2. Outline
Why Do We get Cancer?
How Does the Immune System Protect Us from Cancer?
Types of Immune Responses
Why Does the Immune System Fail to Control Cancer Cells?
Strategies to Harness the Immune System to Fight Cancer Cells
Improving Antigen-Presentation to Prime More Immune Cells
Immunotherapies in Oncology
History of Cancer Immunotherapy
Immunotherapy uses in India?
How does immunotherapy work against cancer?
What are the types of immunotherapy?
How is immunotherapy given?
How often do you receive immunotherapy?
What is the current research in immunotherapy?
What types of cancer can be treated with immunotherapy?
What are potential risks or complications of immunotherapy?
How effective is immunotherapy?
5. The immune system is a network
of biological processes that protects
an organism from diseases. It detects and
responds to a wide variety of pathogens,
from viruses to parasitic worms, as well as cancer
cells.
7. Immunity is the capability of multicellular organisms to resist harmful
microorganisms. Immunity involves both specific and nonspecific components.
The nonspecific components act as barriers or eliminators of a wide range of
pathogens irrespective of their antigenic make-up.
9. • Cancer is a cellular disease resulting from the uncontrolled growth of tumor cells.
• A massive amount of tumor cells accumulate in one or more parts of the body or
spread throughout the blood.
• Documentation of human cancer can be found in literature dating as far back as 3,000
years ago in Egypt, and the search for the cause never comes to an end.
• While inheritance and environmental factors (ultraviolet radiation, pollution, etc.)
are attributed as major causes of human cancer, a recent report pointed out that
random errors in replication of genetic materials (genome) in our bodies seem to
play a key role in cancer generation (Tomasetti et al. 2017).
10. • Once a genomic error happens, its consequence may or may not be harmful to
our bodies and the cells harboring the error.
• The error or mutation (changes) in the genome can cause a normal cell to become
a tumor cell. These errors in the genome are responsible for two-thirds of the
mutations in human cancers (Greenman et al. 2007).
• However, not all mutations or errors in our cells will lead to cancer. We have
both internal- and external-checking systems to monitor what happens to the cells
in our bodies.
• If all these checking systems fail, tumor cells will proliferate and take control—the
disease spreads throughout the body, eventually resulting in death if not treated.
11. • The internal-checking system consists mainly of tumor suppressor genes that
suppress the development and growth of mutant cells in a process called
“programmed cell death.”
• In this process, some enzymes will be activated to cut the genetic material of cells into
small fragments that will stop the proliferation and survival of the cells.
• Basically, our cells are programmed to die if they detect any mutations within their
genes that they cannot correct. If the tumor cells escape this internal check, they will
face an external check that is mediated by the immune system.
• Our immune system has developed the ability to check for tiny changes in cells.
Immune cells have very specific “eyes” to identify any subtle changes in nearby cells
and will activate our immune cells accordingly.
12. How Does the Immune System
Protect Us from Cancer?
13. • Many of us have tumor cells in our bodies, but most of us do not develop cancer as a
disease. Our immune system prevents spontaneously generated tumor cells from
developing into cancers.
• This phenomenon has been reproduced in animal models and has prompted a theory of
“immune surveillance.” There are four pieces of evidence that support this theory that
the immune system indeed responds to cancer.
• First, humans with genetic defects in their immune systems tend to have a higher
incidence of cancer than those whose immune systems are intact.
• Second, humans who have their immune systems suppressed by medicine in order to
avoid rejection of transplants have higher cancer generation than people with normal
immune function.
14. • Third, some cancer patients have “paraneoplastic syndromes” (consequence of cancer
in the body) that are caused by the immune system’s response to a cancer. For example,
patients with lung cancer may develop disorders in the central nervous system (CNS) due
to immune responses to certain proteins shared by CNS and lung cancers.
• Fourth, Immunotherapy regimens do not directly kill tumor cells but boost the
immune system to find and destroy cancer cells. The success of this therapy provides
direct evidence that we have pre-existing immune responses to cancer in our body, but
at times they do not function as well as they should.
16. • The two types of immune responses differ in their specificity of recognition and
speed of response.
• One is called the innate immune response, in which innate immune cells lack
precise specificity in recognition of their targets but have a rapid response to
them.
