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Tumor markers > Oncology > Flashcards

Oncology Flashcards

1
Q

THYROID CANCER - Types

A
  • Differentiated (papillary, follicular and Hürthle cell)
  • Medullary
  • Anaplastic (an aggressive cancer)
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2
Q

THYROID CANCER - most common

A
  • papillary 8/10
  • most common & most favorable
  • most common mixed papillary follicular variant
  • Other less common quicker growth subtypes (columnar, tall, insular, diffuse sclerosing)
    Slow, LN spread, rarely fatal
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3
Q

THYROID CANCER - worst prognosis

A

anaplastic

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4
Q

THYROID CANCER - staging

A

AJCC TNM pathologic and clinical

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5
Q

THYROID CANCER - stage 1

A

<55, any T, any N, M0
>55, T1 N0 M0
>55 T2 N0

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6
Q

Hurthel cells (AKA)

A

oxyphil cell carcinoma
Hard to treat
3% thyroid cancers

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7
Q

Medullary thyroid cancer MTC

A

4% of thyroid cancer
from C cells
Makes calcitonin
LN, lung, liver
Sporadic 80% (older) vs familial 20% (younger)

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8
Q

thyroid ca favorable and non favorable prognosis for follicular and papillary

A

age <40
low stage
medullary thyroid ca asso. with MEN2B is BAD

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9
Q

Adenocarcinoma

A

Adenocarcinomas start in the cells that would normally secrete substances such as mucus.

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10
Q

NSCLC - KRAS

A

Unfavorable
20 -25% of NSCLCs have changes in the KRAS gene that cause them to make an abnormal KRAS protein which helps the cancer cells grow and spread. NSCLCs with this mutation are often adenocarcinomas, resistant to other drugs such as EGFR inhibitors, and are most often found in people with a smoking history.

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11
Q

NSCLC - EGFR

A

EGFR is a protein that appears in high amounts on the surface of 10% to 20% of NSCLC cells and helps them grow. Some drugs that target EGFR can be used to treat NSCLC with changes in the EGFR gene, which are more common in certain groups, such as those who don’t smoke, women, and Asians. But these drugs don’t seem to be as helpful in patients whose cancer cells have changes in the KRAS gene.

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12
Q

NSCLC ALK

A
  • 5% of NSCLCs have a change in the ALK gene
  • most often seen in people who don’t smoke
  • most in adenocarcinoma subtype
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13
Q

NSCLC

A

unfavorable
- KRAS (20-25%) - increase resistance to EGFR inhibitors, often in adenocarcinomas

favorable
- EGFR 10-20% non-smoker, F, asian
- AKL 5%
- ROS1 1-2%
- RET
- BRAF 5%
- MET
- HER2
- NTRK
- protein PD-L1 - favorable respond to immunotherapy

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14
Q

5 yr relative survival rate NSCLC

A

SEER stage NSCLC
- localised 64%
- regional 37%
- Distant 8%
all SEER stages combined 26%

SEER stage SCLC
- localised 29%
- regional 18%
- Distant 3%
all SEER stages combined 7%

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15
Q

Breast cancer proteins

A

ER/PR
PD-L1 protein (in triple -ve), response to immunotherapy

Gene
BRACA 1/2
PIK3CA gene (drug alpelisib)
ESR1 gene mutation - unfavorable response to hormone drugs
MSI Microsatellite instability - defect in mismatch repear gene, if high level present, pembrolizumab may help
NTRK fusion gene > changes are favorable to target therapy larotrectinib

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16
Q

Breast ca
tumor markers

A

CEA, Ca 15.3, CA 27, 29

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17
Q

BREAST CA 5 yr survival

A

localised - 99%
Regional - 86%
Distant 29%
All stages combined 90%

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18
Q

Gliomas IDH1 or IDH2 gene mutations

A

that are found to have IDH1 or IDH2 gene mutations tend to have a better outlook than gliomas without these gene mutations.

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19
Q

presence of MGMT promoter methylation In high-grade gliomas

A

In high-grade gliomas, the presence of MGMT promoter methylation is linked with better outcomes and a higher likelihood of responding to chemotherapy.

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20
Q

brain tumour tests

A

ATRX, TERT, H3F3A, BRAF, and HELA.
Chromosomal 1p19q co-deletions

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21
Q

IDU mutant vs wild type

A

IDH-mutated glioma exhibits a favourable disease outcome compared with its wild-type counterpart.

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22
Q

Any one of the following 5 criteria is sufficient to designate an IDH-wildtype diffuse astrocytic glioma as a glioblastoma

A

IDH-wildtype is characterized by the following
- microvascular proliferation
- necrosis
- TERT promotor mutation
- EGFR gene amplification
- +7/–10 chromosome copy number changes.

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23
Q

Pineal Tumors

A
  • SMARCB1mutant
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24
Q

WHO 5th edition introduced 14 new gliomas and glioneuro tumours, 8 other neuropathologic lexicons

A
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25
Q

WHO 2021 The critical importance of identifying mutations other than the canonical IDH1 R132H mutation in diffuse gliomas, especially in patients younger than 55 years of age, is emphasized

A
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26
Q

Gliomas essential

A

1p/19q codeletion on fluorescence in situ hybridization (FISH)
isocitrate dehydrogenase (IDH) mutant or IDH-wildtype on immunohistochemistry
loss of ATRX expression
TERT promoter mutations
TP53
histone H3 mutations
EGFR amplification
CDKN2A/B alterations- BAD (grade 4 astrocytoma)

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27
Q

glioma essental groups

A

Four general groups of diffuse gliomas are recognized in the 2021 WHO classification:
1) adult-type diffuse gliomas,
2) pediatric-type diffuse low-grade gliomas,
3) pediatric-type diffuse high-grade gliomas
4) circumscribed astrocytic gliomas.

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28
Q

Grade 2 - 4 gliomas

A

Adult-type diffuse gliomas are astrocytoma
IDH-mutant; oligodendroglioma
IDH-mutant and 1p/19q-codeleted
glioblastoma, IDH-wildtype.
IDH-mutant diffuse astrocytomas

the terms IDH-mutant “anaplastic astrocytoma” and “glioblastoma” have been dropped.

