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Y2 MCD Cancer > clinical oncology > Flashcards

clinical oncology Flashcards

leukaemia: define leukaemia, explain the difference between lymphoid and myeloid leukaemia, and acute and chronic leukaemia; summarise the clinical, haematological features and genetic features of acute lymphoblastic leukaemia

1
Q

define leukaemia

A

bone marrow disease normally causing increased WBC (“white blood”) - hence “cancer of blood”

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2
Q

epidemiology of leukaemia: common and mortality

A

most common cancers in men/women ages 15-24, main cause of cancer death between 1-34

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3
Q

leukaemia mechanism

A

mutations in single lymphoid or myeloid stem cell, leading progeny to show abnormalities in proliferation (too rapid), differentiation (don’t reach end cell) or cell survival (too long), leading to steady expansion of leukaemic clone

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4
Q

cells that can be mutated to be involved in leukaemia

A

pluripotent haematopoietic stem cell (mixed phenotype leukaemia), myeloid stem cell, lymphoid stem cell, pre-B lymphocyte, pre-T lymphocyte

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5
Q

2 hit hypothesis in leukaemia

A

first mutation gives growth/survival advantage to that line of cells, so expand at expense of normal cells; acquire second mutation to get leukaemia

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6
Q

how is leukaemia different to other cancers: tumours

A

most cancers exist as solid tumour, with other tumours present in leukaemia patients being uncommon (more often have leukaemic cells replacing normal bone marrow cells and circulating freely in blood stream)

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7
Q

how is leukaemia different to other cancers: cells

A

haemopoietic and lymphoid cells behave differently from other body cells: normal haemopoietic stem cells can circulate in blood and both stem cells and cells derived from them can enter tissues, and normal lymphoid stem cells recirculate between tissues and blood

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8
Q

how is leukaemia different to other cancers: benign and malignant, and impact on treatment

A

invasion and metastasis cannot be applied to cells that normally travel around body and enter tissues (must have another way to distinguish benign vs malignant), so treatment must be systemic

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9
Q

what are leukaemias that behave relatively benignly called

A

chronic

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10
Q

what are leukaemias that behave malignantly called, and outcome if not treated

A

acute (if not treated, disease is very aggressive and patient dies quite rapidly)

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11
Q

2 classifications of leukaemia

A

acute vs chronic, lymphoid (B/T cell) vs myeloid (granulocyte, monocyte, erythroid, megakaryocyte)

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12
Q

4 types of leukaemia

A

acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML), chronic lymphocytic leukaemia (CLL), chronic myeloid leukaemia (CML)

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13
Q

describe the 2 types of influences which cause a series of mutations in a single stem cell to cause leukaemia (causing characteristics due to proliferation of leukaemic cells and loss of function of normal cells)

A

some are identifiable oncogenic, while others are random errors that occur throughout life and accumulate in individual cells

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14
Q

3 important leukaemogenic mutations

A

mutation in known proto-oncogenes, creation of novel gene (e.g. chimaeric or fusion gene when chromosomes translocate), dysregulation of gene when translocation brings it under influence of promoter or enhancer of another gene

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15
Q

what other gene can be affected to contribute to leukaemogenesis

A

loss of function of tumour-suppressor gene (resulting from deletion or mutation of gene)

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16
Q

what 2 genetic tendencies can increase risk of leukaemia

A

tendency to increased chromosomal breaks, if cell cannot repair DNA (error persists)

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17
Q

what 4 inherited/other constitutional abnormalities can contribute to leukaemogenesis

A

Down’s syndrome, chromosomal fragility syndromes, defects in DNA repair, inherited defects of tumour-suppressor genes

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18
Q

4 identifiable causes (not mechanisms) of leukaemogenic mutations

A

irradiation, anti-cancer drugs, cigarette smoking, chemicals e.g. benzene

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19
Q

why might leukaemia be, in part, an inevitable result of ability of humanity to change through evolution

A

some mutations appear to be random events rather than caused by exogenous influence, so may result from nature of human genome

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20
Q

2 outcomes of cells continuing to proliferate but being unable to mature in acute myeloid leukaemia (AML)

A

build up of most immature cells (myeloblasts) in bone marrow with spread into blood; failure of production of normal functioning end cells e.g. neutrophils, monocytes, erythrocytes, platelets, so crowded out (plateles also consumed by intravascular coagulation)

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21
Q

what do mutations in AML usually affect

A

transcription factors (so transcription of multiple genes is affected)

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22
Q

what does the product of an oncogene prevent (usually acts in dominant manner)

A

normal function of protein encoded by its normal homologue, disturbing cell behaviour

23
Q

what to mutations in CML usually affect

A

gene encoding a protein in signalling pathway between cell surface receptor and nucleus (either membrane receptor or cytoplasmic protein)

24
Q

CML vs AML: cell kinetics and function

A

cell kinetics and function not as seriously affected in CML compared to AML

25
Q

3 features of CML to ensure cell survives longer and leukaemic clone expands progressively

