current cancer treatments riya n sandra (1)
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Introduction
Current Cancer Treatments
Cancer is a nearly invincible disease that has plagued humankind for centuries. Only in recent
decades have doctors found effective ways to treat it. In that time we have also found better
methods for early detection of this devastating disease. Despite great efforts to develop better
treatments, more than 6 million people worldwide died from cancer in 1997. And we are still
years away from any possible cure for cancer, something that many scientists think is impossible.
While early detection is your best form of prevention, there are several techniques that are used
to treat cancer, these techniques include:
Surgery Radiation therapy Chemotherapy Hormone therapy Immunotherapy
Surgery is the oldest and most widely used treatment available for cancer patients. About 60
percent of people diagnosed with cancer will undergo surgery, according to theAmerican CancerSociety.If a growth is found early, doctors may opt to remove it before it has a chance to grow.
Surgery is also used when there is a good chance to remove an entire tumor before it spreads.
Surgery is rarely used as a stand-alone treatment. Usually, it is combined with radiation therapy
and /or chemotherapy.
In radiation therapy, the specific part of the body containing a cancerous growth is exposed to
radiation energy to attack reproducing cancer cells. However, the radiation cannot affect the
cancer cells without affecting normal cells, which can lead to several unpleasant side effects,
including fatigue, dryness and peeling of skin, nausea and vomiting. Radiation therapy is often
used to shrink a tumor so that it can be removed through surgery, or to prevent tumor growth
following surgery.
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In these two categories, there are more specific types of cancer vaccines. Each type of cancer
vaccine works on the same basic idea: The vaccine, which contains tumor cells or antigens,
stimulates the patient's immune system, which produces special cells that kill cancer cells and
prevent relapses of the cancer. Unlike vaccines for other disease that prevent the occurrence of
the disease, there isn't a vaccine in development that can prevent the onset of cancer. Cancer
vaccines are used only as a treatment after the cancer has been found in a patient. Here is a list of
five kinds of cancer vaccines being developed:
Antigen vaccines Anti-idiotype vaccines Dendritic cell vaccines
DNA vaccines Tumor cell vaccines
Antigen vaccines use tumor-specific antigens -- proteins displayed on a tumor cell -- to stimulate
the immune system. By injecting these antigens into the cancerous area of the patient, the
immune system will produce an increased amount of antibodies or cytotoxic T lymphocytes, also
known as killer T cells, to attack cancer cells that carry that specific antigen. Multiple antigens
can be used in this type of vaccine to vary the immune system response.
In some instances, some antibodies, called idiotype antibodies, act as antigens, triggering an
immune response similar to that described above. In this case, the immune system will produce
anti-idiotype antibodies to attack the idiotypes. Scientists have found a way to mass-produce
anti-idiotype antibodies to produce a vaccine that can be injected to treat cancer.
Dendritic cells break the antigens on the cancer cell surfaces into smaller pieces. The dendritic
cells then act as most-wanted posters for the immune system, displaying those antigen pieces to
the killer T cells. To make a dendritic cell vaccine, scientists extract some of the patient's
dendritic cells and use immune cell stimulants to reproduce large amounts of dendritic cells in
the lab. These dendritic cells are then exposed to antigens from the patient's cancer cells. This
combination of dendritic cells and antigens is then injected into the patient, and the dendritic
cells work to program the T cells.
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With recent DNA (deoxyribonucleic acid) research, scientists are finding ways to use the genetic
code of proteins produced in cells to aid the immune systems fight against cancer. Bits of DNA
from the patient's cells are injected into the patient, which instructs the other cells to
continuously produce certain antigens. This DNA vaccine increases production of antigens,
which forces the immune system to respond by producing more T cells.
Tumor cell vaccines can be produced using cancer cells from the patient or another patient.
These cells are killed and injected into the patient. While the cells are dead, the antigens are still
recognized by the the immune system, which responds by attacking the dead cells. The immune
system will also attack the live cancer cells carrying the antigen that was displayed on the dead
cells.
While scientists have had some success with each of these cancer vaccines, it is still much too
early to predict when a true cancer vaccine will be developed. However, science has brought us
closer than ever to being able to develop a method that could eradicate some forms of cancer in
our lifetime, if not all cancer entirely.
Cancer treatment that PUNCHES HOLES in tumours could be latestweapon in war against disease
New treatment uses millions of electric pulses per second to make holes in cancer cellsand kill them
Therapy does not damage surrounding healthy tissue Now experts want to carry out larger clinical trials
A minimally invasive cancer treatment that punches microscopic holes in tumours - without
harming surrounding healthy tissue - could be the latest weapon in the war against
cancer.Irreversible electroporation (IRE) uses millions of electrical pulses per second to kill
cancer cells but spare nearby tissue.IRE may be especially beneficial in treating liver, lung,
pancreatic and other cancers that are close to blood vessels, nerves and other sensitive
structures.
