Learning Objectives:
Introduction
Definition of CML
Philadelphia Chromosome
Normal Granulopoiesis
Pathogenesis of CML
Aetiology
Incidence
Clinical Features
Phases of CML
Lab Diagnosis of CML
Course & Prognosis
Differential Diagnosis
Brief Overview of Treatment
Learning Objectives:
- Introduction
- Definition
- Classification
- Acute Leukaemia
- Predisposing Factors
- Acute Myeloid Leukaemia
- FAB & WHO Classification of AML
- Pathogenesis
- Clinical Features of AML
- Lab Diagnosis of AML
- Treatment of AML
Acute Myeloid Leukemia (AML): Cancer of the Blood & Bone MarrowKumaraguru Veerasamy
These slides covers one of the most common types of acute leukemia in adults. AML makes up 32% of all adult leukemia cases. 1.8% of cancer deaths are caused by AML, meaning that it is quite rare. Xeraya Capital is currently working with Oncomyx and Imago Bio on novel treatments for patients with AML.
Learning Objectives:
Introduction
Definition of CML
Philadelphia Chromosome
Normal Granulopoiesis
Pathogenesis of CML
Aetiology
Incidence
Clinical Features
Phases of CML
Lab Diagnosis of CML
Course & Prognosis
Differential Diagnosis
Brief Overview of Treatment
Learning Objectives:
- Introduction
- Definition
- Classification
- Acute Leukaemia
- Predisposing Factors
- Acute Myeloid Leukaemia
- FAB & WHO Classification of AML
- Pathogenesis
- Clinical Features of AML
- Lab Diagnosis of AML
- Treatment of AML
Acute Myeloid Leukemia (AML): Cancer of the Blood & Bone MarrowKumaraguru Veerasamy
These slides covers one of the most common types of acute leukemia in adults. AML makes up 32% of all adult leukemia cases. 1.8% of cancer deaths are caused by AML, meaning that it is quite rare. Xeraya Capital is currently working with Oncomyx and Imago Bio on novel treatments for patients with AML.
acute leukemia
For More Medicine Free PPT - http://playnever.blogspot.com/
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
3. Introduction
• Acute Leukemia (AL) is a clonal neoplastic disorder characterized by the
proliferation & accumulation of immature and malignantly transformed
cells in the BM and PB.
• The abnormal cells replace the normal BM tissue.
• The result is abnormal /insufficient hematopoiesis.
– Anemia
– Thrombocytopenia
– Leukocytosis/leukopenia
• Infiltrate other organ tissues
4. Introduction...
• AL is basically one of the two types
– Acute Myelogenous Leukemia(AML)
– Acute Lymphoblastic Leukemia(ALL)
• Other very rare variants of AL
– Biphenotypic Leukemia
– Bilineage Leukemia
– Other rare variant in WHO classification
• AL can be
– De novo
– Secondary/ transformed
• Distinction b/n AML & ALL should be the first step in the diagnosis and
management.
5. Epidemiology
Rare disease but has huge impact on cancer survival statistics
The annual incidence of AML( in Western pop)
3.6 cases/100,000
80% of AL
The annual incidence of ALL
1.4 cases/100,000
20% of AL
The incidence of AML
Increases with age
Median age at presentation 60-65yrs
6. Epidemiology...
The peak incidence of ALL
3-4yrs of age
Incidence decreases after 9yrs of age
Rare after 40
Sex distribution
M:F in AML = 1.3:1
M:F in ALL = 1.5:1
The relative frequency of the 4 leukemias
ALL (11%) AML (46%)
CLL (29%) CML (14%)
7. Classification of AL
The classification is based on biological features
Clinical feature
Morphology based on Wright or Giemsa stain
Cytochemical studies
Electron Microscope
Flowcytometry
Cytoplasmic markers
Cytogenetic or molecular study
Microarray analysis
8. Classification of AL...
French-American and British(FAB)
Based on morphology & cytochemical studies
ALL into L1-L3
AML into M0-M7
Immunological classification
Specially for ALL into the different stages of B-Cell & T-Cell groups
WHO classification
For all hematological malignancies
Cytogenetic studies included
Comprehensive but not applicable in all setting
9.
