Treatment Agents for Peripheral T-Cell Lymphoma
Treatment Agents for Peripheral T-Cell
Lymphoma
Treatment Agents for Peripheral T-Cell Lymphoma
Below are some medicines your doctor might use to treat peripheral T-cell lymphoma (PTCL). Some of these medicines are FDA-approved specifically for certain types or stages of PTCL. This means they were carefully studied and shown to be safe and effective for this disease. Others are used “off-label.” This means the medicine is approved by the FDA for a different cancer, but doctors may still use it for PTCL as research, clinical trial results, or medical experience suggest it can help. Off-label use is common for rare cancers like PTCL, where there are fewer approved treatments. This approach helps patients get access to promising medicines that may work against their type of lymphoma.
Below, we will discuss some FDA-approved and off-label drugs in PTCL.
Chemotherapy: “DNA Blocking” Agents
Chemotherapy is a main treatment for PTCL. It’s usually given through a vein at a clinic or hospital, so the medicine can travel through your bloodstream and reach cancer cells almost anywhere in your body. These medicines work by attacking cells that grow and divide quickly, which is what cancer cells do. They damage the cancer cells’ DNA or stop them from multiplying, which helps slow or stop the lymphoma.
Chemotherapy is a main treatment for PTCL. It’s usually given through a vein at a clinic or
hospital, so the medicine can travel through your bloodstream and reach cancer cells almost
anywhere in your body. These medicines work by attacking cells that grow and divide quickly,
which is what cancer cells do. They damage the cancer cells’ DNA or stop them from multiplying, which helps slow or stop the lymphoma.
Chemotherapy can also affect some healthy cells that grow quickly, such as those in your hair, skin, and digestive system. This is why side effects like hair loss, mouth sores, or nausea can happen. The good news is that healthy cells can usually repair themselves, and your body gets time to recover between treatment cycles.
Below are some of the chemotherapy drugs used to treat PTCL.
Chemotherapy can also affect some healthy cells that grow quickly, such as those in your hair, skin, and digestive system. This is why side effects like hair loss, mouth sores, or nausea can happen. The good news is that healthy cells can usually repair themselves, and your body gets time to recover between treatment cycles. Below are some of the chemotherapy drugs used to treat PTCL.
Alkylating agents: Cyclophosphamide, Ifosfamide, Bendamustine
Mechanism of action: These drugs work by adding chemical tags (alkyl groups) to DNA, preventing cancer
cells from copying themselves. When the cell tries to divide, the tagged DNA cannot copy correctly, causing
breaks or “cross-links” between DNA strands—like tying the two halves of a zipper together so it can’t
unzip. While normal cells can repair some of this damage, rapidly dividing cancer cells become overwhelmed, ultimately triggering cell death.
Mechanism of action: These drugs work by adding chemical tags (alkyl groups) to DNA, preventing cancer cells from copying themselves. When the cell tries to divide, the tagged
DNA cannot copy correctly, causing breaks or “cross-links” between DNA strands—like
tying the two halves of a zipper together so it can’t unzip. While normal cells can repair
some of this damage, rapidly dividing cancer cells become overwhelmed, ultimately triggering cell death.
b. Route: Intravenous
Anthracyclines: Doxorubicin (Hydroxydaunorubicin)
Mechanism of action: Anthracyclines work in two main ways to kill cancer cells. They create unstable
molecules called free radicals that can damage DNA, and they also slip between the strands of DNA (a
process called intercalation), which causes the DNA to break. These effects make it harder for cancer cells to grow and divide.
Mechanism of action: Anthracyclines work in two main ways to kill cancer cells. They
create unstable molecules called free radicals that can damage DNA, and they also slip
between the strands of DNA (a process called intercalation), which causes the DNA to break. These effects make it harder for cancer cells to grow and divide.
b. Route: Intravenous
Topoisomerase Inhibitors: Etoposide
Mechanism of action: Topoisomerase inhibitors work by blocking enzymes called topoisomerases, which
normally act like tiny scissors to cut, untangle, and repair DNA. When these enzymes are blocked, cancer
cells can’t unzip and copy their DNA, which stops them from dividing. Drugs like etoposide use this process to kill lymphoma cells.