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NEW ICE THERAPY IS FREEZING OUT CANCERSCryoablation has potential as a treatment for cancer that has spread to the lungs from other parts
of the body and could prolong the lives of patients who are running out of options, said David
Woodrum of the Mayo Clinic in Minnesota, who helped lead the study. Cryoablation may not be
able to cure the cancer, but it can at least slow it down significantly and allow patients to enjoy
greater quality of life longer.The study involved 22 people who suffered with a total of 36
tumours in their lungs.After undergoing 27 cryoablation sessions, researchers found that the
treatment was 100 per cent successful in killing the tumours after a three month follow-up
treatment.After six months, five of the 22 patients still showed no sign of tumour regrowth. The
researchers plan to follow the same patients for another four and a half years.
Cryoablation is performed using a small needle-like probe guided through a nick in the skin to
cancerous tumours inside the lung.Once in position, the tip of the instrument is cooled with gas
to as low as minus 100 degrees Celsius. The resulting halo of ice crystals can destroy cancer by
interrupting its cellular function, protecting nearby healthy, delicate lung tissue.
New radiation therapy for cancer patients that has NO side-effects such hair
loss or nausea
humans
-effects of radiotherapy occur because it damages healthy cells as well as destroying
cancerous ones
-engineered boron chemical spares neighboring healthy
cells
The team got cancer cells to take in and store a boron chemical designed by
Professor Hawthorne. When those boron-infused cancer cells were exposed to neutrons, a
subatomic particle, the boron atom shattered and selectively tore apart the cancer cells, sparing
neighboring healthy cells - and avoiding side-effects.The reaction is said to be 'like pool balls
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careening around a billiards table' and cancer cells are destroyed from the inside without harming
the surrounding tissues.
Angiogenesis InhibitorsAngiogenesis is the formation of new blood vessels. This process involves the migration, growth,
and differentiation ofendothelial cells,which line the inside wall of blood vessels.
The process of angiogenesis is controlled by chemical signals in the body. These signals can
stimulate both the repair of damaged blood vessels and the formation of new blood vessels.
Other chemical signals, called angiogenesis inhibitors, interfere with blood vessel formation.
Normally, the stimulating and inhibiting effects of these chemical signals are balanced so that
blood vessels form only when and where they are needed.
Angiogenesis plays a critical role in the growth and spread of cancer. A blood supply is
necessary for tumors to grow beyond a few millimeters in size. Tumors can cause this blood
supply to form by giving off chemical signals that stimulate angiogenesis. Tumors can also
stimulate nearby normal cells to produce angiogenesis signaling molecules. The resulting new
blood vessels feed growing tumors with oxygen and nutrients, allowing the cancer cells to
invade nearby tissue, to move throughout the body, and to form new colonies of cancer cells,called metastases.
Because tumors cannot grow beyond a certain size or spread without a blood supply, scientists
are trying to find ways to block tumor angiogenesis. They are studying natural and synthetic
angiogenesis inhibitors, also calledantiangiogenic agents, with the idea that these molecules will
prevent or slow the growth of cancer.
Mechanism of action
Angiogenesis requires the binding of signaling molecules, such as vascular endothelial growth
factor (VEGF), to receptors on the surface of normal endothelial cells. When VEGF and other
endothelial growth factors bind to their receptors on endothelial cells, signals within these cells
are initiated that promote the growth and survival of new blood vessels.
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Angiogenesis inhibitors interfere with various steps in this process. For example, bevacizumab
(Avastin) is a monoclonal antibody that specifically recognizes and binds to VEGF. When
VEGF is attached to bevacizumab, it is unable to activate the VEGF receptor. Other angiogenesis
inhibitors, including sorafenib and sunitinib, bind to receptors on the surface of endothelial cells
or to other proteins in the downstream signaling pathways, blocking their activities.
Drugs Having Antiangiogenic Activity
The U.S. Food and Drug Administration (FDA) has approved bevacizumab to be used alone for
glioblastoma that has not improved with other treatments and to be used in combination with
other drugs to treat metastatic colorectal cancer, some non-small cell lung cancers, and
metastaticrenal cell cancer.Bevacizumab was the first angiogenesis inhibitor that was shown to
slow tumor growth and, more important, to extend the lives of patients with some cancers.
The FDA has approved other drugs that have antiangiogenic activity, including sorafenib
(Nexavar),sunitinib (Sutent),pazopanib (Votrient), andeverolimus (Afinitor). Sorafenib
is approved for hepatocellular carcinoma and kidney cancer, sunitinib and everolimus for both
kidney cancer and neuroendocrine tumors, and pazopanib for kidney cancer. Researchers are
exploring the use of angiogenesis inhibitors to treat other types of cancer . In addition,
angiogenesis inhibitors are being used to treat some diseases that involve the development ofabnormal blood vessel growth in noncancer conditions, such asmacular degeneration.
Side Effects
Initially, it was thought that angiogenesis inhibitors would have mild side effects, but more
recent studies have revealed the potential for complications that reflect the importance of
angiogenesis in many normal body processes, such aswound healing, heart and kidney function,
fetal development, and reproduction. Side effects of treatment with angiogenesis inhibitors can
include problems with bleeding, clots in the arteries (with resultant stroke or heart attack),
hypertension, and protein in the urine . Gastrointestinal perforation andfistulas also appear to be
rare side effects of some angiogenesis inhibitors. Animal studies have revealed the potential for
birth defects, although there is no clinical evidence for such effects in humans.