• Macrophages (large eater cells) and natural killer (NK) cells are the main innate
immune cells. They recognize their targets based on the general patterns of
molecules expressed by target cells or pathogens.
17. • The second response is called the adaptive immune response. Adaptive immune
cells have a very restricted specificity in recognition of their targets, but usually
have a delayed response to their targets because they need more time to divide and
produce attacking molecules.
• There are two major sub-populations of adaptive immune cells: T cells and B cells,
also called T lymphocytes and B lymphocytes (since they were originally identified in
lymph nodes).
• The “T” in T cells means that these cells develop in the thymus, and the “B” in B
cells means they develop in bone marrow. They recognize their target cells or
pathogens using receptors (eyes) that are designed only for a very specific antigen.
18. • An antigen is a protein molecule or any substance capable of inducing an
immune response that produces antibodies (antigen-binding proteins) or
attacking molecules. As this specificity is so detailed, T cells or B cells can
recognize any tiny changes in a protein molecule.
• In order to recognize any potentially changed proteins or pathogens, our
bodies have been bestowed with 300 billion T cells and 3 billion B cells.
• Normally we only have a few T cells for each single antigen in our bodies, but we
can have thousands of them once they are activated by antigen stimulation and
undergo expansion (proliferation). Although we cannot see the expansion of T
cells, we can feel them. When you feel enlarged lymph nodes in body after
infection, these signs usually tell that millions of immune cells proliferated.
20. • The innate immune response is fast, but not restricted to specific antigens. It is still
unclear how innate immune cells recognize tumor cells, but they do have the ability to
kill tumor cells once they are activated by environmental cues.
• Macrophages and NK cells are the two major types of innate immune cells that can
attack tumors.
• There are other innate immune cells that do not directly kill tumor cells, but can
present proteins expressed by tumor cells to other immune cells to instruct them to
target these tumors.
• For example, dendritic cells (DCs) are innate immune cells that can present tumor
proteins to adaptive immune cells (like T cells) and help activate T-cell responses; thus,
the dendritic cells act as a “bridge” between the innate immune system and the
adaptive immune.
21. • Macrophages are big eater cells. Macrophages are present within most tissues of our
body in order to clean up dead cells and pathogens.
• Once activated by environmental cues (like materials released from bacteria,
viruses, or dead cells), macrophages infiltrate deep into tumor tissues and destroy
cells via production of toxic oxygen derivatives and tumor necrosis factor (TNF), or
they directly eat the tumor cells (known as phagocytosis).
• In order to escape being eaten by macrophages, some tumor cells express “don’t
eat me” signal molecules to fool macrophages and escape them. Recently, reagents
have been developed to block the “don’t eat me” molecules on tumor cells. An
example of a “don’t eat me” molecule is CD47.
22. • NK cells are circulating immune cells in our blood system and are believed to serve as the earliest
defense against blood-borne metastatic tumor cells. Expressing something abnormal and/or failing to
express something normal.
• NK cells are called natural killers because they do not need to be “coached” to see very specific
antigens for their activation. T
• They respond to their target cells by searching whether something is “missing” on the cell surface.
In this regard, NK cells help us clean out many cancer cells in very early stages or those cancer cells
circulating in our blood where we have plenty of NK cells.
• Patients with metastases have abnormal NK activity, and low NK levels are predictive of eventual
metastasis. Recent studies suggest that some NK cells have a “memory” capability to recognize
certain tumors or pathogens.
23. • First, only tumor cells with “missing” markers can be detected by NK cells.
Second, there are a limited number of NK cells present in the bloodstream, as
only 10% of lymphocytes are NK cells.
• To improve NK cell function, a cytokine called interleukine-2 has been used to
activate NK cells for expansion.
25. • The adaptive response is slower, specific to certain antigens, and has memory (can provide life-long
protection). Since adaptive immune cells can remember antigens from their first encounter, they can
respond to antigens much faster when they encounter the same antigens again. This process is called
“immune memory” and is the foundation of protective immunization.
• They need a very close cell-to-cell contact to clearly and specifically “see” their antigen on the target
cells. In order to remember their target antigens, adaptive immune cells need professional antigen-
presenting cells (APCs) to “teach” them how to see and how to respond.
• Dendritic cells are professional APCs. Dendritic cells are extend to surrounding tissues to catch proteins
released from pathogens or tumors, but they cannot eat whole cells like macrophages. Once they catch
proteins (antigens), they will “eat” (phagocytosis) and “digest” them using enzymes (degradation), and
then “present” them in an antigen-presenting structure on their surfaces.
