Chapter 12_2 flashcards

Question 1

Myelodysplastic Syndrome (MDS): Definition

Answer 1

Broad term for disorders of stem cells in bone marrow. Hematopoiesis is dysfunctional/ineffective; differentiation of precursor stem cells impaired, leading to deficient numbers of WBCs, RBCs, or platelets (or all).

Question 2

MDS: Epidemiology

Answer 2

Uncommon; ~10,000 US cases/year, increasing to 30,000-40,000. Majority >70 years; slight male predominance. Rare in children.

Question 3

MDS: Etiology/Risk Factors

Answer 3

Environmental exposures (radiation, benzene). Secondary MDS from prior radiation/cytotoxic cancer treatment. Cytogenetic abnormality: del 5q (gene deletion on chromosome 5q).

Question 4

MDS: Pathophysiology

Answer 4

Dysfunctional hematopoiesis leads to cytopenias (anemia, leukopenia, thrombocytopenia). Classified as low- or high-risk. High-risk can transition to AML or complete bone marrow failure.

Question 5

MDS: Signs & Symptoms

Answer 5

Nonspecific; related to diminished blood cells. Anemia (fatigue, weakness), Infections (lack of WBCs), Bleeding/bruising (lack of platelets).

Question 6

MDS: Diagnosis

Answer 6

Peripheral blood smear, bone marrow aspirate/biopsy (shows cytopenia, morphological dysplasia). Karyotype, molecular genetic testing, flow cytometry, immunophenotyping. Key: persistent, unexplained cytopenia and significant dysplasia. Del 5q abnormality.

Question 7

MDS: Treatment

Answer 7

Low-risk (mild, asymptomatic): No treatment. High-risk: Erythropoiesis-stimulating agents (for anemia), transfusions, chemotherapy (e.g., Lenalidomide - inhibits cell cycle in malignant cells), allogeneic stem cell transplant.

Question 8

Clinical Concept: High-Risk MDS

Answer 8

Often leads to Acute Myelogenous Leukemia (AML) or complete bone marrow failure.

Question 9

Leukemia: General Definition

Answer 9

Cancer of developing WBCs within bone marrow. Cancerous WBCs arrested at early stage (blasts), proliferate uncontrollably, do not function, crowd out healthy cells.

Question 10

Leukemia: Myelocytic vs. Lymphoblastic

Answer 10

Myelocytic (myelogenous, myeloblastic, nonlymphocytic): Affect myeloid lineage.
Lymphoblastic (lymphogenous): Affect lymphoid lineage.

Question 11

Four Main Classifications of Leukemia

Answer 11

1. Acute Lymphoblastic Leukemia (ALL)
2. Chronic Lymphocytic Leukemia (CLL)
3. Acute Myelogenous Leukemia (AML)
4. Chronic Myelogenous Leukemia (CML)

Question 12

Acute Lymphoblastic Leukemia (ALL): Definition & Epidemiology

Answer 12

Aggressive cancer of T or B lymphoblasts. Most common pediatric cancer (75% of cases, peak 3-4 years, most <5). Bimodal: highest in young children, increases again in adults >50.

Question 13

ALL: Etiology/Risk Factors

Answer 13

Interaction of environmental & genetic factors. Chromosomal alterations (aneuploidy, Ph chromosome/BCR-ABL t(9;22) - Ph+ ALL, Ph-like ALL). Risk factors: Previous chemo/radiation, prenatal radiation (children), male, white, >70yrs, pesticides, genetic disorders (Down syndrome), viruses (EBV, HTLV-1), advanced parental age.

Question 14

ALL: Pathophysiology

Answer 14

Stem cell precursors for T/B lymphocytes in bone marrow don’t mature beyond lymphoblast stage. Lymphoblasts proliferate, crowding out healthy WBCs (neutropenia -> infection), RBCs (anemia), platelets (thrombocytopenia). Lymph nodes enlarge. CNS, kidneys, testicles can be infiltrated (meningeal involvement common, esp. T-cell ALL).

Question 15

ALL: Signs & Symptoms

Answer 15

Frequent infections, anemia (fatigue, weakness, dizziness, dyspnea, pallor), flu-like symptoms (fever, chills, night sweats), enlarged lymph nodes/spleen/liver (nausea, fullness, weight loss), bone pain (sternum, tibia, femur), bleeding/bruising, CNS symptoms (headaches if infiltrated).