In addition, if an IDH-mutant diffuse astrocytoma exhibits CDKN2A/B homozygous deletion, it is designated as a CNS WHO grade 4 neoplasm, even if histologic features of malignancy such as necrosis and microvascular proliferation are absent.

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29
Q

GBM syndromes

A

p53 (NF1, Li-Fraumeni
Turcot
Ollier
Maffucci
Radiation M>F
White>black>asian
Peak age 65-75, usually after 40s

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30
Q

TP53 gene

A

TP53 gene, located on chromosome 17, is a tumor suppressor gene, responsible for the production of the p53 protein, a transcription regulatory protein which works in concert with a number of other proteins, together forming the p53 pathway

Inherited mutations in this gene result in the rare hereditary cancer condition known as Li-Fraumeni syndrome, which predisposes to a wide variety of malignancies 1

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31
Q

Isocitrate dehydrogenase (IDH) gene mutations are increasingly being recognized as key genetic prognostic markers for diffuse gliomas, and form the basis for diffuse adult-type gliomas in the WHO CNS 2021 classification.
FUNCTION:

A

Isocitrate dehydrogenases are enzymes that catalyze the oxidative decarboxylation of isocitrate to 2-oxoglutarate (α-ketoglutarate). This reaction also produces NADPH (IDH1 and IDH2) or NADH (IDH3) 4,5. Isocitrate dehydrogenase acts at the rate-limiting step of the tricarboxylic acid cycle (also known as Krebs cycle).

IDH1
- located on the long arm of chromosome 2 (2q32)
- encodes for cytosolic isocitrate dehydrogenase
mutations affect a single amino acid residue 132, in – most instances (>85%) resulting in arginine being replaced with histidine and thus denoted R132H 8

IDH2 - located on the long arm of chromosome 15 (15q21) -encodes for mitochondrial isocitrate dehydrogenase -  mutations affect a single amino acid residue 172, analogous to the R132 residue in IDH1

MUTANT ARE BETTER TTHAN WILD
mutant prognosis than gliomas without the mutation (WILDTYPE) 3. In other words:

IDH-wildtype = IDH negative = no mutation = poor prognosis ((ALL GBM ARE WILD)
IDH-mutant = IDH positive = mutation present = better prognosis (LOW GRADE ARE MUTANT)

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32
Q

Somatic mutations of IDH

A

Somatic mutations of IDH result in enchondromatosis syndromes: Ollier disease and Maffucci syndrome

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33
Q

IDH WILD (IDH -ve)/no mutation

A

POOR PROGNOSIS (All GBMs are IDH WILD)

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34
Q

IDH detection via immunohistochemistry

A

The majority (90%) of IDH mutations in gliomas affect IDH1 with a single amino acid missense mutation at arginine(R)132 replaced by histidine (H); thus denoted as IDH1 R132H. This is the mutation generally tested by immunohistochemistry

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35
Q

in individuals over the age of 55 years with a new diagnosis of glioma that is IDH1 R132H negative on immunohistochemistry,…

A

… the chances of an IDH mutation being detected by next-generation sequencing is low and not considered mandatory

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36
Q

MGM2

A

IDH1 R132H negative tumor actually harbors a less common mutation. Generally IDH mutated (IDH1 and IDH2) tumors are more likely to also have MGMT methylation (80% for IDH-mutant compared to 60% of IDH-wildtype tumors)

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37
Q

MGMT +ve is ….

A

bad prognosis
High activity of MGMT (i.e. unmethylated) results in reduced efficacy of alkylating agents, and thus is a poor prognostic factor
It is also predictive of pseudoprogression following Stupp protocol

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38
Q

TERT

A

Ch5
GBM!
can be seen in oligodendroglioma, follicular thyroid, melanoma, TCC, HCC

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39
Q

Oligodendroglioma is characterised by

A

They are characterized by IDH mutation and 1p19q codeletion and can be WHO CNS grade 2 or 3.

third most common glioma

Middle age men 40s 50s, older > higher grade

Male 1.3:1

Rare in children

well-circumscribed, gelatinous, grey mass

often calcified (70-90% of histological oligodendrogliomas: one of the most frequently calcifying tumors)

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40
Q

Grade 3 oligodendrogliomas (formerly known as anaplastic oligodendrogliomas) demonstrate ……

A

Grade 3 oligodendrogliomas (formerly known as anaplastic oligodendrogliomas) demonstrate increased cellular density, increased mitotic activity, microvascular proliferation and necrosis. Nuclear anaplasia is also common.

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41
Q

Importantly, and unlike astrocytomas, oligodendrogliomas with necrosis and microvascular proliferation are considered…..

A

Importantly, and unlike astrocytomas, oligodendrogliomas with necrosis and microvascular proliferation are considered only WHO grade 3 and NOT grade 4 tumors

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42
Q

oligodendrogliomas -other mutations are

A

TERT promoter mutation

CIC mutation

FUBP1 mutation

NOTCH1 mutations
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43
Q

Astrocytic tumors
three groups:

A

Astrocytic tumors are primary central nervous system tumors that either arises from astrocytes or appear similar to astrocytes on histology having arisen from precursor cells. They are the most common tumors arising from glial cells and can be broadly divided into three groups:

  • diffuse, adult-type
    Astrocytoma IDHm WHO2-4
    GBM IDH wild, WHO 4
  • diffuse, pediatric type
    low vs high grade
    LOW GRADE: angiocentric; diffuse astrocytoma MYB1/MYBL1; MAPK altered
    HIGH GRADE 4: H3 K27, G34, IDHw,
  • circumscribed grade 1 - 3
    PXA WHO1
    pleomorphic xanthoastrocytoma , chordoid glioma, astroblastoma
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44
Q

Pleomorphic xanthoastrocytomas (PXA)

A

Temporal lobe epilepsy
young adults
seziure 75% presentations
WHO 2-3
difficult to distingish between it and epitheloid glioblastomas
can have spindles, MNC, polygons

GFAP and S100 _ve, and synaptophysin, MAP2

NF1

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45
Q

DNET Dysembryoplastic neuroepithelial tumors (DNET)

A

WHO 1
Cortical or deep grey matter Temporal>frontal>caudate>cerebellum and pons
Asso. cortical dysplasia 80% , noonan
Temporal lobe epilepsy
Children
specific glioneuronal element (SGNE)”+

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46
Q

DNET genetic mutations

A

Importantly, DNETs are negative for IDH mutations, TP53 mutations, and do not demonstrate 1p19q co-deletion 8. These features are helpful in distinguishing DNETs from low-grade astrocytomas (usually IDH mutated) and oligodendrogliomas (IDH mutated and 1p19q co-deleted).