26. • There are two types of adaptive immunity: cellular (T-cell) and humoral (B-cell)
immunity.
• T cells consist of CD8 and CD4 T cells.
• CD8 T cells are also called cytotoxic T lymphocytes (CTLs). They are the primary
killers of tumor cells because they can distinguish cancer cells from normal cells and
directly destroy cancer cells.
• CTLs kill cancer cells via a quick yet well controlled cell-to-cell contact process.
They start by digging a hole in the cancer cells and inject enzymes that can dissolve
their inner materials.
27. • As for CD4 T cells, their major function is producing soluble proteins called
cytokines. These cytokines are messages sent by CD4 T cells to regulate or help the
function of other immune cells during an immune response.
• Some cytokines are called interleukins (ILs), because they deliver messages
between leukocytes (white blood cells). CD4 T cells that use these messages to
help other immune cells are called T helper cells (Th).
• We have several types of T helper cells according to their different production of
cytokines (Th1, Th2, Th17, etc.).
28. • B cells do not kill tumor cells directly, but produce antibodies as their attack molecules.
Their antibodies function like “catchers” that can grasp their target antigens.
• There are five classes of antibodies: IgG, IgM, IgA, IgD, and IgE, based on their different
chemical structures and functions.
• IgG is the major antibody type that crosses the placenta to provide protection for the
baby.
• IgM is the largest antibody in our bodies.
• IgA can be released to our intestines to control infections in our digestion system.
• IgE is the major antibody to control parasites but also causes allergies.
• IgD functions like a receptor for the activation of B cells.
29. • Each antibody can only bind to one antigen.
• Once antibodies bind to antigens, they either block the function of their target
molecules or direct other immune cells (like macrophages and NK cells) to kill the
target cells that express the antigens, a process called antibody-dependent cell-
mediated cytotoxicity (ADCC).
• ADCC plays a key role in the treatment of human cancers, especially cancer cells in
the blood.
30. Why Does the Immune
System Fail to Control
Cancer Cells?
31. • It has been observed that in many patients, cancer cells are surrounded by immune cells in
tissues or co-exist with tumor-reactive immune cells in the peripheral blood. Despite this,
their cancer continues to progress and spread all over the body. We have a name for this
enigma: the Hellström paradox, after Ingegerd and Karl Erik Hellström, two
immunologists who first described this paradox more than 50 years ago (Hellström et al. 1968).
• Most recently, we realized that even if there are plenty of immune cells capable of killing
cancer cells, these immune cells can be killed or suppressed by cancer cells at tumor sites. The
fight back from cancer cells is so powerful that many tumor vaccine therapies and T-cell
transfer therapies failed to control cancer due to the barriers built up in the tumor sites.
• The discovery of B7-H1 (also named PD-L1) expressed by human tumor cells opened a door
for us in our understanding of how tumor cells escape immune surveillance (Dong et al. 2002).
33. • Cancer immunotherapy works through the immune system to control cancer; therefore, its
direct target is the immune cells rather than the tumor cells.
• Cancer immunotherapy is aimed at restoring or enhancing the capability of immune cells to
recognize and destroy cancer cells, and the therapeutic effects will be determined by the
extent to which the immune cells eliminate tumor cells.
• While it is unreasonable to expect the immune system to deal with large tumor masses,
reducing the tumor burden seems to increase the chance of success of immunotherapy. The
ideal scenario is that sufficient numbers of tumor-reactive T cells are generated by
appropriate tumor-antigen stimulation, and T cells are able to move to tumor sites where they
can destroy cancer cells with cytotoxic enzyme (granzyme B) or cytokines (TNF-alpha or IFN-
gamma).
34. Successful immunity will lead to another round of immune response by
releasing more tumor antigens through destruction of tumor cells. This process is
called the cancer-immunity cycle (Chen and Mellman 2013).
36. • Activation of the immune system to bring therapeutic benefit to cancer patients has been the
subject of more than 100 years of study.
• Dr. Coley is believed to be the first physician to perform clinical trials in the treatment of
cancer patients using dead bacteria (Coley 1906). His idea was that a strong immune
response triggered by pathogens that can cure an infection would be able to cure a cancer as
well. Thus, the so-called Coley’s toxin was originally used as a trigger of the immune system
to treat human cancer.