Question 16

ALL: Diagnosis

Answer 16

High WBC on CBC. Bone marrow biopsy: hypercellularity, >20% lymphoblasts. Lumbar puncture (CSF for blasts). Immunophenotyping (cell surface antigens for prognosis/therapy). Cytogenetic/molecular analyses (subtype, Ph chromosome).

Question 17

ALL: Treatment

Answer 17

Aims: Restore bone marrow, prophylactic sanctuary site treatment (CNS), maintenance. Phases: Prephase, Induction (achieve remission), Consolidation (eliminate sanctuary sites), Maintenance (often targeted therapy). TKIs (imatinib, dasatinib) for Ph+ ALL. Monoclonal antibodies (rituximab, blinatumomab). CAR-T cell therapy. Bone marrow transplant (children/young adults). Chemo (older adults).

Question 18

Chronic Lymphocytic Leukemia (CLL): Definition & Epidemiology

Answer 18

Most common leukemia in US/Western countries. B-cell lymphocyte malignancy. >17,000 US cases/year. Median age at diagnosis: 70 years. Male:Female 2:1. Primary risk: family history of CLL/B-cell malignancy.

Question 19

CLL: Etiology/Risk Factors

Answer 19

Genetic changes fundamental. Risk factors: Male, advanced age, Caucasian, family history, herbicides/insecticides (Agent Orange), reduced sun exposure, atopic conditions, hepatitis C. Chromosomal abnormalities (>80% patients): Trisomy 12 (most common), deletions (13q, 11q, 17p). Mutations in NOTCH1, SF3B1, MYD88, ATM, TP53 (chemo resistance). Altered antiapoptotic protein genes (BCL2).

Question 20

CLL: Pathophysiology

Answer 20

Proliferation of mature, functionally incompetent CD5+ B cells (B-CLL lymphocytes) in blood, bone marrow, lymph nodes, spleen. B-CLL cells contain BCL2 protein (allows constant proliferation). Synthesize low/mutated/no Igs (hypogammaglobulinemia). Classified by IGHV mutation status (IGHV-M better prognosis than IGHV-UM). Crowding of bone marrow -> anemia, neutropenia, thrombocytopenia. Lymphadenopathy, splenomegaly.

Question 21

CLL: Signs & Symptoms

Answer 21

Often asymptomatic early (incidental finding on CBC). Later: painless lymphadenopathy, fatigue, fever, upper-left abdominal pain (splenomegaly), night sweats, weight loss, frequent infections.

Question 22

CLL: Diagnosis

Answer 22

Hallmark: Lymphocytosis on CBC (>20,000/mcL total WBC; specifically >5,000 B-lymphocytes/µL for ≥3 months). Flow cytometry confirms. Bone marrow hypercellular. Immunophenotyping: B-CLL cells coexpress CD5, CD19, CD20, CD22, CD23, CD52. Genetic/chromosomal testing (deletions, trisomy 12, t(11;14)). LP/CT for spread.

Question 23

CLL: Staging Systems

Answer 23

Rai Staging System (Stages 0-IV, classifies as low, intermediate, high risk). Binet Staging System (Stages A, B, C based on lymphoid areas, anemia/thrombocytopenia).

Question 24

CLL: Treatment

Answer 24

Asymptomatic/early stage: Monitor. Progressive/symptomatic: Treat. Leukapheresis for very high counts. Chemo (Fludarabine combinations like FCR; alkylating agents like chlorambucil). Corticosteroids. Monoclonal antibodies (Rituximab, Obinutuzumab, Ofatumumab - target CD20; Alemtuzumab - targets CD52; Moxetumomab pasudotox - targets CD22). TKIs (Idelalisib, Ibrutinib - target BTK, PI3K). BCL-2 inhibitors (Venetoclax). Allogeneic stem cell transplant (relapsed/refractory).

Question 25

CLL: Complication - Richter's Transformation

Answer 25

Transformation of CLL to a high-grade/aggressive non-Hodgkin’s lymphoma (DLBCL) or Hodgkin’s lymphoma. Occurs in 2-10% of cases. Hard to treat, may need stem cell transplant.

Question 26

Acute Myelogenous Leukemia (AML): Definition

Answer 26

Also acute myeloid leukemia. Proliferation of undifferentiated myeloblasts (non-lymphoid WBC precursors) in bone marrow (>20% blasts). Reduces healthy blood cell production -> anemia, bleeding, infections.