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It is likely that some of the possible complications of angiogenesis inhibitor therapy remain
unknown. As more patients are treated with these agents, doctors will learn more about possible
rare side effects.
Gene Therapy for CancerAdvances in understanding and manipulating genes have set the stage for scientists
to alter a person's genetic material to fight or prevent disease. Gene therapy is an experimental
treatment that involves introducing genetic material (DNA or RNA) into a person's cells to fight
disease. Gene therapy is being studied in clinical trials (research studies with people) for many
different types of cancer and for other diseases. It is not currently available outside a clinical
trial.
target healthy cells to enhance their ability to fight cancer. Other approaches target cancer cells,
to destroy them or prevent their growth. Some gene therapy techniques under study are described
below.
In one approach, researchers replace missing or altered genes with healthy genes.Because some missing or altered genes (e.g., p53) may cause cancer, substituting
working copies of these genes may be used to treat cancer. Researchers are also studying ways to improve a patient'simmune response to cancer. In
this approach, gene therapy is used to stimulate the body's natural ability to attack cancer
cells. In one method under investigation, researchers take a small blood sample from a
patient and insert genes that will cause each cell to produce a protein called a T-cell
receptor (TCR). The genes are transferred into the patient's white blood cells (called T
lymphocytes)and are then given back to the patient. In the body, the white blood cells
produce TCRs, which attach to the outer surface of the white blood cells. The TCRs then
recognize and attach to certain molecules found on the surface of the tumor cells. Finally,
the TCRs activate the white blood cells to attack and kill the tumor cells.
Scientists are investigating the insertion of genes into cancer cells to make them moresensitive to chemotherapy, radiation therapy, or other treatments. In other studies,
researchers remove healthy blood-forming stem cells from the body, insert a gene that
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makes these cells more resistant to theside effects of highdoses of anticancer drugs, and
theninject the cells back into the patient.
In another approach, researchers introduce suicide genes into a patient's cancer cells. Apro-drug (an inactive form of a toxic drug) is then given to the patient. The pro-drug is
activated in cancer cells containing these suicide genes, which leads to the destruction
of those cancer cells.
Other research is focused on the use of gene therapy to prevent cancer cells fromdeveloping newblood vessels (angiogenesis).
How are genes transferred into cells so that gene therapy can take place?
In general, a gene cannot be directly inserted into a person's cell. It must be delivered to the cell
using a carrier, or vector. The vectors most commonly used in gene therapy are viruses.Viruses have a unique ability to recognize certain cells and insert genetic material into them.
In some gene therapy clinical trials, cells from the patient's blood orbone marrow are removed
and grown in the laboratory. The cells are exposed to the virus that is carrying the desired gene.
The virus enters the cells and inserts the desired gene into the cells DNA. The ce lls grow in the
laboratory and are then returned to the patient by injection into a vein. This type of gene therapy
is calledex vivobecause the cells are grown outside the body. The gene is transferred into the
patient's cells while the cells are outside the patient's body.
In other studies, vectors (often viruses) or liposomes (fatty particles) are used to deliver the
desired gene to cells in the patient's body. This form of gene therapy is called in vivo,because
the gene is transferred to cells inside the patient's body.
Process Of Gene Transferation
In general, a gene cannot be directly inserted into a person's cell. It must be delivered to the cell
using a carrier, or vector. The vectors most commonly used in gene therapy are viruses.
Viruses have a unique ability to recognize certain cells and insert genetic material into them.
In some gene therapy clinical trials, cells from the patient's blood orbone marrow are removed
and grown in the laboratory. The cells are exposed to the virus that is carrying the desired gene.
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The virus enters the cells and inserts the desired gene into the cells DNA. The cells grow in the
laboratory and are then returned to the patient by injection into a vein. This type of gene therapy
is calledex vivobecause the cells are grown outside the body. The gene is transferred into the
patient's cells while the cells are outside the patient's body.
In other studies, vectors (often viruses) or liposomes (fatty particles) are used to deliver the
desired gene to cells in the patient's body. This form of gene therapy is called in vivo,because
the gene is transferred to cells inside the patient's body.
Viruses Used In Gene Therapy
Many gene therapy clinical trials rely on retroviruses to deliver the desired gene. Other viruses
used as vectors include adenoviruses, adeno-associated viruses, lentiviruses, poxviruses, and
herpes viruses.These viruses differ in how well they transfer genes to the cells they recognize
and are able to infect, and whether they alter the cell's DNA permanently or temporarily. Thus,
researchers may use different vectors, depending on the specific characteristics and requirements
of the study.
Scientists alter the viruses used in gene therapy to make them safe for humans and to increase
their ability to deliver specific genes to a patient's cells. Depending on the type of virus and the
goals of the research study, scientists may inactivate certain genes in the viruses to prevent them
from reproducing or causing disease. Researchers may also alter the virus so that it better
recognizes and enters the target cell.