DNETs usually harbor fibroblast growth factor receptor tyrosine kinase domain duplication (FGFR1-TKDD),

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47
Q

Ganglioganglioma

A

ganglion cells (large mature neuronal elements): ganglio-

neoplastic glial element: -glioma

    primarily astrocytic, although oligodendroglial or pilocytic astrocytoma components are also encountered 9
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48
Q

Ganglioglioma

A

synaptophysin: positive

neurofilament protein: positive

MAP2: positive

chromogranin-A: positive (usually negative in normal neurons) 9

CD34: positive in 70-80%

The glial component may also show cytoplasmic positivity for GFAP.

Genetics

BRAF V600E mutations are encountered in 20-60% of cases 9

IDH: negative (if positive then the tumor is most likely a diffuse glioma)
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49
Q

CDKN2A/p16

A

tumor suppressor gene (cyclin-dependent kinase inhibitor 2A) that encodes for the p16 protein, involved in the CDK4/6–RB1 cell-cycle pathway

  • p16 +ve in HNSCC indicates a better prognosis
  • upregulated by HPV
  • p16 +ve cervical scc associated with high grade SIL (HSIL)
  • CDNK2A gene inactivation (p16-ve) by somatic mutation/deletion is seen in GBM is BAD
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50
Q

head and neck SCC
demographics
Gender
Age
Location

A

M > F
peak 50-70s, second peak in young adults HPV/p16+ve
oropharynx most common, decreasing
oropharyngeal increasing

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51
Q

HNSCC association syndrome

A

plummer vinson syndrome

classic triad of dysphagia, iron-deficiency anemia and upper esophageal webs.

?iron deficiency anaemia

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52
Q

Mucoepidermoid carcinoma of salivary glands
epidemiology

A

In the parotid gland, they are the most common malignant primary neoplasm. A slight female predilection
most common in middle age (35-65 years of age) However, it is the most common malignant salivary gland tumor of childhood

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53
Q

Mucoepidermoid carcinoma of salivary glands
pathology

A

The tumors are composed of a mixture of:

mucus-secreting cells (muco-)
squamous cells (-epidermoid)
lymphoid infiltrate often also present 3
  • low/intermediate or high grade
  • clear mucin-containing cells, which stain reddish pink with the mucicarmine stain
    80% MAML2: alteration that appears to be specific for mucoepidermoid carcinoma
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54
Q

Multiple myeloma
epidemiology

A

Multiple myeloma is a common malignancy in patients above 40
- 70% of cases are diagnosed between ages 50 and 70 with a median age of diagnosis being 70 years
- male predilection (M: F 2:1)
- Black populations are affected at nearly twice the rate as White populations 14.

55
Q

Multiple myeloma
complications

A

Fracture
Amyloidosis
recurrent infection sec. to leukopenia
plasmacytoma (solitary lesion in bone OR extramedullary) typically progress to MM

56
Q

Multiple myeloma

A

Monoclonal proliferation of MALIGNANT PLASMA cells
Produce immunoglobulin (commonly IgG)
Infiltrate haemopoietic locations (red marrow)

  • renal failure common
  • obstructive casts form in tubules (BJP, Ig,albumin, tamm-horsfall proteins)
    direct nephrotoxicity to renal tubules BJP
    high calc, dehydration, hyperuricemia and urate nephropathy
    amyloidosis AL type
57
Q

WHO CNS layerd report structure

A

Integrated diagnosis (combined tissue-based histological and
molecular diagnosis)
Histological diagnosis
CNS WHO grade
Molecular information (listed)

e.g.
Diffuse low-grade glioma, MAPK pathway-altered
Subtype: Diffuse low-grade glioma, FGFR1 TKD-duplicated
Histopathological classification: Oligodendroglioma
CNS WHO grade: Not assigned
Molecular information Duplication of the FGFR1 tyrosine kinase domain (next-generation sequencing)

58
Q

Newly Recognized Tumor Types in the 2021 WHO Classification of Tumors of the Central Nervous System

A

Newly Recognized Tumor Types
Diffuse astrocytoma, MYB- or MYBL1-altered
Polymorphous low-grade neuroepithelial tumor of the young
Diffuse low-grade glioma, MAPK pathway-altered
Diffuse hemispheric glioma, H3 G34-mutant
Diffuse pediatric-type high-grade glioma, H3-wildtype and IDH-wildtype
Infant-type hemispheric glioma
High-grade astrocytoma with piloid features
Diffuse glioneuronal tumor with oligodendroglioma-like features and nuclear clusters (provisional type)
Myxoid glioneuronal tumor
Multinodular and vacuolating neuronal tumor
Supratentorial ependymoma, YAP1 fusion-positive
Posterior fossa ependymoma, group PFA
Posterior fossa ependymoma, group PFB
Spinal ependymoma, MYCN-amplified
Cribriform neuroepithelial tumor (provisional type)
CNS neuroblastoma, FOXR2-activated
CNS tumor with BCOR internal tandem duplication
Desmoplastic myxoid tumor of the pineal region, SMARCB1-mutant
Intracranial mesenchymal tumor, FET-CREB fusion positive (provisional type)
CIC-rearranged sarcoma
Primary intracranial sarcoma, DICER1-mutant
Pituitary blastoma

59
Q

Meningiomas 15 subtypes

A

emphasized that the criteria defining atypical or anaplastic (ie, grade 2 and 3) meningioma should be
applied regardless of the underlying subtype.

