Chronic Myeloid Leukemia Cancer from Diagnosis to Treatment
What is Chronic Myeloid Leukemia?
Chronic Myeloid Leukemia is a slow-growing cancer of the blood and bone marrow that starts in the myeloid cells, which normally develop into red blood cells, white blood cells, and platelets.
CML occurs when a genetic change called the Philadelphia chromosome forms - a swap between chromosomes 9 and 22.
This mutation creates an abnormal gene called BCR-ABL1, which produces a protein that causes cells to grow uncontrollably.
Over time, CML can progress from a mild, chronic phase to a more aggressive accelerated or blast crisis phase, similar to acute leukemia.
Chronic Myeloid Leukemia is a slow-growing cancer of the blood and bone marrow that starts in the myeloid cells, which normally develop into red blood cells, white blood cells, and platelets.
CML occurs when a genetic change called the Philadelphia chromosome forms - a swap between chromosomes 9 and 22.
This mutation creates an abnormal gene called BCR-ABL1, which produces a protein that causes cells to grow uncontrollably.
Over time, CML can progress from a mild, chronic phase to a more aggressive accelerated or blast crisis phase, similar to acute leukemia.
1. Early Signs and Symptoms
• Fatigue and weakness
• Weight loss without trying
• Fever or night sweats
• Fullness or pain under the ribs
• Bone pain or discomfort
• Frequent infections
• Easy bruising or bleeding
• Fatigue and weakness
• Weight loss without trying
• Fever or night sweats
• Fullness or pain under the ribs
• Bone pain or discomfort
• Frequent infections
• Easy bruising or bleeding
2. Causes and Risk Factors
The exact cause of CML is often unknown, but risk factors include
• Genetic mutation
• Older age
• Exposure to high-dose radiation
Note: CML is not inherited - it develops after birth due to genetic mutation in bone marrow cells
The exact cause of CML is often unknown, but risk factors include
• Genetic mutation
• Older age
• Exposure to high-dose radiation
Note: CML is not inherited - it develops after birth due to genetic mutation in bone marrow cells
3. Diagnostic Procedure
Physical Examination
The doctor checks for enlarged spleen, signs of anemia, and reviews medical symptoms.
Blood Tests
Complete Blood Count:
Shows elevated white blood cell count with immature cells | myelocytes and blasts
Peripheral Blood Smear:
Reveals a mix of mature and immature white blood cells characteristic of CML.
Bone Marrow Aspiration and Biopsy
Confirms diagnosis and helps determine the phase | chronic, accelerated, or blast.
Cytogenetic Testing
Detects the Philadelphia chromosome
Molecular Testing | PCR or FISH
Identifies the BCR-ABL1 fusion gene and measures its activity.
Used to monitor treatment response over time.
Imaging Tests
Ultrasound or CT scan may check for enlarged spleen or liver.
Physical Examination
The doctor checks for enlarged spleen, signs of anemia, and reviews medical symptoms.
Blood Tests
Complete Blood Count:
Shows elevated white blood cell count with immature cells | myelocytes and blasts
Peripheral Blood Smear:
Reveals a mix of mature and immature white blood cells characteristic of CML.
Bone Marrow Aspiration and Biopsy
Confirms diagnosis and helps determine the phase | chronic, accelerated, or blast.
Cytogenetic Testing
Detects the Philadelphia chromosome
Molecular Testing | PCR or FISH
Identifies the BCR-ABL1 fusion gene and measures its activity.
Used to monitor treatment response over time.
Imaging Tests
Ultrasound or CT scan may check for enlarged spleen or liver.
4. Phases of CML
CML progresses in three main stages.
Chronic Phase
Most patients are diagnosed here.
Few or no symptoms; treatment works well.
Accelerated Phase
Disease progresses; blood counts become abnormal, and symptoms worsen.
Blast Crisis
Resembles acute leukemia; many immature cells | blasts | appear.
Harder to treat and more aggressive.
CML progresses in three main stages.
Chronic Phase
Most patients are diagnosed here.
Few or no symptoms; treatment works well.
Accelerated Phase
Disease progresses; blood counts become abnormal, and symptoms worsen.
Blast Crisis
Resembles acute leukemia; many immature cells | blasts | appear.
Harder to treat and more aggressive.
5. Treatment Options
➛ Targeted Therapy | Tyrosine Kinase Inhibitors
TKIs are the main treatment for CML, blocking the BCR-ABL1 protein that drives the cancer.
Common TKIs include:
Imatinib | Gleevec
Dasatinib | Sprycel
Nilotinib | Tasigna
Bosutinib | Bosulif
Ponatinib | Iclusig
Patients usually take TKIs daily as long-term oral medication.
➛ Chemotherapy
Used when CML does not respond to TKIs or during the blast crisis phase.
Drugs such as cytarabine or hydroxyurea may be used.
➛ Maintenance Therapy
Lower-dose chemotherapy for 2-3 years to maintain remission.
Common drugs:
Methotrexate
6-mercaptopurine
Vincristine
Prednisone.
➛ Stem Cell Transplant
The only potential cure for CML, though rarely needed now due to effective TKIs.
Considered for patients who don’t respond to multiple TKIs or have blast crisis.
➛ Immunotherapy
Monoclonal antibodies and immune checkpoint inhibitors are under study for AML.
➛ Interferon Therapy
Sometimes used in patients who cannot tolerate TKIs, such as pregnant women.
➛ Supportive Care
Blood transfusions for anemia
Antibiotics or antivirals to treat infections
Treatment for enlarged spleen if necessary
➛ Targeted Therapy | Tyrosine Kinase Inhibitors
TKIs are the main treatment for CML, blocking the BCR-ABL1 protein that drives the cancer.
Common TKIs include:
Imatinib | Gleevec
Dasatinib | Sprycel
Nilotinib | Tasigna
Bosutinib | Bosulif
Ponatinib | Iclusig
Patients usually take TKIs daily as long-term oral medication.
➛ Chemotherapy
Used when CML does not respond to TKIs or during the blast crisis phase.
Drugs such as cytarabine or hydroxyurea may be used.
➛ Maintenance Therapy
Lower-dose chemotherapy for 2-3 years to maintain remission.
Common drugs:
Methotrexate
6-mercaptopurine
Vincristine
Prednisone.
➛ Stem Cell Transplant
The only potential cure for CML, though rarely needed now due to effective TKIs.
Considered for patients who don’t respond to multiple TKIs or have blast crisis.
➛ Immunotherapy
Monoclonal antibodies and immune checkpoint inhibitors are under study for AML.
➛ Interferon Therapy
Sometimes used in patients who cannot tolerate TKIs, such as pregnant women.
➛ Supportive Care
Blood transfusions for anemia
Antibiotics or antivirals to treat infections
Treatment for enlarged spleen if necessary
6. Follow-Up
➛ With TKIs, most people with CML can live normal lifespans.
➛ Regular PCR testing monitors BCR-ABL1 levels and treatment response.
➛ If deep molecular remission is achieved for several years, some patients may safely stop therapy under medical supervision.
➛ Without treatment, CML can progress to acute leukemia within 3–5 years.
➛ With TKIs, most people with CML can live normal lifespans.
➛ Regular PCR testing monitors BCR-ABL1 levels and treatment response.
➛ If deep molecular remission is achieved for several years, some patients may safely stop therapy under medical supervision.
➛ Without treatment, CML can progress to acute leukemia within 3–5 years.
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