Risks are associated with current gene therapy trials
Viruses can usually infect more than one type of cell. Thus, whenviral vectors are used to carry
genes into the body, they might infect healthy cells as well as cancer cells. Another danger is that
the new gene might be inserted in the wrong location in the DNA, possibly causing harmful
mutations to the DNA or even cancer.
In addition, when viruses or liposomes are used to deliver DNA to cells inside the patient's body,
there is a slight chance that this DNA could unintentionally be introduced into the patient's
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reproductive cells.If this happens, it could produce changes that may be passed on if a patient
has children after treatment.
Other concerns include the possibility that transferred genes could be overexpressed,
producing so much of the missing protein as to be harmful; that the viral vector could cause
inflammation or an immune reaction; and that the virus could be transmitted from the patient to
other individuals or into the environment. Scientists use animal testing and other precautions to
identify and avoid these risks before any clinical trials are conducted in humans.
Cryosurgery in Cancer TreatmentCryosurgery (also calledcryotherapy)is the use of extreme cold produced by liquid nitrogen (or
argon gas) to destroy abnormaltissue.Cryosurgery is used to treat external tumors, such as those
on the skin. For external tumors, liquid nitrogen is applied directly to the cancer cells with a
cotton swab or spraying device.
Cryosurgery is also used to treat tumors inside the body (internal tumors and tumors in the bone).
For internal tumors, liquid nitrogen or argon gas is circulated through a hollow instrument called
a cryoprobe, which is placed in contact with the tumor. The doctor uses ultrasound orMRI to
guide the cryoprobe and monitor the freezing of the cells, thus limiting damage to nearby healthy
tissue. (In ultrasound, sound waves are bounced offorgans and other tissues to create a picture
called a sonogram.) A ball of ice crystals forms around the probe, freezing nearby cells.
Sometimes more than one probe is used to deliver the liquid nitrogen to various parts of the
tumor. The probes may be put into the tumor during surgery or through the skin
(percutaneously). After cryosurgery, the frozen tissue thaws and is either naturally absorbed by
the body (for internal tumors), or it dissolves and forms a scab (for external tumors).
Cryosurgery is used to treat several types of cancer, and some precancerous or noncancerousconditions. In addition to prostate and liver tumors, cryosurgery can be an effective treatment for
the following:
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Retinoblastoma (a childhood cancer that affects the retina of the eye). Doctors have foundthat cryosurgery is most effective when the tumor is small and only in certain parts of the
retina.
Early-stage skin cancers (bothbasal cell andsquamous cell carcinomas). Precancerous skin growths known asactinic keratosis. Precancerous conditions of the cervix known as cervical intraepithelial neoplasia
(abnormal cell changes in the cervix that can develop intocervical cancer).
Cryosurgery is also used to treat some types of low-grade cancerous and noncancerous tumors of
the bone. It may reduce the risk of joint damage when compared with more extensive surgery,
and help lessen the need foramputation.The treatment is also used to treatAIDS-related Kaposi
sarcoma when the skinlesions are small andlocalized.
Researchers are evaluating cryosurgery as a treatment for a number of cancers, includingbreast,
colon,andkidney cancer. They are also exploring cryotherapy in combination with other cancer
treatments, such ashormone therapy,chemotherapy,radiation therapy,or surgery.
Treatment Area
Cryosurgery can be used to treat men who have early-stage prostate cancer that is confined to the
prostate gland. It is less well established than standard prostatectomy and various types of
radiation therapy. Long-term outcomes are not known. Because it is effective only in small areas,
cryosurgery is not used to treat prostate cancer that has spread outside the gland, or to distant
parts of the body.
Some advantages of cryosurgery are that the procedure can be repeated, and it can be used to
treat men who cannot have surgery or radiation therapy because of their age or other medical
problems.
Cryosurgery may be used to treat primary liver cancer that has not spread. It is used especially if
surgery is not possible due to factors such as other medical conditions. The treatment also may
be used for cancer that has spread to the liver from another site (such as the colon or rectum). In
some cases, chemotherapy and/or radiation therapy may be given before or after cryosurgery.
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Cryosurgery in the liver may cause damage to thebile ducts and/or majorblood vessels,which
can lead to hemorrhage (heavy bleeding) orinfection.
Side Effects
Cryosurgery does have side effects, although they may be less severe than those associated with
surgery or radiation therapy. The effects depend on the location of the tumor. Cryosurgery for
cervical intraepithelial neoplasia has not been shown to affect a woman's fertility, but it can
cause cramping, pain, or bleeding. When used to treat skin cancer (including Kaposi sarcoma),
cryosurgery may cause scarring and swelling; if nerves are damaged, loss of sensation may
occur, and, rarely, it may cause a loss of pigmentation and loss of hair in the treated area. When
used to treat tumors of the bone, cryosurgery may lead to the destruction of nearby bone tissue
and result in fractures, but these effects may not be seen for some time after the initial treatment
and can often be delayed with other treatments. In rare cases, cryosurgery may interact badly
with certain types of chemotherapy. Although the side effects of cryosurgery may be less severe
than those associated with conventional surgery or radiation, more studies are needed to
determine the long-term effects.