60
Q
A

chordoid and clear cell meningioma are
noted to have a higher likelihood of recurrence than the
average CNS WHO grade 1 meningioma and have hence
been assigned to CNS WHO grade 2

61
Q

chordoid and clear cell meningioma

A

chordoid and clear cell meningioma are
noted to have a higher likelihood of recurrence than the
average CNS WHO grade 1 meningioma and have hence
been assigned to CNS WHO grade 2

62
Q

rhabdoid and papillary meningioma historically…

A

historically,
rhabdoid and papillary morphology qualified for CNS
WHO grade 3 irrespective of any other indications for malignancy.

63
Q
A

SMARCE1 (clear cell subtype),
BAP1 (rhabdoid and papillary subtypes), and KLF4/TRAF7
(secretory subtype) mutations, TERT promoter mutation and/or homozygous deletion of CDKN2A/B (CNS WHO grade 3), H3K27me3 loss of nuclear expression (potentially worse prognosis), and methylome profiling64
(prognostic subtyping).

64
Q

Medulloblastomas

A

4 principal molecular groups:
WNT-activated,
sonic hedgehog (SHH)-activated (SSH1 or SSH 2 poor prognosis)
TP53 status Wild or mutant

4 subgroups of SHH and 8 subgroups of

medulloblastoma, WNT-activated
medulloblastoma, SHH-activated and TP53-wildtype
medulloblastoma, SHH-activated and TP53-mutant
medulloblastoma, non-WNT/non-SHH
65
Q

Ependymomas classification

A

Histopathological
Molecular
Anatomical site
posterior fossa (60%)
supratentorial (30%) (children)
spinal cord (10%)

  • supertentorial - ZFTA (BAD), YAP1 (GOOD); GFAP almost always +ve; EMA , S100 and vermentin +ve, OLIG2 negative
  • posterior fossa - Group A (good) /B (bad)
  • spinal NOS or MYCN amplification (aggressive), (most common spinal tumour in adults, asso NF2) Myxopapillary

-myxopapillary ependymoma is now
considered CNS WHO grade 2, high recurrence

66
Q

Benign salivary tumours

A

epithelial
pleomorphic adenoma: this is the most
common (≈50%) tumor of the parotid
Warthin tumor: essentially only found in the parotid, in older, usually male patients; it is bilateral in 10-15%
intraductal papilloma of salivary glands
oncocytoma of salivary glands
myoepithelioma: until recently considered a
subtype of pleomorphic adenoma; they can
also originate in breast and bronchus

non-epithelial
hemangioma
lymphangioma
lipoma

67
Q

Malignantsalivary tumours

A

Malignant

mucoepidermoid carcinoma: most of the malignant lesions*

adenoid cystic carcinoma
myoepithelioma
adenocarcinoma (not otherwise specified)
acinic cell carcinoma of salivary glands
squamous cell carcinoma of salivary glands
lymphoepithelial carcinoma
malignant mixed tumors of the salivary glands
carcinoma ex pleomorphic adenoma
carcinosarcoma (true mixed tumor of the salivary glands)

metastasizing pleomorphic adenoma
salivary duct carcinoma

metastases (mostly to intraparotid lymph nodes)
cutaneous squamous cell carcinoma
malignant melanoma
testicular seminoma (rare)
lymphoma (rare)
primary: arising from the parotid gland as a MALToma 6
secondary: involving the intraparotid lymph nodes

68
Q

maligannt salivary gland ca classification

A

Malignant

mucoepidermoid carcinoma: most of the malignant lesions
adenoid cystic carcinoma
myoepithelioma
adenocarcinoma (not otherwise specified)
acinic cell carcinoma of salivary glands
squamous cell carcinoma of salivary glands
lymphoepithelial carcinoma
malignant mixed tumors of the salivary glands
    carcinoma ex pleomorphic adenoma
    carcinosarcoma (true mixed tumor of the salivary glands)
    metastasizing pleomorphic adenoma
salivary duct carcinoma 7
metastases (mostly to intraparotid lymph nodes) 
    cutaneous squamous cell carcinoma
    malignant melanoma
    testicular seminoma (rare)  
lymphoma (rare)
    primary: arising from the parotid gland as a MALToma 
    secondary: involving the intraparotid lymph nodes
69
Q

tumors of the salivary gland
Warthin tumor

A

Warthin tumors are the 2nd most common benign parotid tumor (after pleomorphic adenoma)

Lymphomatous papillary cystadenomas
benign
lymphoid origin
most commonly arise from the parotid tail.
bilateral or multifocal in up to 20% of cases
most common neoplastic cause of multiple solid parotid masses.
typically 6th decade, Men 2.2 vs 1
Associated with smoking and radiation
1% transformation

70
Q

Adenoid cystic carcinomas

A

rare histological subtype of adenocarcinoma.
NOTABLE TENDENCY FOR PERINEURAL SPREAD
generally low grade

71
Q

perineural tumour is most commonly associated with…

A

Perineural tumor spread is more frequently associated with 1,2,5:

mucosal/cutaneous squamous cell carcinoma
    oral cavity/laryngeal (2-30%) > cutaneous (3-8%)
    most common overall 5
salivary gland carcinoma
    adenoid cystic carcinoma (highest incidence per individual tumor 5)
    mucoepidermoid carcinoma
mucosal/cutaneous basal cell carcinoma (2-5% demonstrate perineural tumor spread) 4
melanoma 
    0.8 - 2.6% demonstrate perineural spread8 
        65% are desmoplastic subtype 
lymphoma
sarcoma
meningioma (rare) 6
72
Q

Pleomorphic adenomas of the salivary glands, also known as benign mixed tumors (see below), are the most common salivary gland tumors

A

70-80% of benign salivary gland tumors
females than males (2:1)
ill defined margins, can locally recur
large size risk for maligancy

73
Q

GBM

A

Glioblastomas have been defined as diffuse astrocytic tumors in adults that MUST** be IDH-wildtype