Question 27

AML: Etiology/Risk Factors

Answer 27

Mutations turn on oncogenes (FLT3, c-KIT, RAS) or off tumor suppressor genes (RUNX1, RARa). Risk factors: Previous chemo/radiation, radiation exposure (Chernobyl), male, smoking, childhood ALL/MDS, benzene exposure. Genetic diseases (Down syndrome, Fanconi's anemia, etc.). Possible links: electromagnetic fields, diesel/gasoline/solvents, herbicides/pesticides.

Question 28

AML: Pathophysiology

Answer 28

Proliferation of myeloblasts infiltrates bone marrow, blood, tissues, spleen, liver. Can invade skin (rash/nodules) and lungs (pneumonia-like symptoms).

Question 29

AML: Signs & Symptoms

Answer 29

Neutropenia (infection, fever, chills, night sweats), Anemia (fatigue, weakness, dizziness), Thrombocytopenia (bruising, nosebleeds, gingival bleeding). Swollen lymph nodes, splenomegaly/hepatomegaly (abdominal pain, poor appetite, weight loss). Autoimmune hemolytic anemia possible.

Question 30

AML: Diagnosis

Answer 30

CBC with differential, bone marrow biopsy (>20% blasts). FISH, PCR for genetic/chromosomal abnormalities: t(8;21), t(15;17), inv(16), del(7), trisomy 8. Oncogenes: FLT3, IDH1, IDH2, c-Kit, RAS. Biomarker: CD33 protein.

Question 31

AML: Treatment

Answer 31

Chemo phases: Remission induction (e.g., 7+3 regimen: cytarabine + anthracycline like daunorubicin/idarubicin), Consolidation (postremission, e.g., HiDAC - high-dose cytarabine). Leukapheresis for very high WBCs. Allogeneic/autologous stem cell transplant. Targeted therapy: TKIs (Midostaurin for FLT3 mutation; Ivosidenib/Enasidenib for IDH mutations). Monoclonal antibody (Gemtuzumab for CD33+ AML). BCL-2 inhibitor (Venetoclax with decitabine/azacitadine for resistant cases).

Question 32

Chronic Myelogenous Leukemia (CML): Definition & Epidemiology

Answer 32

Also chronic myeloid leukemia. Overproduction of mature but non-functioning myeloid cells in bone marrow. Most affected ≥65 years. 15-20% of adult leukemias. Slightly more males.

Question 33

CML: Etiology/Risk Factors

Answer 33

Exposure to ionizing radiation. 95% of adults have Ph chromosome (BCR-ABL oncogene t(9;22)) in a pluripotent hematopoietic stem cell. This triggers production of tyrosine kinase, inhibiting apoptosis and causing unrelenting proliferation.

Question 34

CML: Clinical Phases

Answer 34

1. Chronic Phase: <10% blasts in blood/marrow. Mild symptoms. Often diagnosed here, responds to treatment. 2. Accelerated Phase: <30% blasts. Low platelets, Ph chromosome apparent. Moderate symptoms (fever, appetite loss, weight loss). Less responsive. 3. Blast Crisis Phase: Large clusters of blasts in marrow, high % in blood. Spread to organs. Severe symptoms.

Question 35

CML: Signs & Symptoms

Answer 35

Anemia (fatigue, weakness), Leukopenia (infection, fever, chills, night sweats), Thrombocytopenia (bleeding, bruising), Bone pain. Abdominal fullness (hepatosplenomegaly). WBC >100,000; can cause respiratory distress (blasts in lungs).

Question 36

CML: Poor Prognostic Factors (Box 12-5)

Answer 36

Accelerated/blast phase, splenomegaly, bone damage, high basophils/eosinophils, very high/low platelets, age ≥60, multiple chromosome changes. (Sokal system, Euro score used for prognosis).

Question 37

CML: Diagnosis

Answer 37

CBC with differential, bone marrow biopsy. FISH and PCR find Ph chromosome translocation (t(9;22)).

Question 38

CML: Treatment

Answer 38

Standard: TKIs (e.g., Ponatinib, Imatinib) inhibit tyrosine kinase from BCR-ABL, can induce complete remission (>90%). Different response types (hematological, cytogenetic, molecular - see Box 12-6). Splenectomy if severe splenomegaly. Allogeneic bone marrow transplant for some.

Question 39

Lymphoma: General Definition & Main Categories

Answer 39

Most common US blood cancer. Solid tumors of proliferating lymphoid cells (B or T). Two major categories: 1. Hodgkin’s Lymphoma (HL), 2. Non-Hodgkin’s Lymphoma (NHL).