Advantages Of Cryosurgery
Cryosurgery offers advantages over other methods of cancer treatment. It is less invasive than
surgery, involving only a small incision or insertion of the cryoprobe through the skin.
Consequently, pain, bleeding, and other complications of surgery are minimized. Cryosurgery is
less expensive than other treatments and requires shorter recovery time and a shorter hospital
stay, or no hospital stay at all. Sometimes cryosurgery can be done using onlylocal anesthesia.
Because physicians can focus cryosurgical treatment on a limited area, they can avoid the
destruction of nearby healthy tissue. The treatment can be safely repeated and may be used along
with standard treatments such as surgery, chemotherapy, hormone therapy, and radiation.
Cryosurgery may offer an option for treating cancers that are considered inoperable or that do
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not respond to standard treatments. Furthermore, it can be used for patients who are not good
candidates for conventional surgery because of their age or other medical conditions.
Disadvantages Of Cryosurgery
The major disadvantage of cryosurgery is the uncertainty surrounding its long-term
effectiveness. While cryosurgery may be effective in treating tumors the physician can see by
usingimaging tests (tests that produce pictures of areas inside the body), it can missmicroscopic
cancer spread. Furthermore, because the effectiveness of the technique is still being assessed,
insurance coverage issues may arise.
Hyperthermia in Cancer TreatmentHyperthermia (also called thermal therapy or thermotherapy) is a type of cancer treatment inwhich body tissue is exposed to high temperatures (up to 113F). Research has shown that high
temperatures can damage and kill cancer cells, usually with minimal injury to normal tissues. By
killing cancer cells and damagingproteins and structures within cells, hyperthermia may shrink
tumors.Hyperthermia is under study in clinical trials (research studies with people) and is not
widely available
Treatment
Hyperthermia is almost always used with other forms of cancer therapy, such as radiation
therapy and chemotherapy. Hyperthermia may make some cancer cells more sensitive to
radiation or harm other cancer cells that radiation cannot damage. When hyperthermia and
radiation therapy are combined, they are often given within an hour of each other. Hyperthermia
can also enhance the effects of certain anticancerdrugs.
Numerous clinical trials have studied hyperthermia in combination with radiation therapy and/or
chemotherapy. These studies have focused on the treatment of many types of cancer, including
sarcoma,melanoma,and cancers of the head and neck, brain, lung,esophagus,breast,bladder,
rectum,liver,appendix,cervix,andperitoneal lining (mesothelioma). Many of these studies, but
not all, have shown a significant reduction in tumor size when hyperthermia is combined with
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perfused area; however, most of theseside effects are temporary. Whole-body hyperthermia can
cause more serious side effects, including cardiac and vascular disorders, but these effects are
uncommon Diarrhea, nausea, and vomiting are commonly observed after whole-body
hyperthermia
Photodynamic Therapy for CancerPhotodynamic therapy (PDT) is a treatment that uses a drug, called a photosensitizer or
photosensitizing agent, and a particular type of light. When photosensitizers are exposed to a
specific wavelength of light, they produce a form of oxygen that kills nearbycells.Thus, doctors
use specific photosensitizers and wavelengths of light to treat different areas of the body with
PDT
Treatment
In the first step of PDT for cancer treatment, a photosensitizing agent is injected into the
bloodstream. The agent is absorbed by cells all over the body but stays in cancer cells longer
than it does in normal cells. Approximately 24 to 72 hours after injection, when most of the
agent has left normal cells but remains in cancer cells, the tumor is exposed to light. The
photosensitizer in the tumor absorbs the light and produces an active form of oxygen that
destroys nearby cancer cells.
In addition to directly killing cancer cells, PDT appears to shrink or destroy tumors in two other
ways. The photosensitizer can damageblood vessels in the tumor, thereby preventing the cancer
from receiving necessary nutrients. PDT also may activate the immune system to attack the
tumor cells.
The light used for PDT can come from a laser or other sources. Laser light can be directed
through fiber optic cables (thin fibers that transmit light) to deliver light to areas inside the body.
For example, a fiber optic cable can be inserted through anendoscope (a thin, lighted tube used
to look at tissues inside the body) into the lungs or esophagus to treat cancer in these organs.
Other light sources include light-emitting diodes (LEDs), which may be used for surface tumors,
such as skin cancer.
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PDT is usually performed as an outpatient procedure. PDT may also be repeated and may be
used with other therapies, such assurgery,radiation,orchemotherapy.
Extracorporeal photopheresis (ECP) is a type of PDT in which a machine is used to collect the
patients blood cells, treat them outside the body with a photosensitizing agent, expose them to
light, and then return them to the patient. The U.S. Food and Drug Administration (FDA) has
approved ECP to help lessen the severity of skin symptoms of cutaneous T-cell lymphoma that
has not responded to other therapies. Studies are under way to determine if ECP may have some
application for other blood cancers, and also to help reduce rejection after transplants.
The FDA has approved the photosensitizing agent called porfimer sodium, or Photofrin, for
use in PDT to treat or relieve the symptoms ofesophageal cancer andnon-small cell lung cancer.
