trend in 2025
A rapidly expanding field is the use of immunotherapy before and/or after surgery (perioperative):
- Neoadjuvant (preoperative): to reduce the size of the tumor and increase the chances of complete resection.
- Adjuvant (postoperative): to eliminate remaining microscopic tumor cells and prevent recurrence.
Recent studies (e.g. MATTERHORN, KEYNOTE-590) have established perioperative immunotherapy as the standard of care in several types of upper gastrointestinal cancer and bladder cancer.
Frequently Asked Questions (FAQ)
❓ Does immunotherapy work for every type of cancer? No. It works best in tumors with certain molecular characteristics (high PD-L1, MSI-H, TMB-H). There are approved indications for a large number of cancers, but the benefit varies significantly from one patient to another.
❓ Can I have immunotherapy at the same time as chemotherapy? Yes, in many current protocols, immunotherapy is combined with chemotherapy. Major studies have demonstrated superior benefits over chemotherapy alone in lung, gastric, esophageal, and other cancers.
❓ How long does it take to see the effects of immunotherapy? Response may occur more slowly than with chemotherapy – on average 2 months after starting treatment. Durable responses are specific to immunotherapy.
❓ If I have diabetes or an autoimmune disease, can I have immunotherapy? Pre-existing autoimmune diseases are a relative contraindication. They are evaluated individually, with careful monitoring. Discuss your specific situation with your oncologist.
❓ Is immunotherapy available in Romania? Yes. Pembrolizumab, nivolumab, atezolizumab and others are available in Romania, partly through national reimbursement programs. Access may vary, so a second opinion may be valuable.
Conclusion
Immunotherapy is no longer the “medicine of the future” – it is the medicine of the present . With 30% of all FDA new drug approvals in 2024 and dramatically expanding the oncology treatment landscape, immunotherapy offers real hope for cancers that were once considered incurable. The key is proper patient selection based on biomarkers, careful monitoring of side effects, and access to up-to-date information .
📊 Summary Diagrams: Immunotherapy in Cancer
Visual guide for patients – oncoexpertai.com
🔬 TABLE 1 – Types of Immunotherapy: What are they and how do they work?
| Type of Immunotherapy | How it works (in your understanding) | For what type of cancer | How to administer |
| Checkpoint inhibitors (ex: Pembrolizumab, Nivolumab) | The tumor “puts a brake” on your immune system. These drugs take the brake off and let the immune cells attack freely. | Melanoma, lung, colorectal, gastric, kidney, bladder, breast, cervical cancer and many more | IV infusion every 3 or 6 weeks (or injection under the skin – new formulation 2024-2025) |
| CAR-T therapy (ex: Kymriah, Yescarta, Carvykti) | Your immune cells are harvested, genetically reprogrammed in the lab to recognize the tumor, then reinfused into your body. | Leukemias, aggressive lymphomas, multiple myeloma | Single infusion after specific preparation (conditioning chemotherapy) |
| TIL therapy (Lifileucel) (Amtagvi – approved 2024) | Immune cells that have already penetrated the tumor are extracted , multiplied in the laboratory in large numbers, then reinfused. | Advanced metastatic melanoma | Single infusion |
| Therapeutic vaccines (ex: Sipuleucel-T, BCG, T-VEC) | It stimulates the immune system to recognize and attack existing cancer cells. | Prostate cancer, bladder cancer, melanoma | Direct injection into tumor / intravesical / intravenous |
| Bispecific antibodies (ex: Blinatumomab, Tarlatamab) | It functions as a molecular bridge : it simultaneously links an immune cell to the tumor cell, bringing them face to face. | Acute lymphoblastic leukemia, small cell lung cancer | Continuous or intermittent IV infusion |
| cytokines (e.g. IL-2, Interferon) | Natural molecules of the body that directly stimulate the activity of the immune system. | Metastatic melanoma, kidney cancer, hairy cell leukemia | Subcutaneous/IV injection |
🧬 TABLE 2 – Biomarkers: What do they mean for your eligibility for immunotherapy?