A

cell becomes independent of external signals, alterations in interaction with stroma, reduced apoptosis

26
Q

CML vs AML: production of end cells (anaemia occurs due to crowding out of erythrocytes)

A

in AML there is failure of production of end cells, in CML there is increased production of end cells

27
Q

ALL vs CLL: maturity of cells

A

ALL has increase in very immature cells (lymphoblasts) which fail to develop into mature T and B cells; CLL has abnormal mature T and B cells

28
Q

what 7 things can accumulation of abnormal cells in leukaemia lead to

A

leucocytosis, bone pain (if leukaemia is acute), hepatomegaly, splenomegaly, lymphadenopathy (if lymphoid), thymic enlargement (if T lymphoid), skin infiltration (leukaemia cutis)

29
Q

4 metabolic effects of leukaemic cell proliferation

A

hyperuricaemia -> renal failure; weight loss; low grade fever; sweating

30
Q

3 effects of crowding out of normal cells in leukaemia

A

anaemia, neutropenia, thrombocytopenia

31
Q

acute myeloid leukaemia consequence of thrombocytopenia

A

bruises and small haemorrhages

32
Q

why could a sufferer of AML have an intraventricular haemorrhage

A

associated with disseminated intravascular coagulation, so consumes platelets, causing haemorrhages which can’t be plugged

33
Q

2 abnormalities in buccal cavity due to AML

A

haemorrhage, swelling of gums (infiltration of gums by leukaemic cells)

34
Q

what causes leukaemic cells to infiltrate gums in AML

A

chemotaxic stimli

35
Q

what is a feature of CLL due to loss of normal T and B cell function

A

loss of normal immune function

36
Q

main age groups affected by ALL, and mechanism for later peak

A

largely in children (later peak in middle and old age, which is genetically different - same as CML translocation)

37
Q

what might B-lineage ALL result from

A

delayed exposure to common pathogen (early exposure to pathogen protects from ALL)

38
Q

what can affect exposure to common pathogens affecting B-lineage ALL

A

family size, new towns, socio-economic class, early social interactions, variations between countries

39
Q

other causes of ALL in young children

A

irradiation in utero, in utero exposure to certain chemicals; unlikely due to exposure of mutagenic drug (normally AML)

40
Q

6 clinical features of ALL resulting from accumulation of abnormal cells

A

bone pain, hepatomegaly, splenomegaly, lymphadenopathy, thymic enlargement, testicular enlargement

41
Q

4 clinical features of ALL, caused by anaemia, resulting from crowding out normal cells

A

fatigue, lethargy, pallor, breathlessness

42
Q

2 clinical features of ALL, caused by neutropenia, resulting from crowding out normal cells

A

fever, other features of infection

43
Q

3 clinical features of ALL, caused by thrombocytopenia, resulting from crowding out normal cells

A

bruising, petechiae, bleeding

44
Q

5 haematological features of ALL

A

leucocytosis (due to lymphoblasts in blood), anaemia (normocytic, normochromic), neutropenia, thrombocytopenia, replacement of normal bone marrow cells by lymphoblasts

45
Q

6 investigations for ALL

A

blood count and film, liver function, renal function and uric acid, bone marrow aspirate, cytogenetic/molecular analysis, chest x-ray

46
Q

immunophenotyping ALL to determine lineage (myeloid can have granules so this aids diagnosis)

A

antibody binding to antigen (CD) to find lineage e.g. B-lineage and maturity of cells

47
Q

why is cytogenetic/molecular analysis of ALL useful for managing individual patient and for advancing knowledge of leukaemia

A

gives information about prognosis (ALL is not single disease or even 2 diseases, and has multiple different leukaemogenic mechanisms giving different disease phenotypes), permits discoveries of leukaemogenic mechanisms and specific treatments

48
Q

good and poor prognosis for ALL found by cytogenetic analysis

A

hyperdiploidy is a good prognosis, t(4;11) is a poor prognosis

49
Q

3 leukaemogenic mechanisms of ALL

A

formation of fusion gene (due to translocation e.g. t(4;11)), dysregulation of proto-oncogene by juxtaposition of it to promoter of another gene (e.g. TCR gene), point mutation in proto-oncogene

50
Q

cytogenetics of ALL (translocation causing fusion gene), and process by which FISH detect fusion gene

A

t(12;21)(p12;q22) leading to a ETV6-RUNX1 fusion gene; FISH (flurescence in situ hybridisation) using 2 fluorescent probes (green probe for ETV6 and red probe for RUNX1), so when a fusion gene is formed the two colours fuse to give a yellow fluorescent signal

51
Q

advantage of FISH over immunophenotyping

A

can look for fusion gene without cell going into mitosis

52
Q

3 types of treatment for ALL

A

supportive, systemic chemotherapy, intrathecal chemotherapy (into CSF and through BBB)

53
Q

3 types of supportive treatment for ALL

A

red cells, platelets, antibiotics

54
Q

EFS vs OS survival

A

event-free survival vs overall survival

Y2 MCD Cancer (20 decks)

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