Question 40

Lymphoma: Epidemiology Comparison (HL vs. NHL)

Answer 40

NHL: 83% of cases, ~77,000 new US cases/year, more common in older people. HL: 17% of cases, ~8,500 new US cases/year, common in 15-20 yrs and >50 yrs.

Question 41

Lymphoma: Distinguishing HL from NHL

Answer 41

Microscopic examination is key. HL: specific abnormal B lymphocyte line (Reed-Sternberg cells). NHL: abnormal B or T cells. Both have unique genetic markers.

Question 42

Lymphoma: General Risk Factors (Box 12-7)

Answer 42

Age >60, male, Caucasian, autoimmune disorders, infections (HIV, EBV, H. pylori, HCV, HTLV-1), radiation, immunosuppressive therapy, occupational chemical exposure (pesticides, herbicides, benzene), family history.

Question 43

Lymphoma: General Signs & Symptoms (Box 12-8)

Answer 43

Often painless enlarged lymph node (neck, armpit, groin) - may press on structures causing swelling, pain, numbness. Splenomegaly, hepatomegaly, abdominal pain/fullness, fever, chills, weight loss, headache, seizure (if CNS involved), SVC syndrome, frequent infections, chest pain, SOB, easy bruising/bleeding, night sweats, rash/itching.

Question 44

Lymphoma: Staging System

Answer 44

Lugano Staging System (based on Ann Arbor system). Stages I-IV based on location/number of lymph node regions involved, extranodal sites, and presence (B) or absence (A) of systemic symptoms (fever, night sweats, weight loss >10%).

Question 45

Non-Hodgkin’s Lymphoma (NHL): Definition & Cell Origin

Answer 45

Caused by cancerous T cells, B cells, or NK cells. Most (85%) are B-cell origin. >20 subtypes. Most common type: Diffuse Large B-cell Lymphoma (DLBCL).

Question 46

NHL: Etiology

Answer 46

Chromosomal translocations are hallmark (e.g., t(8;14) in follicular lymphoma). Oncogenic pathogens may be involved (HIV, EBV, H. pylori, HTLV-1, HCV, HHV-8) by introducing genes causing mutations (oncogene stimulation, tumor suppressor inhibition).

Question 47

NHL: Pathophysiology (Growth Patterns & Aggressiveness)

Answer 47

Follicular/nodular pattern: Generally less aggressive. Diffuse pattern: More aggressive. Small lymphocyte lymphomas: Milder course. Large lymphocyte lymphomas: Intermediate/high-grade aggressiveness.

Question 48

NHL: Diagnosis

Answer 48

Mainstay: Lymph node biopsy. CBC, liver function, serum protein electrophoresis, beta-2 microglobulin, LDH, HIV/hepatitis testing, bone marrow aspiration. Imaging (CT, MRI, PET, bone scan - FDG-PET highly sensitive). LP, fluid sampling. FISH, PCR, immunophenotyping, gene expression profiling.

Question 49

NHL: Treatment (Depends on aggressiveness, symptoms, type, stage)

Answer 49

Chemo (e.g., CHOP: Cyclophosphamide, Doxorubicin, Vincristine, Prednisone; R-CHOP with Rituximab). Immunotherapy (Rituximab, Tafasitamab). Targeted therapy (TKIs like Ibrutinib, proteasome inhibitors). CAR-T cell therapy (for resistant CD19+ B-cell lymphomas like DLBCL). Radiation. Stem cell transplant (autologous or allogeneic). Surgery (rarely).

Question 50

NHL: Prognosis - International Prognostic Index (IPI) Factors (Box 12-10)

Answer 50

1. Age (>60 poor). 2. Stage (III/IV poor). 3. Extranodal involvement (>1 organ poor). 4. Performance status (lack of independence poor). 5. LDH level (high poor). Score 0-5, higher score = poorer prognosis. Four risk groups: Low, Low-intermediate, High-intermediate, High.

Question 51

Hodgkin’s Lymphoma (HL): Definition & Subtypes

Answer 51

Malignancy of B lymphocytes. Most common in adolescents/young adults (15-34) and older (>55). Subtypes: Classic HL (cHL, >90%, aggressive - further subdivided) and Nodular Lymphocyte Predominant HL (NLPHL, less aggressive).

Question 52

HL: Classic HL Subtypes

Answer 52

Nodular Sclerosis (NSCHL - most common), Mixed Cellularity (MCCHL), Lymphocyte Rich (LRCHL), Lymphocyte Deficient (LDCHL).