Mechanism of action: Topoisomerase inhibitors work by blocking enzymes called topoisomerases, which normally act like tiny scissors to cut, untangle, and repair DNA.
When these enzymes are blocked, cancer cells can’t unzip and copy their DNA, which stops them from dividing. Drugs like etoposide use this process to kill lymphoma cells.
b. Route: Intravenous
Platinums: Cisplatin, Carboplatin
Mechanism of action: Platinum drugs work by attaching “sticky” tags to DNA, creating cross-links,
connections that tie pieces of DNA together. These cross-links act like knots, tangling the DNA so cancer
cells can’t copy it and divide. Because they target rapidly dividing cells, they are especially effective against cancer cells.
Mechanism of action: Platinum drugs work by attaching “sticky” tags to DNA, creating cross-links, connections that tie pieces of DNA together. These cross-links act like knots,
tangling the DNA so cancer cells can’t copy it and divide. Because they target rapidly
dividing cells, they are especially effective against cancer cells.
b. Route: Intravenous
Pralatrexate
Mechanism of action: Pralatrexate works by blocking cancer cells from using folate, a vitamin they need to
make the building blocks of DNA. Without these building blocks, the cancer cells can’t make new DNA and are unable to divide.
Mechanism of action: Pralatrexate works by blocking cancer cells from using folate, a
vitamin they need to make the building blocks of DNA. Without these building blocks, the cancer cells can’t make new DNA and are unable to divide.
b. Route: Intravenous
Gemcitabine
Mechanism of action: Gemcitabine works by mimicking one of the building blocks of DNA. When cancer
cells try to copy their DNA, they accidentally use gemcitabine instead. This stops the DNA from being built
correctly and prevents the cell from finishing the copying process. As a result, the cancer cell can’t divide and eventually dies.
Mechanism of action: Gemcitabine works by mimicking one of the building blocks of DNA. When cancer cells try to copy their DNA, they accidentally use gemcitabine instead. This stops the DNA from being built correctly and prevents the cell from finishing the copying process. As a result, the cancer cell can’t divide and eventually dies.
b. Route: Intravenous
Vincristine
Mechanism of action: Vincristine works by stopping cancer cells from building the “machinery” they need
to divide. Normally, cells build tiny structures called microtubules that act like ropes to pull the cell apart into
two new cells. Vincristine blocks the formation of these microtubules, so cancer cells can’t divide and eventually die.
Mechanism of action: Vincristine works by stopping cancer cells from building the “machinery” they need to divide. Normally, cells build tiny structures called microtubules
that act like ropes to pull the cell apart into two new cells. Vincristine blocks the formation of these microtubules, so cancer cells can’t divide and eventually die.
b. Route: Intravenous
Chemotherapy: “DNA Blocking” Agents
Chemotherapy is a main treatment for PTCL. It’s usually given through a vein at a clinic or
hospital, so the medicine can travel through your bloodstream and reach cancer cells almost
anywhere in your body. These medicines work by attacking cells that grow and divide quickly,
which is what cancer cells do. They damage the cancer cells’ DNA or stop them from multiplying, which helps slow or stop the lymphoma.
Chemotherapy can also affect some healthy cells that grow quickly, such as those in your hair, skin, and digestive system. This is why side effects like hair loss, mouth sores, or nausea can happen. The good news is that healthy cells can usually repair themselves, and your body gets time to recover between treatment cycles. Below are some of the chemotherapy drugs used to treat PTCL.