Porfimer sodium is approved to relieve symptoms of esophageal cancer when the cancer
obstructs the esophagus or when the cancer cannot be satisfactorily treated with laser therapy
alone. Porfimer sodium is used to treat non-small cell lung cancer in patients for whom the usual
treatments are not appropriate, and to relieve symptoms in patients with non-small cell lung
cancer that obstructs the airways. In 2003, the FDA approved porfimer sodium for the treatment
of precancerous lesions in patients with Barrett esophagus, a condition that can lead to
esophageal cancer.
Side effects
Porfimer sodium makes the skin and eyes sensitive to light for approximately 6 weeks after
treatment. Thus, patients are advised to avoid direct sunlight and bright indoor light for at least 6
weeks.
Photosensitizers tend to build up in tumors and the activating light is focused on the tumor. As a
result, damage to healthy tissue is minimal. However, PDT can cause burns, swelling, pain, and
scarring in nearby healthy tissue. Otherside effects of PDT are related to the area that is treated.
They can include coughing, trouble swallowing,stomachpain, painful breathing, or shortness of
breath; these side effects are usually temporary.
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Limitations of PDT
The light needed to activate most photosensitizers cannot pass through more than about one-third
of an inch of tissue (1centimeter). For this reason, PDT is usually used to treat tumors on or just
under the skin or on the lining of internal organs or cavities. PDT is also less effective in treating
large tumors, because the light cannot pass far into these tumors. PDT is a local treatment and
generally cannot be used to treat cancer that has spread (metastasized).
Lasers in Cancer TreatmentThe term laser stands for light amplification by stimulated emission of radiation. Ordinary
light, such as that from a light bulb, has many wavelengths and spreads in all directions. Laser
light, on the other hand, has a specific wavelength. It is focused in a narrow beam and creates a
very high-intensity light. This powerful beam of light may be used to cut through steel or toshape diamonds. Because lasers can focus very accurately on tiny areas, they can also be used for
very precise surgical work or for cutting through tissue (in place of ascalpel).
Treatment
Laser therapy uses high-intensity light to treat cancer and other illnesses. Lasers can be used to
shrink or destroy tumors or precancerous growths. Lasers are most commonly used to treat
superficial cancers (cancers on the surface of the body or the lining of internalorgans)such as
basal cell skin cancer and the very earlystages of some cancers, such ascervical,penile,vaginal,
vulvar, andnon-small cell lung cancer.
Lasers also may be used to relieve certainsymptoms of cancer, such as bleeding orobstruction.
For example, lasers can be used to shrink or destroy a tumor that is blo cking a patientstrachea
(windpipe) or esophagus. Lasers also can be used to remove colon polyps or tumors that are
blocking the colon orstomach.
Laser therapy can be used alone, but most often it is combined with other treatments, such as
surgery,chemotherapy,orradiation therapy.In addition, lasers can seal nerve endings to reduce
pain after surgery and seallymph vessels to reduce swelling and limit the spread of tumor cells.
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Laser therapy is often given through a flexible endoscope (a thin, lighted tube used to look at
tissues inside the body). The endoscope is fitted with optical fibers (thin fibers that transmit
light). It is inserted through an opening in the body, such as the mouth, nose, anus,orvagina.
Laser light is then precisely aimed to cut or destroy a tumor.
Laser-induced interstitial thermotherapy (LITT), or interstitial laser photocoagulation, also uses
lasers to treat some cancers. LITT is similar to a cancer treatment called hyperthermia,which
uses heat to shrink tumors by damaging or killing cancer cells.During LITT, an optical fiber is
inserted into a tumor. Laser light at the tip of the fiber raises the temperature of the tumor cells
and damages or destroys them. LITT is sometimes used to shrink tumors in theliver.
Photodynamic therapy (PDT) is another type of cancer treatment that uses lasers. In PDT, a
certain drug, called a photosensitizer or photosensitizing agent, is injected into a patient and
absorbed by cells all over the patients body. After a couple of days, the agent is found mostly in
cancer cells. Laser light is then used toactivate the agent and destroy cancer cells. Because the
photosensitizer makes the skin and eyes sensitive to light afterwards, patients are advised to
avoid direct sunlight and bright indoor light during that time.
Types Of Lasers
Three types of lasers are used to treat cancer:
carbon dioxide (CO2) lasers, argon lasers, (Nd:YAG) lasers.
Each of these can shrink or destroy tumors and can be used with endoscopes.CO2 and argon
lasers can cut the skins surface without going into deeper layers. Thus, they can be used to
remove superficial cancers, such as skin cancer. In contrast, the Nd:YAG laser is more
commonly applied through an endoscope to treat internal organs, such as theuterus,esophagus,
and colon.
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Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser light can also travel through optical
fibers into specific areas of the body during LITT. Argon lasers are often used to activate the
drugs used in PDT.