Question 53

HL: Etiology

Answer 53

Cause unknown. EBV found in malignant B cells (RS cells) in ~50% of patients. Immunosuppression increases risk. Proposed: carcinogens, viruses, genetic/immune mechanisms.

Question 54

HL: Pathophysiology - Reed-Sternberg (RS) Cells

Answer 54

Classic HL diagnosed by presence of RS cells in lymphoid tissue. RS cell: large malignant B cell, two nuclei (owl's eyes appearance). Malignancy starts in one area (e.g., lymph node), spreads through lymphatic system. Common sites: cervical/mediastinal nodes, spleen.

Question 55

HL: Clinical Presentation & Signs/Symptoms

Answer 55

Often painless enlarged lymph node (neck, chest, groin). Sore throat, fever, dysphagia, SOB, abdominal pain. Symptoms depend on site. Waldeyer’s ring common. Chest tumor -> pain, SVC syndrome. Sub-diaphragmatic -> abdominal distention, splenomegaly.

Question 56

HL: Diagnosis

Answer 56

Biopsy of nodal/extranodal sites (shows RS cells). Flow cytometry, DNA analysis. Bone marrow biopsy if cytopenias. FDG-PET/CT for staging and treatment response. Immunophenotyping for CD15, CD30 (on RS cells).

Question 57

HL: Treatment

Answer 57

Mainstays for cHL: Chemo & Radiation. Combination chemo (e.g., ABVD: Adriamycin, Bleomycin, Vinblastine, Dacarbazine - standard US regimen). Involved Site Radiotherapy (ISRT). Immunotherapy (Brentuximab vedotin targets CD30 - antibody-drug conjugate; Rituximab for NLPHL targets CD20; Nivolumab/Pembrolizumab - checkpoint inhibitors). High-dose chemo + stem cell transplant (autologous or allogeneic).

Question 58

HL: Prognostic Factors (Box 12-13)

Answer 58

Male, age >45, advanced stage, bulky disease, constitutional 'B' symptoms (fever, night sweats, weight loss), high WBC, low Hgb, low lymphocyte count, low albumin, high ESR indicate more serious disease.

Question 59

Multiple Myeloma (MM): Definition

Answer 59

Hematological neoplasm of B lymphocytes that become plasma cells, proliferating uncontrollably in bone marrow. Secrete excessive abnormal immunoglobulins (Igs) or Ig fragments (M-proteins).

Question 60

MM: Epidemiology

Answer 60

~35,000 US cases/year. 2nd most common US hematological neoplasm. Higher in men (2:1), African Americans (2:1). Most prevalent >65 years.

Question 61

MM: Etiology/Risk Factors

Answer 61

Trigger unknown. Genetic/chromosomal changes in myeloma cells (duplications, deletions - del(17p) high risk; translocations - t(4;14), t(14;16) high risk, associated with oncogenes). Excessive IL-6 production. Risk factors: Male, firefighter, obesity, dioxin/Agent Orange, 9/11 first responder.

Question 62

MM: Pathophysiology Progression (MGUS, SMM)

Answer 62

Begins as Monoclonal Gammopathy of Undetermined Significance (MGUS) -> progresses to MM in 1-2%/20yrs. Smoldering Multiple Myeloma (SMM) more advanced -> 10% progress to MM/year.

Question 63

MM: Pathophysiology - Core Mechanisms

Answer 63

Neoplastic plasma cells proliferate in marrow, crowding out healthy cells (anemia, leukopenia, thrombocytopenia). Abnormal Igs (M-proteins, Bence Jones proteins - light chains) can cause renal failure (myeloma cast nephropathy). Cytokines stimulate osteoclasts, inhibit osteoblasts -> bone destruction, hypercalcemia, vertebral lesions (risk of spinal cord compression - emergency!). Hyperviscosity of blood from high Igs (esp. IgM).

Question 64

MM: Clinical Presentation & Symptoms

Answer 64

Bone pain (esp. back) common at diagnosis (from lytic lesions, plasmacytomas). Anemia (weakness, pallor, fatigue). Infections (from leukopenia, lack of normal Igs). Renal disease (hypercalcemia, myeloma cast nephropathy). Radiculopathy (spinal nerve compression). Concurrent light chain amyloidosis (protein deposits in heart/kidney). Extramedullary disease (plasmacytomas outside marrow, CNS involvement, plasma cell leukemia).