Alkylating agents: Cyclophosphamide, Ifosfamide, Bendamustine
Mechanism of action: These drugs work by adding chemical tags (alkyl groups) to DNA, preventing cancer cells from copying themselves. When the cell tries to divide, the tagged DNA cannot copy correctly, causing breaks or “cross-links” between DNA strands—like tying the two halves of a zipper together so it can’t unzip. While normal cells can repair some of this damage, rapidly dividing cancer cells become overwhelmed, ultimately triggering cell death.
b. Route: Intravenous
Anthracyclines: Doxorubicin (Hydroxydaunorubicin)
Mechanism of action: Anthracyclines work in two main ways to kill cancer cells. They
create unstable molecules called free radicals that can damage DNA, and they also slip between the strands of DNA (a process called intercalation), which causes the DNA to break. These effects make it harder for cancer cells to grow and divide.
b. Route: Intravenous
Topoisomerase Inhibitors: Etoposide
Mechanism of action: Topoisomerase inhibitors work by blocking enzymes called topoisomerases, which normally act like tiny scissors to cut, untangle, and repair DNA.
When these enzymes are blocked, cancer cells can’t unzip and copy their DNA, which stops them from dividing. Drugs like etoposide use this process to kill lymphoma cells.
b. Route: Intravenous
Platinums: Cisplatin, Carboplatin
Mechanism of action: Platinum drugs work by attaching “sticky” tags to DNA, creating cross-links, connections that tie pieces of DNA together. These cross-links act like knots, tangling the DNA so cancer cells can’t copy it and divide. Because they target rapidly dividing cells, they are especially effective against cancer cells.
b. Route: Intravenous
Pralatrexate
Mechanism of action: Pralatrexate works by blocking cancer cells from using folate, a
vitamin they need to make the building blocks of DNA. Without these building blocks, the cancer cells can’t make new DNA and are unable to divide.
b. Route: Intravenous
Gemcitabine
Mechanism of action: Gemcitabine works by mimicking one of the building blocks of DNA. When cancer cells try to copy their DNA, they accidentally use gemcitabine instead. This stops the DNA from being built correctly and prevents the cell from finishing the copying process. As a result, the cancer cell can’t divide and eventually dies.
b. Route: Intravenous
Vincristine
Mechanism of action: Vincristine works by stopping cancer cells from building the “machinery” they need to divide. Normally, cells build tiny structures called microtubules
that act like ropes to pull the cell apart into two new cells. Vincristine blocks the formation of these microtubules, so cancer cells can’t divide and eventually die.
b. Route: Intravenous
Targeted Pathway Inhibitors
Targeted pathway inhibitors are a newer type of treatment for PTCL that focus on blocking specific molecules or signals that cancer cells use to grow and survive. Unlike chemotherapy, which affects all rapidly dividing cells, targeted therapies are designed to act on particular pathways that are more active or abnormal in cancer cells. By disrupting these signals, targeted inhibitors can slow or stop cancer growth while often causing fewer effects on healthy cells. They are generally most effective when the cancer cells have known corresponding molecular changes, making them more likely to respond to the specific targeted therapy.
PI3K Inhibitors: Duvelisib
Mechanism of action: Duvelisib works by blocking two key signals (called PI3K-delta and PI3K-gamma) that cancer cells use to grow and stay alive. These signals act like “on
switches” that tell the cells to keep dividing and help them hide from the immune system.
By turning off these switches, duvelisib slows down cancer cell growth and allows the immune system to find and attack the cancer cells.
b. Route: Oral
JAK Inhibitors: Ruxolitinib, Golidocitinib
Mechanism of action: JAK inhibitors work by blocking overactive growth signals (JAK proteins) in PTCL. These signals act like a stuck “on switch,” telling cancer cells to keep growing. By turning them off, these medicines can slow cancer cell growth.
b. Route: Oral
Gene Expression Modifiers
Gene expression modifiers are a type of cancer treatment that works by changing how certain genes are turned on or off inside cancer cells. In PTCL, some genes that control cell growth and survival can become abnormally activated or silenced, helping the cancer grow. Gene expression modifiers target these abnormalities, restoring a more normal pattern of gene activity and making the cancer cells more likely to stop growing or die.