• Most of his trials failed, but occasionally some of his cancer patients experienced tumor
regression. From his pioneering work on cancer immunotherapy, immunologists have
learned the immuno-stimulatory power of his “toxin” and dissected its effective components to
discover new functions of immune adjuvants (enhancers).
37. • These adjuvants have been tested to help immune responses to tumor
vaccination. For example, the dead bacteria bacille Calmette-Guérin (BCG) that
causes tuberculosis has been successfully used in the treatment of human
bladder cancer.
• Some defined tumor antigens or irradiated tumor cells can be used as vaccines
in combination with certain powerful adjuvants to prevent tumor growth.
39. • Cancer is a leading cause of death in the industrialized world second only to
cardiovascular diseases. It is estimated that the number of people living with
cancer is increasing.
• The most commonly diagnosed malignancy in women is breast cancer and
that in men is prostate cancer. Lung cancer and colorectal cancer are the
second and third most commonly diagnosed cancers, respectively, in both men and
women (Siegel et al. 2015).
• Cancer immunotherapy aims to augment the patient’s own immune system,
especially T cells, to fight cancer. In recent years cancer immunotherapy has
emerged to be a promising modality in cancer treatment (Mellman et al. 2011).
40. • Approved agents used in clinical practice that aim to achieve a therapeutic
benefit by modulating pre-existing anti-tumor immunity.
47. • The first cancer immunotherapies used nonspecific immunostimulants with then-
unknown mechanisms of action that rarely limited tumor growth but provided impetus
for creation of the Biologic Response Modifiers Program of the National Cancer Institute
(NCI; prior to 1980s).
• The second generation of immunotherapies utilized well-characterized recombinant
cytokines including interleukin-2 (IL-2) and interferon alpha (IFNα). These agents were
associated with substantial toxicity when utilized at effective doses, but demonstrated
deep responses in less than 10% of patients (prior to 1990s).
• Other cytokines, including IFNγ, IL-4, IL-7, IL-10, IL-12, IL-15, IL-18, IL-25, and so on,
failed to provide substantive benefit, although anecdotal responses were observed. These
were the first effective immunotherapies.
48. • The third generation of immunotherapies utilized humanized and human
monoclonal antibodies (mAbs) to cell surface receptor proteins present on tumor
cells (human epidermal growth factor receptor 2 [HER2]/Neu, epidermal growth
factor receptor [EGFR], etc) and were integrated into cancer care (prior to 2000s).
• Vaccination strategies using the available peptide, whole tumor, recombinant
proteins, dendritic cells (DCs), and adjuvants were only modestly successful 100
vaccine with IL-2, anti-idiotype vaccines following effective chemotherapy, and
long peptides for human papillomavirus [HPV] E6, E7 in precancerous lesions)
(prior to 2000s).
49. • The modern era of immunotherapy launched with the extraordinary novel
efficacy to immune checkpoints in patients with lung cancer, melanoma, renal
cancer, bladder cancer, and head and neck cancer (2005–current).
• The modern treatment of patients with cancer will integrate immunotherapy
with conventional surgical, chemotherapeutic, and radiation oncologic
strategies (the future).
51. • Immunotherapy is treatment that uses a person's own immune system to fight
cancer. Immunotherapy can boost or change how the immune system works so it
can find and attack cancer cells.
• Immunotherapy is a type of biological therapy.
52. Cancer immunotherapy, also known as immuno-oncology, is a form of cancer
treatment that uses the power of the body’s own immune system to prevent, control,
and eliminate cancer.
Immunotherapy can:
• Educate the immune system to recognize and attack specific cancer cells
• Boost immune cells to help them eliminate cancer
• Provide the body with additional components to enhance the immune response
54. Immunotherapy for cancer in India can be done either by:-
• Stopping or halting the growth of cancer in the body.
• Stopping cancer from travelling to other parts of the body.
• Enhancing, and strengthening patient’s immune system
55. • Cancer immunotherapy comes in a variety of forms, including targeted
antibodies, cancer vaccines, adoptive cell transfer, tumor-infecting viruses,
checkpoint inhibitors, cytokines, and adjuvants.