Now an entirely separate diagnosis from astrocytoma, IDH-mutant grade 2, 3 or 4

Primary GBM are largely wild type
Secondary GBM now equates to astrocytoma IDH MUTANT

Histology variants
giant cell glioblastoma
gliosarcoma
epithelioid glioblastoma

74
Q

GBM immunophenotyping

A

GFAP: positive but of variable intensity
S100: positive
nestin: positive
p53 protein: positive if TP53 mutated
EGFR: positive in 40-98% of cases 16

IDH-1 R132H: negative (by definition, otherwise not an IDH-wildtype glioblastoma, but rather an astrocytoma, IDH-mutant WHO CNS grade 4) 16

H3 K27M mutation: negative (if positive then diffuse midline glioma H3 K27-altered)
75
Q

GBM genetics

A

EGFR gene amplification

TERT promoter mutations

combined gain of whole chromosome 7, loss of chromosome 10 [+7/-10]

alterations of the CDK4/6–RB1 cell-cycle pathway: 80% due to deletions of CDKN2A

76
Q

Prognosis GBM 6 factors

A

Despite all of this, even in the best-case scenario, glioblastoma carries a poor prognosis with a median survival of <2 years 15.

Negative prognostic factors include:

increased necrosis 
greater enhancement 
deep location (e.g. thalamus)
MGMT not-methylated
increased age
lower pre-diagnosis functional status (e.g. ECOG performance status)
77
Q

terminology CNS WHO grading

A

Arabic numbers
Grading
emphasize molecular markers in grading
Essential and desirable diagnostic criteria
NOS
NEC not elsewhere classified -fully characterised but not fitting in established classification system
Dropping variant and anaplastic

78
Q

Pediatric-type diffuse low vs high-grade gliomas

A

Pediatric-type diffuse low-grade gliomas

  • diffuse astrocytoma, MYB- or MYBL1-altered
  • angiocentric glioma
  • polymorphous low-grade neuroepithelial tumor of the young
  • diffuse low-grade glioma, MAPK pathway-altered

Pediatric-type diffuse high-grade gliomas
- diffuse midline glioma, H3 K27-altered
- diffuse hemispheric glioma, H3 G34-mutant
- diffuse pediatric-type high-grade glioma, H3-wildtype and IDH-wildtype
- infant-type hemispheric glioma

79
Q

Adult-type diffuse gliomas
the importance of IDH and 1p19q codeletion

A

Adult-type diffuse gliomas
- astrocytoma, IDH-mutant
- oligodendroglioma, IDH-mutant, and 1p/19q-codeleted
- glioblastoma, IDH-wildtype

IDH positive + 1p19q codeletion = oligodendroglioma = BETTER prognosis
IDH positive + no 1p19q codeletion = astrocytoma

When diffuse adult gliomas have non-mutated IDH (i.e. “wild-type”), the status of 1p19q is of uncertain clinical significance and the tumor is considered to be not elsewhere classified (NEC) 6,7.

Similarly, if deletion is partial (e.g. 1p loss with 19q retention), then tumors should also be considered NEC

IDH-wildtype = IDH negative = no mutation = poor prognosis
IDH-mutant = IDH positive = mutation present = better prognosis
80
Q

IDH

A

In most instances, IDH status is obtained by performing immunohistochemistry on surgical biopsy specimens. The majority (90%) of IDH mutations in gliomas affect IDH1 with a single amino acid missense mutation at arginine(R)132 replaced by histidine (H); thus denoted as IDH1 R132H. This is the mutation generally tested by immunohistochemistry

IDH-wildtype (negative)
As of the 5th edition (2021) of the WHO classification, all glioblastomas are now, by definition, IDH-wildtype

81
Q

Syndromes associated with IDH Isocitrate dehydrogenase gene mutation

A

enchondromatosis syndromes: Ollier disease and Maffucci syndrome

82
Q

Pilocytic astrocytoma

A

WHO grade 1
75% in first 2 decades, M=F
Most common primary brain tumor of childhood
Strong association with NF1 (optic pathway glimas)
60 % PF ; 30% Optic pathway >brainstem and spine
supratentorial in adults,

83
Q

Pilocytic astrocytoma immunophenotyping

A

GFAP: positive
S100: positive
OLIG2: positive
IDH R132H mutation: negative
p53 protein: negative or weak

Pilocytic astrocytoma, as well as pleomorphic xanthoastrocytomas, frequently have BRAF alterations (present in ~70% of cases). Importantly they, along with other pediatric low-grade gliomas, lack IDH mutations and TP53 mutations

84
Q

Pilocytic astrocytoma prognosis

A

10 yr survival >95%

85
Q

High grade astrocytoma with piloid features

A
  • middle age and elderly
  • NF1 association
  • **Defined by characteristic DNA methylation profile
  • Prognosis similar to GBM

Other molecular characteristics, common alteration
NF1
BRAF
FGFR1
CDKN2A/B deletion
ATRX (mutations or loss)a
MGMT promoter methylation

86
Q

GBM molecular profiling

A

IDH status - IDH stands for “Isocitrate Dehydrogenase.” This is an enzyme involved in the production of energy by brain tumour cells, and in GBM it may have a mutation which confers a better prognosis. Research has indicated that different forms of GBMs have differences between these enzymes, though their role in tumour initiation (how a tumour first begins) and tumour growth is still being explored. As part of this research, a number of drugs that can potentially influence IDH enzymes are being investigated.

IDH ‘wild’ type status - This occurs in about 90% of GBM brain tumours and usually indicates that the tumour formed as glioblastoma since the very beginning (primary GBM) and carries a worse prognosis than those classified as being IDH mutant.

IDH mutant - This represents approximately 10% of GBMs, and indicates a secondary glioblastoma tumour, meaning that it was previously a lower grade glioma and carries a better prognosis than a ‘wild’ type status.

IDH NOS - This stands for “Not Otherwise Specified”, meaning that in rare cases, it cannot be determined whether a GBM is ‘wild’ type or mutant for IDH.