10.
11.
12.
13. Etiology in Acute Leukemias(AL)
• Most AL sporadic
– Acquisition of somatic mutation in hematopioetic progenitors
• Usually not possible to identify a cause
• Valuable clues from
– Rare heritable leukemias
– Cases related to specific environmental exposure
• Variable latency following exposure to causative agent
• Genetic Polymorphism
16. Etiology in AL...
• Familial Disorders leading to Leukemias
• Defective DNA repair syndromes
– Bloom’s Syndrome
– Fanconi’s Anemia
– Neurofibromatosis
– Li-Fraumeni Syndrome
– Wiskott-Aldrich Syndrome
– Blackfan-Diamond Syndrome
– Kostmann’s Syndrome ( Infantile Agranulocytosis)
17. Pathogenesis
Single cell of origin of AL
Leukemic Stem Cell
Clonality
Like other human malignancies, in AL one or more of the following somatic
mutation and genetic abnormalities are involved
Oncogene mutations (Proto-oncogenes)
Tumor Suppressor gene mutation
General Genomic instability
Multistep and multicausal
18. Pathogenesis...
• Two –hit hypothesis
– Mutations giving proliferative& survival advantage
– The next impairing differentiation
• The two models for the explanation of heterogeneous groups in AL
– Transformation at one of the several developmental stages
– Transformation within the primitive multipotent progenitor cells
• Specific or recurrent genetic abnormalities leading to certain leukemia
types
19. Clinical Features of AL
AL presents acutely
Exception- transformed/secondary AL
In general patients manifest signs & symptoms related to
Abnormalities of the 3 blood cell lines
Infiltration of organs & tissues
Certain features are specific to the AL type
Family history of malignancy and history of predisposing factors should be
looked for.
20. Symptoms of AL
Sxs of anemia
Sxs of thrombocytopenia
Fever
High grade due to infections
Low grade with systemic sxs due to the AL
Sxs due to CNS involvement
Seizure, headache, cranial nerves dysfunction
Vomiting, blurring of vision, altered mentation
Abdominal fullness & other GI sxs due to organomegaly and electrolyte
disturbance
Oliguria
21. Signs of AL
Pallor
Bleeding
Mucocutaneous
DIC
Fever and other signs of infection accordingly
22. Signs ...
Signs of tissue or organ infiltration
Gingival hyperplasia
LAP
Hepatosplenomegaly
Bone(sternal tenderness)
Chloromas
Leukemic cutis
Cranial nerve palsies
Mengeal irritation signs
Extramedullary disease
Prominent LAP & signs of mediastinal LAP
23.
24. Investigation in AL
Complete history and physical examination
CBC, differential, platelets, ESR, Blood group
Serological screening ( HIV, HBV, HCV, CMV...)
Examination of peripheral smear
BM aspiration & biopsy
Morphology
Flowcytometry
Cytochemical studies
Cytogenetic study
25. Investigation in AL...
CXR
Coagulation profile
Biochemical tests
Liver & renal functions
Serum electrolytes
Uric acid
Serum LDH
Serum lysozymes
Blood and other specimen for culture
27. Treatment
Requires comprehensive team & good setup
Starts with the confirmation of specific AL dx & prognostication.