• Some immunotherapy treatments use genetic engineering to enhance immune
cells’ cancer-fighting capabilities and may be referred to as gene therapies.
• Many immunotherapy treatments for preventing, managing, or treating different
cancers can also be used in combination with surgery, chemotherapy, radiation, or
targeted therapies to improve their effectiveness.
57. Immune system can prevent or slow cancer growth.
cancer cells have ways to avoid destruction by the immune system.
For example, cancer cells may:
• Have genetic changes that make them less visible to the immune system.
• Have proteins on their surface that turn off immune cells.
• Change the normal cells around the tumor so they interfere with how the immune
system responds to the cancer cells.
Immunotherapy helps the immune system to better act against cancer.
59. Active and Passive Immunotherapy
Active Immunotherapy
Inducing cellular immunity (involving cytotoxic T-cells) in a host that failed to spontaneously
develop an effective response generally involves methods to enhance presentation of tumor antigens
to host effector cells. Cellular immunity can be induced to specific, very well-defined antigens.
Several techniques can be used to stimulate a host response; these may involve presenting
peptides, DNA, or tumor cells (from the host or another patient). T-cells as the ultimate effectors of
adaptive immune response are currently used to treat patients affected by infectious diseases and certain
tumors.
Nonspecific Immunotherapy
Interferons (IFN-α, -β, -γ) are glycoproteins that have antitumor and antiviral activity.
Depending on dose, interferons may either enhance or decrease cellular and humoral immune
functions. Interferons also inhibit division and certain synthetic processes in a variety of cells.
Clinical trials have indicated that interferons have antitumor activity in various cancers,
including hairy cell leukemia, chronic myelocytic leukemia, AIDS- associated Kaposi’s sarcoma, non-
Hodgkin lymphoma (NHL), multiple myeloma, and ovarian carcinoma.
60. Three groups of immunological substances of particular interest are,
Interferon ,
Interleukins and
Tumour necrosis factor ( TNF ).
61. Monoclonal Antibodies
Many attempts have been made to develop antibodies with specific activity against a
particular cancer. In animal studies, this has been possible in a number of different models,
especially with several tumour types in mice. There have been three somewhat different
therapeutic objectives:
1. One is to develop “killer antibodies” that specifically act against a particular cancer.
2. Another is to develop “magic bullets” where antibodies are used to carry an anticancer
chemotherapeutic agent or a radio-isotope or other such agent directly to the cancer cells
wherever they might be.
3. The third potential use of monoclonal antibodies is to identify the presence of cancer cells by
reaction to specific antibodies.
62. • The application of these principles to treatment of clinical cancers in humans has
met with some encouraging results, especially in treating metastatic breast cancer.
• Recently developed techniques in biotechnology have made it possible to
manufacture so-called monoclonal antibodies that are aimed at specific vital targets
in certain cancers.
• These include malignant lymphoma and breast and bowel cancers. The use of these
antibodies is relatively new, e.g. Mabthera for lymphoma, Herceptin in breast
cancer and Erbitux for bowel cancer.
• In general, these antibodies are used in combination with chemotherapy. Despite
their great expense, they are showing considerable effectivity, although their final
role is still being evaluated.
63. Interferon
• It was first recognised in the 1930s that infection of animal cells with one virus would for a time
“interfere” with infection by other viruses. Thirty years later, it was discovered that a protein substance
was released from cells infected with a virus and this substance protects other cells against other viral
infections. This interfering substance is called “interferon”.
• Interferon is found to be species specific. That is, interferon produced by chicken cells is protective to
other chicken cells against virus infection but is not protective for cells of any other animal species.
Similarly, interferon produced from human cells is protective for other human cells but not for cells
of other animal species.
• There is evidence that it may be protective in some viral infections but is too expensive for general use.
A rare form of leukaemia called “hairy cell” leukaemia is one malignancy that often does respond well
to interferon treatment.
64. • AIDS (acquired immune deficiency syndrome) is due to a virus infection. This
condition is an infection and not a cancer, but a particular type of cancer called
Kaposi ’ s sarcoma was found to develop in some of the first patients with AIDS.
• Over a longer term, some types of lymphoma, cancers of the cervix and some
other cancers have been found to develop more commonly in AIDS patients than
in the community at large.
• Early hopes that AIDS might respond well to interferon or any other immune
treatment have so far not been fulfilled.