MGMT methylation - This is short for O6-methylguanine-DNA methyltransferase and whether it is ‘methylated’ or ‘unmethylated’ indicates how effectively the tumour cells can repair the damage inflicted on them by certain chemotherapy drugs, such as Temozolomide. Patients with higher levels of MGMT methylation respond better to Temozolomide treatment. Methylation means the transfer of a methyl group (CH3) from one molecule to another, which affects the way the tumour behaves.

1p/19q deletion - The word “deletion” refers to the fact that when you look at one of the chromosomes, the genes at positions 1p and 19q are missing. Tumours with a 1p/19q deletion may respond better to certain chemotherapy drugs such as Temozolomide or Carmustine, than other tumours without the deletion.

87
Q

GBM molecular profiling

IDH wild vs mutant vs NOS

A

IDH ‘wild’ type status - This occurs in about 90% of GBM brain tumours and usually indicates that the tumour formed as glioblastoma since the very beginning (primary GBM) and carries a worse prognosis than those classified as being IDH mutant.

IDH mutant - This represents approximately 10% of GBMs, and indicates a secondary glioblastoma tumour, meaning that it was previously a lower grade glioma and carries a better prognosis than a ‘wild’ type status.

NOS- cant be determined

88
Q

GBM MGMT

A

MGMT methylation - This is short for O6-methylguanine-DNA methyltransferase and whether it is ‘methylated’ or ‘unmethylated’ indicates how effectively the tumour cells can repair the damage inflicted on them by certain chemotherapy drugs, such as Temozolomide. Patients with higher levels of MGMT methylation respond better to Temozolomide treatment. Methylation means the transfer of a methyl group (CH3) from one molecule to another, which affects the way the tumour behaves.

1p/19q deletion - The word “deletion” refers to the fact that when you look at one of the chromosomes, the genes at positions 1p and 19q are missing. Tumours with a 1p/19q deletion may respond better to certain chemotherapy drugs such as Temozolomide or Carmustine, than other tumours without the deletion.

89
Q

GBM 1p19q

A

1p/19q deletion - The word “deletion” refers to the fact that when you look at one of the chromosomes, the genes at positions 1p and 19q are missing. Tumours with a 1p/19q deletion may respond better to certain chemotherapy drugs such as Temozolomide or Carmustine, than other tumours without the deletion.

90
Q

Ganglioglioma

A

Usually WHO grade 1/2. 955
Anaplastic grade 3

BRAF V600E mutation 10-60% (not specific)
p53 mutation (not specific)

RFx
NF1 TUBEROUS SCLEROSIS

91
Q

Small round blue cell tumours

A

A number of tumours share similar histology, composed of relatively uniform primitive small round blue cells. They also share many demographic, radiographic and clinical similarities. They include:

Ewing sarcoma

peripheral primitive neuroectodermal tumour (pPNET)

Askin tumour

neuroblastoma

Wilms tumour

hepatoblastoma

embryonal rhabdomyosarcoma

medulloblastoma

pineoblastoma

retinoblastoma

embryonal tumour with multilayered rosettes, which was formerly known as CNS primitive neuroectodermal tumour (CNS-PNET)

neuroepithelioma

desmoplastic small round cell tumour

small cell mesothelioma

acute leukaemia

92
Q

Most common bladder cancer is

A

Urothelial carcinoma 90%

93
Q

bladder cancer more common in male or female?

A

Male

94
Q

Bladder SCC is common in what population?

A

Schistosomiasis endemic regions

95
Q

Bladder cancer risk factors

A

Cigarette smoking, occupational carcinogens schistosomiasis
9p9q deletion and TP53 mutations

96
Q

Inverted urothelial papilloma is benign or malignant

A

Entirely benign

97
Q

Non-invasive papillary urothelial neoplasms classification (increase risk of cancer)

A

Papilloma
Papilloma urothelial neoplasm of low grade potential
Low grade papillary urothelial
High grade papillary urothelial carcinoma carcinoma

98
Q

Stages of syphilis

A
99
Q

What stains distinguish Paget disease of the vulva (intradermal proliferation of epithelial malignancy) to melanoma

A

Positive staining for PAS periodic acid Schiff in Paget.

100
Q

Vulva ca. Features Old people vs young

A

Young

Middle age
HPV 16 18
Smoker
Often from precancerous VIN, leukoplakia
HPV forms multifocal and warty

Old people
HPV neg (well differentiated keritanising SCC, uniformed
From Lichen sclerosis or inflammatory disease

101
Q

Vaginal clear cell adenocarcinoma
RFx

A

Diethylstilbestrol during pregnancy
Vaginal adenosis a precursor to clear cell adenocarcinoma

102
Q

Cervical ca. What genetic mutation may have a role

A

LKBI gene
First identitfied in peutz jegher

Cervizlx everts at adolescents
Columnar cells exposed in transitional zone.
Undergo squamous metaplasia
CIN 1 low grade LSIL
2&3 high grade HSIL

103
Q

Cervical ca risk factors

A

HPV (16/18/31/33)
Vaccine protection 16/18
Early age at first sexual intercourse multiple Partners with multiple partners
Smoking
Immunodeficiency
HPV express E6 and E7 proteins inactivating TP53 and Rb tumour suppressor gene
Loss of LKB1 gene 20%
Mets risk 1% under 3mm vs 10+% greater than 3mm

104
Q

Differential Diagnosis - primary lung vs Metastatic adenocarcinoma

colon
breast
thyroid
prostate

A

Differential Diagnosis
❚ Metastatic adenocarcinoma
● Presentation with multiple lung masses favors
metastasis
● Metastatic colonic adenocarcinoma is typically CK7
negative and CK20 positive
● CDX2 is positive in mucinous BAC and
gastrointestinal lesions
● Estrogen and progesterone receptors and gross cystic
disease fluid protein-15 are often positive in breast
carcinomas
● Prostate-specific antigen, prostatic acid phosphatase
are positive in metastatic prostate carcinoma
● TTF-1 is positive in primary lung and metastatic
thyroid carcinoma; thyroglobulin is positive in the
latter, and mucin staining is positive in the former