In general has 2 important components
Supportive
Specific/ Definitive
Certain parameters/ goals related to specific therapy
Remission ( CR, PR)
Survival (leukemia free, overall survival, relapse )
Cure
28. Supportive Care
Fluid & electrolyte management
Blood component therapy
Packed red cells transfusion
Platelet transfusion
Treatment of infection
Broad spectrum IV antibiotics( empiric/emergency)
culture and other studies
Prevention of uric acid nephropathy & tumor lysis syndrome
hydration
Allopurinol & other agents
29. Supportive Care
Recombinant growth factors (GM-CSF, G-CSF, EPO, IL-11, Thrombopoietin)
Hyperleukocytosis/hyperviscosity, leukostasis
Associated with various complications
Leukopheresis
Emergency irradiation of whole-brain
Adminstration of drugs for cytoreduction
Hydroxyurea, steriods
Early dx & Rx of coagulation abnormality
Reverse-barrier ( reverse – isolation)
30. Supportive Care
Vascular access
Birth control and fertility advice
Treatment of comorbid conditions
Psychosocial support
31. Specific Treatment
Chemotherapy
Specific regimen of the AL types
Phases
Remission Induction
Postremission
Hematopoietic Stem Cell Transplantation
Allogeneic-SCT
Syngeneic-SCT
Autologous-SCT
Investigational Therapy
Clinical trails
32. DDX
MDS
Aplastic Anemia
Infectious Mononucleosis ( LAP & atypical lymphocytes)
BM failure syndromes & infiltration
Severe infection with leukocytosis & shift
Aggressive & very aggressive NHL
ITP
34. General remarks about AML
A complex disease
Heterogenous group
Phenotypically
Genotypically
More than 100 recurrent cytogenetic abnormalities.
Patients die of leukemia or Rx complication
Still a challenge both clinically & in genetic study
Certain groups with excellent prognosis
35. Classification
FAB
Based on morphology & cytochemical studies
Blast % in the BM for Dx
Simple & still in wide clinical use but does not incorporate the recent advances
in molecular study
WHO
Comprehensive
Detail molecular and cytogenetic studies
Currently not universally applicable
36. FAB DESCRIPTION %
M0 AML, minimally differentiated 3
M1 AML without maturation 19
M2 AML with maturation 32
M3 Acute Promyelocytic Leukemia 7
M4 Acute Myelomonocytic Leukemia 23
M5 Acute Monoblastic Leukemia 12
M6 Acute Erythroleukemia 3
M7 Acute Megakaryoblastic Leukemia 0.3
37.
38.
39.
40.
41.
42.
43.
44.
45. AML WITH
RECURRENT
GENETIC
ABNORMALITY
AML with t(8;21)(q22;q22), (AML1/ETO)
AML with abnormal bone marrow eosinophils and
inv(16)(p13q22) or t(16;16)(p13;q22), (CBF/MYH11)
Acute promyelocytic leukemia with t(15;17)(q22;q12),
PML/RAR-alpha and variants
AML with 11q23 (MLL) abnormalities
AML WITH
MULTILINEAGE
DYSPLASIA
Following MDS or MDS/MPD
Without antecedent MDS or MDS/MPD, but with dysplasia in at
least 50 percent of cells in two or more myeloid lineages
AML &MDS,
THERAPY
RELATED
Alkylating agent/radiation-related type
Topoisomerase II inhibitor-related type
Other
46. AML, NOT
OTHERWISE
CATEGORIZED
AML, minimally differentiated
AML without maturation
AML with maturation
Acute myelomonocytic leukemia
Acute monoblastic/acute monocytic leukemia
Acute erythroid leukemia (erythroid/myeloid and pure
erythroleukemia variants)
Acute megakaryoblastic leukemia
Acute basophilic leukemia
Acute panmyelosis with myelofibrosis
Myeloid sarcoma
47. AML WITH
RECURRENT
GENETIC
ABNORMALITY
AML with t(8;21)(q22;q22), (AML1/ETO)
AML with abnormal bone marrow eosinophils and
inv(16)(p13q22) or t(16;16)(p13;q22), (CBF/MYH11)
Acute promyelocytic leukemia with t(15;17)(q22;q12),
PML/RAR-alpha and variants
AML with 11q23 (MLL) abnormalities
AML WITH
MULTILINEAGE
DYSPLASIA
Following MDS or MDS/MPD
Without antecedent MDS or MDS/MPD, but with dysplasia in at
least 50 percent of cells in two or more myeloid lineages
AML &MDS,
THERAPY
RELATED
Alkylating agent/radiation-related type
Topoisomerase II inhibitor-related type
Other
48. AML, NOT
OTHERWISE
CATEGORIZED
AML, minimally differentiated
AML without maturation
AML with maturation
Acute myelomonocytic leukemia
Acute monoblastic/acute monocytic leukemia
Acute erythroid leukemia (erythroid/myeloid and pure
erythroleukemia variants)
Acute megakaryoblastic leukemia
Acute basophilic leukemia
Acute panmyelosis with myelofibrosis
Myeloid sarcoma
49. Specific Rx for AML
Chemotherapy
Remission induction
7+3 regimen ( cytarabine + daunorubicin/doxorubicin)
Alternative ( cytarabin + Idarubicin + etoposide)