| biomarkers | What is it, in short | What value indicates benefit | What does it mean to you? | How is it determined? |
| PD-L1 | The protein through which the tumor “camouflages” itself from the immune system | TPS ≥ 50% = maximum benefit (monotherapy) ; TPS ≥ 1% = benefit in combination with chemotherapy | The higher the value, the greater the chances of response to checkpoint inhibitors. | Biopsy + IHC test (immunohistochemistry) |
| MSI-H / dMMR | Defect in the “error correction” system in the tumor’s DNA | Any MSI-H or dMMR value = eligibility | Regardless of the affected organ, you are eligible for pembrolizumab (tissue-agnostic approval) | Biopsy + molecular test (PCR or NGS) |
| TMB (Mutational Tumor Burden) | Number of genetic mutations in the tumor | TMB ≥ 10 mutations/megabase = TMB-high | The more mutations a tumor has, the more easily the immune system recognizes it. | Genomic sequencing (NGS) |
| HER2 | Tumor cell growth protein | Score 3+ on IHC = HER2 positive | Relevant for targeted therapies (not classical immunotherapy), but important in breast and gastric cancer | Biopsy + IHC/FISH |
| Ki-67 | The percentage of tumor cells that are actively dividing | Low Ki-67 (<15%) = slow tumor; High Ki-67 (>30%) = aggressive tumor, but sometimes more sensitive to chemotherapy | Helps in choosing the overall therapeutic strategy | Biopsy + IHC test |
| Hormone receptors (ER/PR) | Indicates whether hormones “feed” cancer | ER+ or PR+ | Relevant for hormonal therapy (breast cancer, endometrium) | Biopsy + IHC test |
🎯 TABLE 3 – Which type of immunotherapy is suitable for which situation?
| Your type of cancer | Relevant biomarker | Immunotherapeutic option | Treatment line |
| Non-small cell lung cancer (NSCLC) | PD-L1 ≥ 50% | Pembrolizumab alone | First line |
| Non-small cell lung cancer (NSCLC) | PD-L1 ≥ 1% | Pembrolizumab + chemotherapy | First line |
| Metastatic melanoma | No specific biomarker required | Pembrolizumab / Nivolumab / Combination Nivolumab + Ipilimumab | First or second line |
| Advanced metastatic melanoma | Previously treated with anti-PD-1 | Lifileucel (TIL therapy) | Later line |
| Colorectal cancer | MSI-H / dMMR | Pembrolizumab / Nivolumab + Ipilimumab (approved 2025) | First line |
| Any solid tumor | MSI-H or TMB ≥ 10 | Pembrolizumab (tissue-agnostic approval) | Later line |
| Kidney cancer | No specific biomarker | Nivolumab + Ipilimumab / Pembrolizumab + Axitinib | First line |
| Aggressive B-cell lymphoma/DLBCL | CD19 positive | CAR-T: Kymriah, Yescarta or Breyanzi | 2nd line or later |
| Acute lymphoblastic leukemia (ALL) | CD19 positive | CAR-T: Kymriah / Blinatumomab | Relapsed or refractory |
| Multiple myeloma | BCMA positive | CAR-T: Carvykti or Abecma | After 1-2 previous lines (approved 2024) |
| Metastatic prostate cancer | Minimal symptoms | Sipuleucel-T (vaccine) | Refractory to castration |
| Bladder cancer (NMIBC) | Non-responsive to BCG | Pembrolizumab | Later line |
| Triple-negative breast cancer | PD-L1 CPS ≥ 10 | Pembrolizumab + chemotherapy | First line |
⚠️ TABLE 4 – Immunotherapy Side Effects: What to Watch for and What to Do
| Side effect | Symptoms to recognize | SEVERITY | What you need to do |
| Colitis (intestinal inflammation) | Persistent diarrhea, abdominal cramps, blood in the stool | ⚠️ Moderate – Severe | Contact your doctor immediately; don’t ignore diarrhea! |
| Pneumonitis (lung inflammation) | New dry cough, shortness of breath, fever | 🔴 Severe – Can be fatal | Go to the emergency room immediately / call the oncologist |
| Hepatitis | Extreme fatigue, dark urine, jaundice (yellowing of the skin) | ⚠️ Moderate – Severe | Urgent blood tests, contact the doctor |
| Hypothyroidism (most common) | Fatigue, weight gain, feeling cold, constipation | 🟡 Easy – Moderate | Thyroid tests, thyroid hormone replacement treatment |
| Hyperthyroidism | Palpitations, sweating, weight loss, agitation | 🟡 Moderate | Contact the doctor, tests |
| Sudden onset of type 1 diabetes | Extreme thirst, frequent urination, fatigue, nausea | ⚠️ Severe | Medical emergency if serious symptoms occur |
| Skin rash/itching | Redness, itching, spots on the skin | 🟡 Easy – Moderate | Inform the doctor; do not apply treatments without advice |
| Nephritis (kidney inflammation) | Decreased urine output, edema | ⚠️ Moderate – Severe | Urgent urine and blood tests |
| Rare neurological reactions | Muscle weakness, numbness, double vision | 🔴 Severe | Neurological emergency |
🩺 Golden rule: Any new symptoms that appear during immunotherapy should be reported to your oncologist immediately – do not wait for your scheduled consultation.