65. The Interleukins
• The interleukins are protein substances, known as cytokines, and are produced from white
cells and are found to activate the immunological defense system.
• The first interleukins were interleukin 1 which is produced from macrophages (giant
white cells) and interleukin 2 that is produced from lymphocytes (small white cells).
• They stimulate reproduction and activity of immune cells against a cancer to which the cells
have been specifically sensitized.
• In experimental animals, interleukins have been shown, under certain conditions, to
stimulate the animal’s natural lymphocyte activity against implanted cancers to such an
extent that the cancers have been eradicated.
66. • However, some cancers, including melanoma and kidney cancers, sometimes
appear to have increased response when certain interleukins are used in
conjunction with other treatments.
67. Tumour Necrosis Factor (TNF)
• TNF is a more recent cytokine protein product of immunological research. TNF does
cause cancer cell destruction in some experimental models but is too toxic for direct use in
human patients.
• However, recent work has shown that TNF enhances the anti-cancer effect of certain other
chemotherapeutic agents and can be used safely and effectively when given exclusively to a
limited part of the body.
• It can be given with safety only in a closed circuit by regional perfusion or regional infusion
to treat malignancies such as melanoma and sarcoma when confined to a limb, but it
cannot be used systemically with safety.
68. • TNF in combination with interleukin 1 and interleukin 6 has been implicated in
promoting cancer cachexia.
• Drugs that suppress the production of TNF, e.g. corticosteroids and thalidomide,
have shown promise as agents that suppress cachexia and tumour growth,
respectively.
• The omega-3 oils are thought to work by suppressing interleukin 6, which
promotes breakdown of adipose tissue and skeletal muscle.
69. Small-Molecule Target Inhibitors
• Basic cancer research has identified a number of key signaling pathways that
coordinate cancer cell growth. Growth signaling cytokines circulate in the blood and
bind to cancer cells via special receptor molecules. Receptors become activated by the
binding cytokine and send a complex series of chemical signals to the cell nucleus
stimulating cell growth and division.
• The principle oncogene proteins responsible have been identified and successfully
targeted for direct inhibition by small molecules (low molecular mass compounds)
that specifically inhibit the enzyme activity that stimulates growth. Examples are
imatinib mesylate (Gleevec) which inhibit the tyrosine kinases.
70. VACCINES
• Prophylactic vaccines have changed the natural history of many infectious diseases; consequently, the
development of vaccines that could stimulate the immune system to recognize and destroy cancer
cells has been a major focus of immunotherapy research for decades.
• Many vaccine approaches have been tried, and several have shown promise in early phase trials
compared to historical controls.
• However, with a few notable exceptions, randomized controlled phase III trials have failed to
confirm the benefit of these vaccines relative to standard therapies, observation, or placebo.
• Nonetheless, examination of these approaches in the light of our recent understanding of tumor
immunology provides insight into the likely limitations of previous vaccine approaches that can inform
current and future cancer vaccine development.
71. • Autologous whole tumor cell vaccines have universally failed to show benefit
in phase III trials, including studies with GVAX (a granulocyte macrophage
colony-stimulating factor [GM-CSF]-transduced autologous tumor cell vaccine)
given alone or in combination with other agents.
• Bacillus Calmette-Guérin (BCG) vaccine for adjunctive therapy for superficial
bladder cancer, Sipuleucel-T is a DC vaccine for prostate cancer, GVAX is a
whole-cell vaccine for prostate cancer cell lines, Gp100 vaccine is a peptide
vaccine for patients with melanoma.
72. Several types of immunotherapy are used to treat cancer. These include:
• Immune checkpoint inhibitors, which are drugs that block immune checkpoints. These
checkpoints are a normal part of the immune system and keep immune responses from being
too strong. By blocking them, these drugs allow immune cells to respond more strongly to
cancer.
• T-cell transfer therapy, which is a treatment that boosts the natural ability of your T
cells to fight cancer. T-cell transfer therapy may also be called adoptive cell therapy,
adoptive immunotherapy, or immune cell therapy.
74. Different forms of immunotherapy may be given in different ways. These include:
• Intravenous (IV)
The immunotherapy goes directly into a vein.
• Oral
The immunotherapy comes in pills or capsules that swallow.
• Topical
The immunotherapy comes in a cream that rub into skin. This type of
immunotherapy can be used for very early skin cancer.