Question 65

MM: Diagnosis - CRAB Criteria & Key Tests

Answer 65

Diagnosis: ≥10% plasma cells in bone marrow + organ/tissue damage. CRAB criteria for end-organ damage: C=Calcium elevation, R=Renal dysfunction, A=Anemia, B=Bone disease. Tests: CBC, chemistry, serum/urine protein electrophoresis (for M-proteins/Bence Jones proteins), beta-2-microglobulin. Flow cytometry. Genetic analysis (FISH for chromosomal changes). Bone marrow aspirate/biopsy (plasma cell morphology, CD138+ quantification). Imaging (CT, MRI, PET for lytic lesions). Echocardiogram (for amyloidosis).

Question 66

MM: Staging - Revised International Staging System (RISS) (Table 12-3)

Answer 66

Stages I, II, III based on: 1. Serum albumin amount. 2. Serum beta-2-microglobulin amount. 3. LDH amount. 4. Specific gene abnormalities (cytogenetics - high-risk changes like del(17p), t(4;14), t(14;16) indicate poorer prognosis).

Question 67

MM: Treatment (Asymptomatic MGUS/SMM vs. Symptomatic MM)

Answer 67

MGUS/SMM (asymptomatic): Monitor; some high-risk SMM may get lenalidomide + dexamethasone. Symptomatic MM: Chemo (immunomodulators like lenalidomide; proteasome inhibitors like bortezomib; often combined with dexamethasone), followed by autologous stem cell transplant. Non-transplant candidates: ~8-12 cycles chemo then maintenance (lenalidomide; bortezomib for high-risk).

Question 68

MM: Treatment for Relapsed Disease & Supportive Care

Answer 68

Relapsed: Daratumumab (anti-CD38 monoclonal antibody)-based regimens. Panobinostat (HDAC inhibitor). Bendamustine (alkylating agent). CAR-T therapy (targeting B cell antigens) under investigation. Supportive: Ca/Vit D, bisphosphonates/denosumab (bone strength), kyphoplasty/vertebroplasty, fluids (renal function), plasmapheresis (hyperviscosity), prophylactic gamma globulin, vaccines, erythropoietin, analgesics, DVT prophylaxis (with lenalidomide).

Question 69

Blast Cells: Definition in Leukemia

Answer 69

Immature leukemic WBCs, proliferation of which is characteristic of acute leukemias. They do not differentiate into mature, functioning cells.

Question 70

Bence Jones Proteins

Answer 70

Abnormal immunoglobulin light chains produced by plasma cells in some types of Multiple Myeloma; found in urine.

Question 71

Plasmacytoma

Answer 71

A tumor made up of neoplastic plasma cells, can occur within bone (common in MM) or outside the bone marrow (extramedullary disease).

Question 72

BCR-ABL Oncogene

Answer 72

Fusion gene resulting from translocation between chromosome 9 (ABL gene) and chromosome 22 (BCR gene) - the Ph chromosome. Produces tyrosine kinase, driving proliferation in CML and some ALL.

Question 73

Richter’s Transformation

Answer 73

A serious complication of CLL where the leukemia transforms into a high-grade or aggressive type of non-Hodgkin’s lymphoma (DLBCL) or, less commonly, Hodgkin’s lymphoma.

Question 74

Tyrosine Kinase (in hematological cancers)

Answer 74

Enzyme (often produced due to genetic mutations like BCR-ABL) that causes uncontrolled proliferation of cancer cells by inhibiting apoptosis. Targeted by Tyrosine Kinase Inhibitor (TKI) drugs.

Question 75

Immunophenotyping: Purpose

Answer 75

Analysis of cancer cells to identify specific surface antigens (e.g., CD markers). Helps in precise diagnosis, subtyping, prognosis, and selection of targeted therapies (like monoclonal antibodies).

Question 76

Allogeneic vs. Autologous Hematological Stem Cell Transplant

Answer 76

Allogeneic: Uses healthy stem cells from a matched donor. Autologous: Uses the patient's own healthy stem cells, harvested before high-dose chemo/radiation and then reinfused.

Question 77

CAR-T Cell Therapy: Basic Mechanism

Answer 77

Patient's T cells are genetically engineered to express chimeric antigen receptors (CARs) that recognize specific antigens on cancer cells. These modified T cells are then reinfused to target and kill the cancer.

Question 78

Monoclonal Antibodies in Cancer Treatment

Answer 78

Laboratory-produced antibodies designed to recognize and bind to specific antigens found on cancer cells, either killing them directly, blocking growth, or delivering toxins/radiation.