🔄 TABLE 5 – Immunotherapy vs. Chemotherapy: The Main Differences
| Criterion | Chemotherapy | Immunotherapy |
| How it works | Directly attacks rapidly dividing cells (including healthy ones) | Activates your own immune system to attack the tumor |
| Hair loss | Yes, frequent | No, in general |
| Nausea/Vomiting | Frequent, sometimes severe | Rarer |
| Main side effects | Anemia, infections, fatigue, mucositis | Autoimmune reactions (colitis, pneumonitis, thyroiditis) |
| Response speed | Relatively fast (weeks) | Slower (2+ months on average) |
| Response time | Usually limited | Long-term potential (years) |
| Pseudoprogression | Does not appear | Possible (2-10% of patients) – the tumor appears larger initially, but later shrinks |
| Patient selection | It applies more broadly | Requires biomarker testing (PD-L1, MSI, TMB) |
💡 TABLE 6 – Essential questions to ask your oncologist (Patient Checklist)
| # | Question | Why is it important? |
| 1 | “Was PD-L1 tested in my biopsy? What is the score?” | Determine eligibility for checkpoint inhibitors |
| 2 | “Is my tumor MSI-H or dMMR?” | It can open access to treatment regardless of the type of cancer |
| 3 | “What is the BMR value of my tumor?” | Important biomarker for tissue-agnostic immunotherapy |
| 4 | “Are there active clinical trials of immunotherapy for my case?” | Access to new therapies, sometimes for free |
| 5 | “Can I combine immunotherapy with my current treatment?” | Many protocols combine immunotherapy with chemotherapy |
| 6 | “What are the warning signs for autoimmune side effects?” | Early recognition can save lives |
| 7 | “If the tumor appears to be growing on the first scan, does that mean the treatment isn’t working?” | Clarifying the phenomenon of pseudoprogression |
| 8 | “Is there a subcutaneous formulation for my medication?” | Increased comfort (available from 2024-2025 for pembrolizumab and nivolumab) |
🤖 Oncoexpertai.com automatically analyzes biomarkers in your medical record and compares them with the international NCCN / ESMO guidelines updated in real time, helping you go to the oncologist prepared with all the data in order.
⚕️ Disclaimer: The information in these tables is purely informative and educational. It does not replace a specialized medical consultation. Any therapeutic decision should be made together with your oncologist.
If you are in the therapeutic decision-making process and want to know if your molecular profile qualifies you for immunotherapy, the Oncoexpertai platform provides you with AI analysis tools and access to specialized oncological expertise.
[Upload your medical record for a complete analysis and an informed second opinion]
Disclaimer: The information in this article is for informational and educational purposes only. It does not constitute medical advice, does not replace consultation with a specialist oncologist, and does not constitute the basis for making therapeutic decisions. Any treatment decision should be made in consultation with your healthcare team, based on your individual medical history.
Article written based on international medical literature (FDA clinical documents, published phase III studies) and updated with available data until 2025 .
Dr. Onisim Florin Senior Medical Oncologist Founder of OncoExpertAI


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