• Intravesical
The immunotherapy goes directly into the bladder.
76. Immunotherapy depends on:
• Type of cancer and how advanced it is
• The type of immunotherapy get
• How body reacts to treatment
• May have treatment every day, week, or month. Some types of immunotherapy
given in cycles. A cycle is a period of treatment followed by a period of rest.
The rest period gives body a chance to recover, respond to the immunotherapy,
and build new healthy cells.
77. What is the current research in immunotherapy?
78. Researchers are focusing on several major areas to improve immunotherapy, including:
• Finding solutions for resistance.
Researchers are testing combinations of immune checkpoint inhibitors and other types of
immunotherapy, targeted therapy, and radiation therapy to overcome resistance to immunotherapy.
• Finding ways to predict responses to immunotherapy.
Only a small portion of people who receive immunotherapy will respond to the treatment. Finding
ways to predict which people will respond to treatment is a major area of research.
• Learning more about how cancer cells evade or suppress immune responses against them.
A better understanding of how cancer cells get around the immune system could lead to the
development of new drugs that block those processes.
• How to reduce the side effects of treatment with immunotherapy.
79. What types of cancer can be treated with immunotherapy?
80. • Immunotherapy has proven beneficial in the treatment of most cancer types.
• The various common types of cancer that can be treated with immunotherapy
include lung cancer, some skin cancers (particularly melanoma), kidney
cancer, bladder cancer, head and neck cancers, lymphoma.
• Not as widely used as radiation therapy, surgery or chemotherapy, some studies
indicate that immunotherapy has shown 20-30% positive results on the
patients.
• Doctors advise for this treatment when the patient’s body fails the first and
second-line treatments.
82. Side effects from immunotherapy vary depending on the drug and cancer types.
• Infusion-related reactions.
• Diarrhea or colitis.
• Bone or muscle pain.
• Fatigue.
• Flu-like symptoms, such as fever and chills.
• Headaches.
• Loss of appetite.
• Mouth sores.
• Skin rash.
• Shortness of breath or pneumonitis.
84. • Success rates for any cancer treatment, including immunotherapy, depend on
individual factors, including the cancer type and stage.
• In general, immunotherapy is effective against many cancers. While some cancers
are more immunogenic than others, in general, immunotherapy is effective across a
wide variety of cancers.
• Immunotherapy can produce durable responses unlike chemotherapy or radiation,
however, these occur only in around 25% patients.
• Some research suggests that the immune system may remember cancer cells
after immunotherapy ends.
87. • Perhaps the greatest hopes for the future are in the fields of immunotherapy ,
genetic engineering and molecular biology .
• Related research indicates that tumour antibodies may not only reveal early evidence
of cancer but may be used in treatment either in a direct attack upon cancer cells or by
carrying cytotoxic chemical agents specifi cally to the cancer cells. In time, a more
reliable means of stimulating the immune defence system to eradicate cancer cells
may also emerge from these studies.
88. References
1. Frederick O Stephens, Karl Reinhard Aigner. Basics of Oncology. Second Edition. New York: Springer; 2016.
2. Lisa H Butterfield, Howard L Kaufman, Francesco M Marincola. Cancer Immunotherapy Principles and Practice.
New York : Demos Medical Publishing; 2017
3. Laurence Zitvogel, Guido Kroemer. Oncoimmunology. Springer International Publishing AG 2018.
4. Aung Naing, Joud Hajjar. Immunotherapy. Second Edition. Springer Nature Switzerland AG 2018.
5. Bonny Libbey Johnson, Jody gross. Handbook of oncology nursing. Third edition. Boston: Jones and bartlett
publishers; 1998.
6. Daniele Gde, Jane Chareffe. Oncology Nursing Care Plans. Africa: Delmar thomson learning; 1995.
7. Bartosz Chmielowski, Mary Territo. Manual of Clinical Oncology. 8th edition. Wolters Kluwer;2017
8. https://www.cancer.gov/about
cancer/treatment/types/immunotherapy#:~:text=Immunotherapy%20is%20a%20type%20of,a%20type%20of%20bio
logical%20therapy.
9. https://cytecare.com/blog/immunotherapy-a-modern-treatment-for-cancer/
10. https://my.clevelandclinic.org/health/treatments/11582-immunotherapy
11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4350348/