105
Q

Lung adeno which pattern is associated with the worst prognosis

A

Micropapillary pattern is associated with poorer
prognosis

106
Q

lung adenocarcinoma major histological patterns

A

acinar pattern
papillary pattern
bronchioalveolar pattern
solid pattern
well differentiated fetal adenocarcinoma WDFA
mucinous adenocarcinoma
mucinous cystoadenocarcinoma
signet ring adenocarcinoma
clear cell adenocarcinoma

lung adeno CK7 +ve!! CK20 -ve, TTF1+ve
bronchiolalveolar carcinoma (BAC) is CK7 +ve!! CK20 -ve, TTF1-ve

107
Q

SCLC

A

●Deletion of chromosome 3p is a consistent finding in SCLC, and this region may include the fragile
histidine triad gene (FHIT) located at 3p14.2
● About 20% of SCLCs show mutations in the Rb gene
● About 70% to 95% of SCLCs show Bcl-2 expression
● SCLC shows the highest rate of p53 mutation of all
lung carcinomas, and consequently a strong nuclear
p53 staining pattern in greater than 10% to 20%
percent of cells is strongly suggestive of a p53 mutation

108
Q

Malignant Mesothelioma
Three histologic categories

A

Three histologic categories: epithelioid70% , sarcomatoid,
and biphasic
● Rare tumor showing a male predominance and an
association with asbestos exposure
● Most patients are between 50 and 70 years old
● Associated with a poor prognosis, with average
survival of less than 1 year
Positive for keratin AE1/AE3, CAM5.2, and CK7;
specific markers include calretinin, CK5/6, WT-1,
D2-40
Other Techniques for Diagnosis
● Inactivation of the CDKN2A/ARF locus at 9p21,
which codes for the tumor suppressor genes
p16INK4a and p14ARF, is a common finding
Calretinin stains both nucleus and cytoplasm with
stronger nuclear staining, which is a helpful feature
of mesothelial cells
● Invasion is the best indication of malignant
mesothelioma
● Patients with purely epithelioid mesothelioma show
the longest survival, whereas the shortest survival
occurs with sarcomatoid histology—yet the difference
between the two survival rates is only a matter of
months

109
Q

Lymphoma markers

A

Lymphoma
● Positive for leukocyte common antigen (LCA) and
other lymphoid markers (e.g., CD3 (T-CELLSs), CD20 (B-cells), CD30) and
negative for cytokeratin

110
Q

Hodgkin’s lymphoma

A

Woman 20s-30s
anterior mediastinal mass most common
nodular sclerosing variant most common
type- best determined by nodal analysis (some Dx features may not be present on extranodal sites)
Classic Reed-Sternberg cells in a background
consistent with Hodgkin lymphoma are needed to
establish a new diagnosis of Hodgkin lymphoma
in an extranodal site
can be cystic (degeneration)
MOST COMMON type of lymphoid malignancy. 2nd on e is DLBCL

111
Q

DLBCL

A

F>M
peak 20-40s

typically anterior mediastinum , usually invovles thymus
complication SVC obstruction

CD19, CD20, CD22, and CD45 positive
● CD10, CD5, CD43, CD21, and immunoglobulin
negative (resembling the phenotype of normal thymic
B cells)
● Negative for CD15
● Significant percentage of these cases can be CD30
positive
● Sclerosis and necrosis are common findings
● Good response to multiagent chemotherapy with
consolidation radiation therapy
● Almost always B-cell lineage
Positive for CD20; negative for TdT, CD99, CD1a

112
Q

castleman disease
aka angiofollicular lymph node hyperplasia

A

M=F, wide age range
3 types - hayline vascular (80), plasma cells, mixed
hepatosplenomegaly, pancytooenia
1/3 have other malignancies
more frequent in HIV
ASSOCIATED WITH HHV8!!!

113
Q

cd45

A

lymphoma, cd45 is a leukocyte common antigen

114
Q

gastric adenocarcinoma vs adenocarcinoma associated with barrett oesophagus

A

Gastric cardia adenocarcinoma
● May be identical to Barrett esophagus–associated
adenocarcinoma
● Staining for CK7 and CK20 can help distinguish Barrett esophagus–related adenocarcinoma (CK7 positive; CK20 negative) from gastric adenocarcinoma

115
Q

Adenocarcinoma Associated with
Barrett Esophagus prognosis

A

● Overall prognosis is dismal for invasive adenocarcinoma (75% 5-year survival); prognosis is better for small, well-differentiated adenocarcinoma with
fewer than four positive nodes

116
Q

Helicobacter pylori–Associated Gastritis
(Chronic Gastritis)

A

Most asymptomatic, some have peptic ulcer sx.
diffuse antral gastritis commonly in whites
multifocal atrophic gastritis - more in blacks, Asians, Hispanic and Scandinavians
strongly associated with duodenal and gastric ulcers
> MALT or gastric adenocarcinoma
Gram neg spiral rods

117
Q

Gastric adenocarcinoma
Single best predictor of survival is

A

Single best predictor of survival is depth of
invasion; survival is 95% for tumors confined to the submucosa but drops to 50% with involvement through the muscularis propria to the subserosa (T3); T2 lesions have intermediate survival

118
Q

gastric lymphoma
most common form is …
what age group
Hpylori infection?

A

DLBCL
many gastric lymphomas derived from MALT
50s-60s
Hpylori involved in 92+%
treatment of H pylori - regression of 77% early lesion

119
Q

gastric MALT prognosis

A

excellent if confined to stomach

120
Q

small bowel carcinoid
distribution
types
age
metastatic risk

A

distribution - Most gastrointestinal carcinoid tumors occur in the vermiform appendix, followed by the small intestine (typically ileum), rectum, stomach, and colon

1% duodenal, 7% jejunal, 80%
ileal, and 10% rectal

● Most patients are 50 to 70 years old

types - hormone antibodies
— Serotonin
— Somatostatin
— Gastrin
— VIP
— ACTH
— Insulin
— chromogranin, synaptophysin +ve

Cytokeratin positive in 65% to 70% of cases

metastatic risk
● All carcinoids are potentially malignant
● Risk for metastasis increases with tumor size
— Less than 1 cm: 2%
— One to 2 cm: 50% (ileal)