Elderly patients – modification
Double induction
Postremission therapy
The best regimen not yet settled
Consolidation/Intensification chemotherapy
Allo-SCT
Auto-SCT
BM transplantation
50. Specific Rx for AML...
CNS prophylaxis or Rx
M4 & M5
Relapsed and refractory AML
Early vs late relapse
Treatment of M3(APL)
Special entity(t(15;17)) & Favourable outcome
All- Trans-Retinoic Acid(ATRA) with other chemo
Maintenance therapy
Arsenic TriOxide(ATO)
Treatment of secondary/ therapy related AML
53. General remarks about ALL
ALL is a malignant d/s characterized by accumulation of lymphoblasts.
Different treatment outcomes in children & adults. Cure rate
Children 2/3
Adults 1/3
Reason for poor outcome in adults with ALL
High rate of adverse prognosis(Ph-chromosome)
high degree of toxicity with the drugs
Different pharmacodynamics
Much less heterogeneous in general and less common ( 20% of AL) in adults
54. Stratification of patient into high- risk & low-risk is
required to select therapy
More intensive chemotherapy
Stem cell transplantation
CNS involvement and relapses are the features
55. Classification of ALL
FAB classification of ALL
L1, L2, L3
Based on the morphology of lymphoblasts
Less relevant in predicting outcome
Immunological classification of ALL
Based on cell marker and other studies
B or T cell variant with their stage of development
Comprehensive
Relevant in predicting outcome
60. Immunological Classification of ALL
Children(%) Adults(%)
B-Lineage
Precursor B ( Pro-B ALL) 5 11
Common ALL 65 51
Pre-B ALL 15 10
Mature B-ALL 3 4
T-Lineage
Early T (T-Precursor) ALL 1 7
Cortical ( Thymic) T-ALL
Mature T-ALL 11 17
61. Specific Treatment in ALL
Chemotherapy
Several phases
Remission Induction
CNS prophylaxis or Treatment
Consolidation/Intensification
Maintenance
Upfront cytoreduction
Cyclophosphamide and steriods
75-85% of adults achieve Complete Remission
62. Specific Treatment in ALL
Consolidation/ Intensification
Difference b/n consolidation & intensification
Early intensification
Maintenance
Continues for upto 22months
Monthly pulse doses (Dexa + Vincristine)
Methotrexate /wk + 6-mercaptopurine/d (orally)
63. Specific Treatment in ALL
Remission Induction
4-6 weekly cycles with the aim of CR
Vincristine + Predinsolone + daunorubicin
+/- L-Asparaginase
CNS prophylaxis or Treatment
Intrathecal(cytarabin,Methotrexate, hydrocortisol)
High dose systemic chemo
Cranial Irradiation
64. Adverse Prognostic Factors for Remission Duration
in Adult ALL
Clinical characteristics Higher age >50 yrs, >60 yrs
High WBC >30000/µL in B-lineage
Immunophenotype Pro B (B-lin., CD10-)
Early T (T-lin., CD1a-, sCD3-)
Mature T (T-lin., CD1a-, sCD3+)
Cytogenetics/molecular
genetics
t(9;22)/BCR-ABL or t(4;11)/ALL1-AF4
Treatment response Late achievement of CR >3 or 4 weeks
MRD positivity
65. Specific Treatment in ALL
Stem Cell Transplantation
Reserved for relapse or refractory ALL
Types
Allo-SCT
Auto-SCT
MUD & NMSCT