Histone Deacetylase Inhibitors: Belinostat, Romidepsin
Mechanism of action: Histone deacetylase (HDAC) inhibitors work by blocking certain enzymes called HDACs that cancer cells use to turn off the body’s normal “stop” signals
for cell growth. By blocking these enzymes, belinostat helps restore these natural signals, which can slow or stop the growth of cancer cells.
b. Route: Intravenous
Hypomethylating Agents: Azacitidine
Mechanism of action: Azacitidine works by changing how cancer cells “read” their DNA. Many cancers turn off important genes that normally help control cell growth. Azacitidine helps turn these genes back on by removing chemical tags (called methyl groups) from the DNA. This can slow cancer growth and make cancer cells.
b. Route: Intravenous, oral, subcutaneous
EZH Inhibitors: Valemetostat, Tazemetostat
Mechanism of action: In some PTCL subtypes, certain proteins called EZH1 and EZH2 become overactive and turn off important genes that normally control cell growth, helping the cancer grow. EZH inhibitors are medicines that block these proteins, allowing the normal “stop” signals to work again and slow cancer growth.
b. Route: Oral
Antibody Drug Conjugates
Antibody-drug conjugates are medicines that combine an antibody - which can find and
attach to cancer cells - with a powerful chemotherapy drug. The antibody acts like a
“guided missile,” delivering the chemotherapy directly to the cancer cells and helping reduce damage to healthy cells.
Brentuximab Vedotin
Mechanism of action: Brentuximab Vedotin attaches to a signal called CD30 on the
cancer cell surface, then delivers a toxin called MMAE inside the cell, killing it while sparing many healthy cells
b. Route: Intravenous
Monoclonal Antibodies
Monoclonal antibodies are medicines designed to find and attach to specific markers on
cancer cells. This helps the immune system recognize and attack the cancer, supporting the body’s natural defense against the disease.
Alemtuzumab
Mechanism of action: Alemtuzumab is a monoclonal antibody that targets a protein called
CD52, found on the surface of certain PTCL subtypes.
b. Route: Intravenous
Targeted Pathway Inhibitors
Targeted pathway inhibitors are a newer type of treatment for PTCL that focus on blocking specific molecules or signals that cancer cells use to grow and survive. Unlike chemotherapy, which affects all rapidly dividing cells, targeted therapies are designed to act on particular pathways that are more active or abnormal in cancer cells. By disrupting these signals, targeted inhibitors can slow or stop cancer growth while often causing fewer effects on healthy cells. They are generally most effective when the cancer cells have known corresponding molecular changes, making them more likely to respond to the specific targeted therapy.
PI3K Inhibitors: Duvelisib
Mechanism of action: Duvelisib works by blocking two key signals (called PI3K-delta and PI3K-gamma) that cancer cells use to grow and stay alive. These signals act like “on switches” that tell the cells to keep
dividing and help them hide from the immune system. By turning off these switches, duvelisib slows down cancer cell growth and allows the immune system to find and attack the cancer cells.
Mechanism of action: Duvelisib works by blocking two key signals (called PI3K-delta and PI3K-gamma) that cancer cells use to grow and stay alive. These signals act like “on
switches” that tell the cells to keep dividing and help them hide from the immune system.
By turning off these switches, duvelisib slows down cancer cell growth and allows the immune system to find and attack the cancer cells.
b. Route: Oral
JAK Inhibitors: Ruxolitinib, Golidocitinib
Mechanism of action: JAK inhibitors work by blocking overactive growth signals (JAK proteins) in PTCL.
These signals act like a stuck “on switch,” telling cancer cells to keep growing. By turning them off, these medicines can slow cancer cell growth.
Mechanism of action: JAK inhibitors work by blocking overactive growth signals (JAK proteins) in PTCL. These signals act like a stuck “on switch,” telling cancer cells to keep growing. By turning them off, these medicines can slow cancer cell growth.
b. Route: Oral
Gene Expression Modifiers
Gene expression modifiers are a type of cancer treatment that works by changing how certain genes are turned on or off inside cancer cells. In PTCL, some genes that control cell growth and survival can become abnormally activated or silenced, helping the cancer grow. Gene expression modifiers target these abnormalities, restoring a more normal pattern of gene activity and making the cancer cells more likely to stop growing or die.