121
Q

— Carcinoid syndrome

A

— Carcinoid syndrome
◆ Occurs in 10% of patients; more common in
patients with an ileal carcinoid tumor
◆ Usually indicates hepatic metastasis
(precluding hepatic degradation of vasoactive
amines)
◆ Symptoms include flushing, sweating, cardiac
symptoms, and diarrhea
◆ About 50% of patients have endocardial right
heart lesion
◆ Symptoms arise because of increased levels of
5-HT and 5-HIAA

122
Q

Insulinoma

A

— May also be associated with MEN-I syndrome and
hypoglycemia
— Usually benign behavior

123
Q

Gastrinoma

A

Gastrinoma
— Often multiple, but typically small
— Associated with Zollinger-Ellison syndrome and
MEN-I syndrome
— Usually malignant behavior

124
Q

colonic polyps
which has the highest risk in developing a malignant lesion

A

Clinically the important distinctions are size, villous component, and presence of high-grade dysplasia or carcinoma

  • colonic adenoma
  • villous architecture
  • presence of high grade dysplasia

Other subtypes
Hyperplastic polyp, most common, asymptomatic, M>F
inflammatory -IBD, trauma etc
adenoma
- tubular most common, 70%, pedunculated
-tubulovillous -larger than tubular
- villous - sessile, flat, broad, small pedicle

<1cm 1% cancer
>2cm, 45% harbor cancer

Carcinoma cells that infiltrate into the muscularis mucosae or lamina propria alone (intramucosal adenocarcinoma) have virtually no risk for metastasis; many advocate classifying these lesions as high-grade dysplasia

Only when the carcinoma cells infiltrate through the muscularis mucosae into the submucosa or beyond are they considered invasive (and
clinically significant)

Pathology report should include
— Highest degree of dysplasia present in the biopsy specimen and presence of villous component
— Degree of differentiation and distance from the margin, if invasive carcinoma is present, as well as the presence or absence of vascular and lymphatic invasion

125
Q

WHO lung nomenclature

A

adenocarcinoma, Squamous cc, adenocarcinoma with lepidic patten
NSCC - favoured adeno/squamous/spindle and/or giant cells
Small cells
NSCC with neuroendocrine morphology, positive neuroendocrine marker, possible large cell nuroendocrine ca

126
Q

WHO 2021 lung
bronchial adenoma/ciliated micronodular papillary tumor

A

bronchial adenoma/ciliated micronodular papillary tumor
benign, peripheral
GGO, some with cavitation
middle age to elderly, median 72yrs, M=F
TTF1 stain and P40

127
Q

thoracic SMARCA4 deficient undifferentiated tumour (WHO 2021 lung)

A

thoracic SMARCA4 deficient undifferentiated tumor
median age 39-59
MF 9:1
rapid progressive tumors
mediastinum>pul hilum, pleura with/out chest wall
often multiple sites and metastatic 77-83%
tumor diameter - large 3-21cm
TP53 mutation 60%

128
Q

lung biopsies - tissue preservation

A

divide cores - 2 tissue block
IHC based on morphology
dual stain
(TTF-1/p40)
p40 (nuclear)/Napsin (cytoplasmic)
CK5/TTF-1

neuroendocrine markers only if morphology indicates
if ordering stains - get unstained - beware of short shelf life of unstained slides

129
Q

WHO 2021 new terminology
Spread through airspace (STAS)

A

tumour cells within airspaces beyond the (MAIN) edge of the main tumor
present in 15-56% NSCLC
patterns: micropapillary structures, solid tumor cell nests, discohesive single tumor cells
should NOT be included in tumor size.
e.g. speculations
occurs in adeno, SQCC, neuroendocrine (all subtype), pleomorphic
increase risk of recurrence or OS
sublobar resection > may indicate further resection/lobectomy

130
Q

WHO bone classification 2020.
Osteosarcoma subtypes

A

OSTEOSARCOMA (NOS) majority
- small
- telangiectatic
- conventional COS

SECONDARY osteosarcomas subtypes
In the latest classification, secondary osteosarcoma is divided
into six subtypes: [4]
a) Osteosarcoma in Paget’s disease of bone, (poorer prognosis)
b) Radiation-induced osteosarcoma (poorer prognosis)
c) Infarct related osteosarcoma
d) Chronic osteomyelitis related
e) Implant-related osteosarcoma
f) Osteosarcoma secondary to fibrous dysplasia.

The prognosis of secondary osteosarcoma occurring as a
result of Paget’s disease of bone and radiation treatment is
poorer than COS.

The previous classification included secondary osteosarcoma in the conventional osteosarcoma (COS) subtype, but now, the recent classification has described it in a separate category. Now osteosarcoma not otherwise specified (NOS) includes only three subtypes: COS, telangiectatic osteosarcoma, and small cell osteosarcoma. COS accounts for the majority of osteosarcoma [Figure 5]. Osteosarcoma NOS can also be subdivided into different types based on the dominant matrix: Osteoblastic, chondroblastic, and fibroblastic;

However, this subdivision has no role in predicting
prognosis. COS and telangiectatic osteosarcoma are more
commonly encountered in the metaphyseal region of long
bones whereas small cell osteosarcoma is predominantly seen in the diaphysis. Recent classification has also removed Clear cell and chondroblastoma-like osteosarcoma subtypes from the osteogenic tumors.[4]

131
Q

GCT specific marker

A

H3F3A 92%

132
Q

ABC

A

USP6

133
Q

Melanoma AJCC8
Prognosis are based on

A

Breslow thickness to the nearest 0.1mm
T1 0.8 vs 0.8-1.0 mm
T2 1-2
T3 2-4mm
T4 >4 mm

Presence of Ulceration

Mitotic index 1mitosis/mm2 vs >1mit/mm2

LDH elevation/no elevation

Node
Clinical vs path (pN0 is better than cN0)
Regional lymph nodes represent the most common first site of metastasis in patients with primary melanoma.

Metastasis status
M1a distal node
M1b lung
M1c viscera
M1d CNS

Tumor markers (3 decks)

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