Advantages of laser therapy
Lasers are more precise than standard surgical tools (scalpels), so they do less damage to normal
tissues. As a result, patients usually have less pain, bleeding, swelling, and scarring. With laser
therapy, operations are usually shorter. In fact, laser therapy can often be done on anoutpatient
basis. It takes less time for patients to heal after laser surgery, and they are less likely to get
infections.Patients should consult with their health care provider about whether laser therapy is
appropriate for them.
Disadvantages of laser therapy
Laser therapy also has several limitations. Surgeons must have specialized training before they
can do laser therapy, and strict safety precautions must be followed. Laser therapy is expensive
and requires bulky equipment. In addition, the effects of laser therapy may not last long, so
doctors may have to repeat the treatment for a patient.
Pharmacological treatment
I. GILOTRIFGeneric name:Afatinib
Category:Metastatic lung cancer
General information:
GILOTRIF is indicated for the first-line treatment of patients with metastatic non-
small cell lung cancer (NSCLC) whose tumors have epidermal growth factor receptor (EGFR)
exon 19 deletions or exon 21 (L858R) substitution mutations as detected by an FDA-approved
test. GILOTRIF is an oral, once-daily kinase inhibitor that is designed to bind and irreversibly
inhibit the following receptors: EGFR (ErbB1), HER2 (ErbB2) and ErbB4.
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Mechanism Of Action
As a a tyrosine kinase inhibitor, Gilotrif works by blocking proteins that are necessary for cancer
cells to develop. The drug will be approved exclusively for patients with tumors that express the
EGFR exon 21 L858R substitution or exon 19 deletions or gene mutations.
Limitation of Use:
Safety and efficacy of GILOTRIF have not been established in patients whose tumors have other
EGFR mutations
Side effects :
Fever Severe rash Decreased appetite Eyeinflammation Decreased weight Lung inflammation Decreased weight Nose bleed Skin infection
DRUG INTERACTIONS
Effect of P-glycoprotein (P-gp) Inhibitors and Inducers
Concomitant taking of P-gp inhibitors (including but not limited to ritonavir,cyclosporine A, ketoconazole, itraconazole, erythromycin, verapamil, quinidine,
tacrolimus, nelfinavir, saquinavir, and amiodarone) with GILOTRIF can increaseexposure to afatinib.
Concomitant taking of P-gp inducers (including but not limited to rifampicin, carbamazepine,
phenytoin, phenobarbital, and St. John's wort) with GILOTRIF can decrease exposure to
afatinib.
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WARNINGS AND PRECAUTIONS
Diarrhea Bullous and Exfoliative Skin Disorders Interstitial Lung Disease (ILD) Hepatic Toxicity Keratitis Embryofetal Toxicity
II. PomalystStructure:
Generic name:Pomalidomide
Category: Relapsed and refractory multiple myeloma
General information:
Pomalidomide (INN, originally CC-4047 or 3-amino-thalidomide, marketed as Pomalyst by
Celgene), is a derivative of thalidomide that is anti-angiogenic and also acts as an
immunomodulator.
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Mechanism of action
Pomalidomide directly inhibits angiogenesis and myeloma cell growth. This dual effect is central
to its activity in myeloma, rather than other pathways such as TNF alpha inhibition, since potent
TNF alpha inhibitors includingrolipram andpentoxifylline do not inhibit myeloma cell growth
nor angiogenesis. Up regulation ofInterferon gamma,IL-2 andIL-10 as well as down regulation
of IL-6 have been reported for pomalidomide. These changes may contribute to pomalidomide's
anti-angiogenic and anti-myeloma activities.
Absorption
Peak plasma time: 2-3 hr
Peak Peak plasma concentration: 75 ng/mL
Distribution
Protein bound: 12-44%
Vd: 62-138 L
Semen concentration: 67% of plasma level at 4 hr post-dose
Metabolism
Metabolized in liver by CYP1A2 and CYP3A4 (primary enzymes involved the hydroxylation);
minor contribution by CYP2C19 and CYP2D6
Elimination
Half-life: 7.5 hr
Total body clearance: 7-10 L/hr
Excretion: 73% urine (2% unchanged); 15% feces (8% unchanged)
Side Effects
Adverse events associated with the use of Pomalyst may include, but are not limited to, the
following:
fatigue and asthenia neutropenia
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anemia constipation nausea diarrhea dyspnea upper-respiratory tract infections back pain pyrexia
III. Sipuleucel-TGeneric name: Provenge
Category:Metastatic prostate cancer
General information:
Sipuleucel-T manufactured byDendreon Corporation, is atherapeuticcancer vaccine forprostate
cancer (CaP). It must be prepared specifically for each patient.
Mechanism of Action
Dendreon is an autologous cellular immunotherapy. While the precise mechanism of action is
unknown, Provenge is designed to induce an immune response targeted against PAP, an antigen
expressed in most prostate cancers.
Pharmacology
Side effects
Serious side effect, such as:
fever redness, swelling, oozing, or other signs of infection where the IV needle was placed; or signs of infection around the veins your cells were collected from.
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Less serious Provenge side effects may include:
back pain mild nausea headache mild body aches.
IV. Radium-223 chlorideGeneric name:Xofigo
Category: Bone metastases
General Information:
Radium-223 chloride , is aradiopharmaceutical to improve survival in patients with bone
metastases from advanced cancer.