Histone Deacetylase Inhibitors: Belinostat, Romidepsin
Mechanism of action: Histone deacetylase (HDAC) inhibitors work by blocking certain enzymes called HDACs that cancer cells use to turn off the body’s normal “stop” signals for cell growth. By blocking these enzymes, belinostat helps restore these natural signals, which can slow or stop the growth of cancer cells.
Mechanism of action: Histone deacetylase (HDAC) inhibitors work by blocking certain enzymes called HDACs that cancer cells use to turn off the body’s normal “stop” signals
for cell growth. By blocking these enzymes, belinostat helps restore these natural signals, which can slow or stop the growth of cancer cells.
b. Route: Intravenous
Hypomethylating Agents: Azacitidine
Mechanism of action: Azacitidine works by changing how cancer cells “read” their DNA. Many cancers
turn off important genes that normally help control cell growth. Azacitidine helps turn these genes back on
by removing chemical tags (called methyl groups) from the DNA. This can slow cancer growth and make cancer cells.
Mechanism of action: Azacitidine works by changing how cancer cells “read” their DNA. Many cancers turn off important genes that normally help control cell growth. Azacitidine helps turn these genes back on by removing chemical tags (called methyl groups) from the DNA. This can slow cancer growth and make cancer cells.
b. Route: Intravenous, oral, subcutaneous
EZH Inhibitors: Valemetostat, Tazemetostat
Mechanism of action: In some PTCL subtypes, certain proteins called EZH1 and EZH2 become overactive
and turn off important genes that normally control cell growth, helping the cancer grow. EZH inhibitors are
medicines that block these proteins, allowing the normal “stop” signals to work again and slow cancer growth.
Mechanism of action: In some PTCL subtypes, certain proteins called EZH1 and EZH2 become overactive and turn off important genes that normally control cell growth, helping the cancer grow. EZH inhibitors are medicines that block these proteins, allowing the normal “stop” signals to work again and slow cancer growth.
b. Route: Oral
Antibody Drug Conjugates
Antibody-drug conjugates are medicines that combine an antibody - which can find and attach to cancer cells - with a powerful chemotherapy drug. The antibody acts like a “guided missile,” delivering the chemotherapy directly to the cancer cells and helping reduce damage to healthy cells.
Antibody-drug conjugates are medicines that combine an antibody - which can find and
attach to cancer cells - with a powerful chemotherapy drug. The antibody acts like a
“guided missile,” delivering the chemotherapy directly to the cancer cells and helping reduce damage to healthy cells.
Brentuximab Vedotin
Mechanism of action: Brentuximab Vedotin attaches to a signal called CD30 on the cancer cell surface,
then delivers a toxin called MMAE inside the cell, killing it while sparing many healthy cells
Mechanism of action: Brentuximab Vedotin attaches to a signal called CD30 on the
cancer cell surface, then delivers a toxin called MMAE inside the cell, killing it while sparing many healthy cells
b. Route: Intravenous
Monoclonal Antibodies
Monoclonal antibodies are medicines designed to find and attach to specific markers on cancer cells. This helps the immune system recognize and attack the cancer, supporting the body’s natural defense against the disease.
Monoclonal antibodies are medicines designed to find and attach to specific markers on
cancer cells. This helps the immune system recognize and attack the cancer, supporting the body’s natural defense against the disease.
Alemtuzumab
Mechanism of action: Alemtuzumab is a monoclonal antibody that targets a protein called CD52, found on
the surface of certain PTCL subtypes.
Mechanism of action: Alemtuzumab is a monoclonal antibody that targets a protein called
CD52, found on the surface of certain PTCL subtypes.
b. Route: Intravenous
Related Reference
Related Reference
Therapeutic Approaches in Peripheral T-Cell Lymphomas: Current Standards and Emerging Options
Sibon D. Peripheral T-Cell Lymphomas: Therapeutic
Approaches. Cancers (Basel). 2022 May 8;14(9):2332.