Mechanism of action
Xofigo usesalpha radiation from radium-223 decay to kill cancer cells. Radium-223 targets to
bone tissue by virtue of its chemical similarity to calcium. Alpha radiation has an effect over arange of 2-10 cells, which is short-range when compared to current radiation therapy which is
based on beta or gamma radiation, and, therefore, causes less damage to surrounding healthy
tissues. Radium-223 has a half life of 11.4 days, making it suitable for cancer treatment, although
the dosage given to the patient must be adjusted based on the half-life of the product being used.
Xofigo that is not taken up by the bone is cleared, primarily via the gut, and excreted.
Pharmacology:
Pharmacokinetics
Absorption:
Since Radium Ra 223 Dichloride is administered I.V., the bioavailability should be 100%.
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Volume of distribution The volume of distribution was not quantified, but after 24 hours, there
is only 1% radium-223 remaining in the blood. The rest of the radium-223 is distributed to bone
(61% of the radioactive dose after 4 hours) and intestine (49% of the radioactive dose after 4
hours). No other organs were found to have significant uptake. Protein binding There is
negligible plasma protein binding.
Metabolism:
Radium-223 does not undergo metabolism because it is a radioisotope that decays.
Side-effects
The most common side effects reported during clinical trials in men receiving Xofigo were
nausea, diarrhea, vomiting and swelling of the leg, ankle or foot. The most commonabnormalities detected during blood testing were anemia, lymphocytopenia, leukopenia,
thrombocytopenia and neutropenia.In clinical trials, Xofigo was administered by intravenous
injection once a month for 4 or 6 months.
V. RegorafenibGeneric name: Stivarga
Category: Colorectal cancer and gastrointestinal stromal tumors.
General information:
Regorafenib is an oral multi-kinase inhibitor which targets angiogenic, stromal and oncogenic
receptor tyrosine kinase (RTK). Regorafenib shows anti-angiogenic activity due to its dual
targeted VEGFR2-TIE2 tyrosine kinase inhibition. It is currently being studied as a potential
treatment option in multiple tumor types.
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INDICATIONS
Colorectal Cancer
Stivarga is indicated for the treatment of patients with metastaticcolorectal cancer (CRC)whohave been previously treated with fluoropyrimidine-, oxaliplatin- and irinotecan-based
chemotherapy,an anti-VEGF therapy, and, if KRAS wild type, an anti-EGFR therapy.
Gastrointestinal Stromal TumorsStivarga is indicated for the treatment of patients with locally advanced, unresectable or
metastaticgastrointestinal stromal tumor (GIST) who have been previously treated with imatinib
mesylate and sunitinib malate.
SIDE EFFECTS
Hemorrhage
Hypertension
Ischemia andInfarction
Posterior Leukoencephalopathy Syndrome (RPLS)
Gastrointestinal Perforation orFistula
Pharmacokinetics
Absorption
(Cmax) of 2.5 g/mL at a median time of 4 hours.The mean relative bioavailability of tablets
compared to an oral solution is 69% to 83%.
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Distribution
Regorafenib undergoes enterohepatic circulation with multiple plasma concentration peaks
observed across the 24-hour dosing interval. Regorafenib is highly bound (99.5%) to human
plasma proteins.
Metabolism
Regorafenib is metabolized by CYP3A4 and UGT1A9. The main circulating metabolites of
regorafenib measured at steady-state in human plasma are M-2 and M-5. M-2 and M-5 are highly
protein bound (99.8% and 99.95%, respectively).
Elimination
Elimination half-lives for regorafenib and the M-2 metabolite in plasma are 28 hours (14 to 58
hours) and 25 hours (14 to 32 hours), respectively. M-5 has a longer mean (range) elimination
half-life of 51 hours (32 to 70 hours).Approximately 71% of a radiolabeled dose was excreted in
feces (47% as parent compound, 24% as metabolites) and 19% of the dose was excreted in urine
(17% as glucuronides) within 12 days after administration of a radiolabeled oral solution at a
dose of 120 mg.
DRUG INTERACTIONS
Effect of Strong CYP3A4 Inducers on Regorafenib Effect of Strong CYP3A4 Inhibitors on Regorafenib
v. Synribo
Generic name:Omacetaxine Mepesuccinate
Category:Chronic Myelogenous Leukemia
Omacetaxine mepesuccinate is analkaloid fromCephalotaxus harringtoniathat is indicated for
treatment ofChronic Myelogenous Leukemia.It was approved by the USFDA on 26th October
2012 for the treatment of adult patients with chronic myeloid leukemia (CML) with resistance
and/or intolerance to two or moretyrosine kinase inhibitors (TKIs).
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Mechanism of action
Omacetaxine is a protein translation inhibitor. It inhibits protein translation by preventing the
initial elongation step of protein synthesis. It interacts with the ribosomal A-site and prevents the
correct positioning of amino acid side chains of incoming aminoacyl-tRNAs. Omacetaxine acts
only on the initial step of protein translation and does not inhibit protein synthesis from mRNAs
that have already commenced translation.