oncology Flashcards

(63 cards)

1
Q

is a growth of tissue that exceeds that of normal tissue
and is not coordinated with it.

A

tumor, or neoplasm,

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2
Q

is a term that includes all malignant tumors.

A

Cancer

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3
Q

is the study of cancer at the molecular level, using
techniques that allow the direct detection of genetic alterations, down to
single-base-pair changes.

A

Molecular Oncology

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4
Q

Cancer is generally divided into two broad groups:

A

Solid tumors
Hematological malignancies

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5
Q

tumor in

Carcinomas-
Sarcomas-
Teratocarcinomas
Benign tumors

A

Carcinomas- epithelial

Sarcomas-bone, cartilage, muscle, blood vessels, fat

Teratocarcinomas consist of multiple cell types.

Benign tumors are named by adding the suffi x - oma to the tissue of origin.

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6
Q

Adenoma is a benign glandular growth.

A

Adenoma is a benign glandular growth.

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7
Q

is the movement of dislodged tumor cells from the original
(primary) site to other locations. O

A

Metastasis

only malignant tumors are metastatic.

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8
Q

Tumors arising from white blood cells are referred to as

A

leukemias and
lymphomas.

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8
Q

is a neoplastic disease of blood-forming tissue in which large
numbers of white blood cells populate the bone marrow and peripheral blood.

A

Leukemia

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9
Q

is a neoplasm of lymphocytes that forms discrete tissue masses.

A

Lymphoma

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10
Q

Cancer is caused by

A

nonlethal
mutations in DNA.

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11
Q

cancer affects mutation of

A

The mutations affect two types
of genes:
Oncogenes
Tumor-suppressor genes.

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12
Q

regulate normal cell growth, division, and survival.

A

oncogenes

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13
Q

can contribute to the development of cancer by promoting abnormal cell
growth and proliferation.

A

oncogenes.

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14
Q

include factors that control transcription, or the translation
of genes required for cell division.

A

Tumor suppressors

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15
Q

They also participate in repairing DNA damage and in promoting apoptosis.

A

TUMOR SUPPRESSORS

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16
Q

Tumor suppressors slow down or stop cell division by counteracting the
movement of the cell from

A

G1 to S or G2 to M phase.

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17
Q

Prevents the cell from entering the S phase if DNA is
damaged.

A

G1 checkpoint:

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18
Q

Stops the cell from entering M phase if DNA is not correctly
replicated.

A

G2 checkpoint:

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19
Q

overexpression of ____ is a predictor of a more aggressive growth and metastasis
of the tumor cells.

A

overexpression of HER2/neu is a predictor of a more aggressive growth and metastasis
of the tumor cells.

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20
Q

is indicated presently for women with HER2/neu -positive
(HER2/neu-overexpressed) breast cancer.

A

Herceptin therapy

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21
Q

using monoclonal and polyclonal antibodies to detect
the HER2/ neu protein.

A

Immunohistochemistry (IHC)

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22
Q

directly detects increased copy numbers of
the HER2/neu gene in DNA likely responsible for the increased protein. Data are
reported as a ratio of the number of HER2 signals to chromosome 17 centromere
signals.

A

Fluorescent in situ hybridization (FISH)-

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23
Q

belongs to a family of receptor tyrosine kinases (RTKs) that are essential
for regulating cell proliferation, survival, and differentiation.

A

Epidermal Growth Factor Receptor, EGFR (7p12)

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24
its binding triggers the release of intracellular signaling cascades, including
egfr
25
mutations in the ____gene can lead to constitutive activation of ____signaling, promoting uncontrolled cell growth and survival characteristic of cancer cells.
EGFR (7p12) Epidermal Growth Factor Receptor,
26
mutations are commonly found in NSCLC, particularly in adenocarcinoma histology and in patients who are non-smokers or light smokers.
EGFR
27
The most common mutations are
small, in-frame deletions in exon 19 and a point mutation in exon 21 (L858R).
28
exon to
Exon 18: G719X (G719A, G719C, and G719S)- Point Mutations Exon 19: deletions and complex mutations Exon 20: S768I, T790M, Insertions Exon 21: L858R and L861Q - Point Mutations
29
These mutations lead to increased EGFR activity and are associated with sensitivity to EGFR tyrosine kinase inhibitors (TKIs).
EGFR Mutations in Lung Cancer:
30
Deletion of specific nucleotides in exon 19 of the EGFR gene.
EGFR deletions
31
Occurs in exon 21 of the EGFR gene, resulting in the substitution of a leucine (L) with an arginine (R) at position 858
L858R Point mutation
32
Substitution of a threonine (T) with a methionine (M) at position 790 in exon 20 of the EGFR gene.
T790M mutation
33
This is associated with acquired resistance to first-generation EGFR TKIs
T790M mutation
34
Involve the insertion of additional nucleotides into exon 20 of the EGFR gene.
Exon 20 insertions
35
inhibit the tyrosine kinase activity of EGFR.
EGFR TKIs, such as gefitinib, erlotinib, and afatinib,
36
competitively bind to the ATP-binding site of the EGFR kinase domain, preventing phosphorylation and downstream signaling.
EGFR TKIs:
37
also called massive parallel sequencing
Next Generation Sequencing (NGS)
38
designed to sequence large numbers of templates carrying millions of bases simultaneously, in a run that takes a few hours.
Next Generation Sequencing (NGS)
39
are both members of the RAS gene family, which encode proteins involved in cell signaling pathways that regulate cell growth and proliferation.
Kirsten Rat Sarcoma Viral Oncogene Homolog, K-ras (12p12); Neuroblastoma ras, N-ras (1p13) KRAS and NRAS
40
Mutations in these genes are commonly found in various cancers, including lung cancer, colorectal cancer, and pancreatic cancer.
KRAS and NRAS
41
Mutations in ___ lead to constitutive activation of downstream signaling pathways, such as the MAPK (Mitogen-Activated Protein Kinase) pathway, which promotes cell proliferation, survival, and tumor progression.
Mutations in KRAS lead to constitutive activation of downstream signaling pathways, such as the MAPK (Mitogen-Activated Protein Kinase) pathway, which promotes cell proliferation, survival, and tumor progression.
42
They are more prevalent in lung adenocarcinomas, particularly in patients with a history of smoking.
KRAS (Kirsten Rat Sarcoma viral oncogene homolog)
43
It is also involved in regulating cell growth and proliferation by activating downstream signaling pathways.
NRAS (Neuroblastoma RAS viral oncogene homolog)
44
significant in significant, particularly in melanoma - associated with more aggressive disease and resistance to targeted therapies.
NRAS (Neuroblastoma RAS viral oncogene homolog)
45
is a proto-oncogene that encodes a protein kinase involved in the RAS- RAF-MEK-ERK signaling pathway, also known as the MAPK pathway.
BRAF (v-Raf Murine Sarcoma Viral Oncogene Homolog B)
46
. This pathway regulates cell proliferation, survival, and differentiation.
MAPK pathway
47
Mutations in the _______gene can lead to constitutive activation of the B______resulting in dysregulated cell growth and proliferation characteristic of cancer cells.
Mutations in the BRAF gene can lead to constitutive activation of the BRAF protein kinase, resulting in dysregulated cell growth and proliferation characteristic of cancer cells.
48
a valine residue is substituted with glutamic acid at position 600 of the BRAF protein.
V600E mutation,
49
This mutation leads to hyperactivation of the BRAF protein kinase, resulting in sustained activation of the MAPK pathway and promotion of tumor growth.,
braf mutation
50
This test is an in vitro diagnostic test for the quantitation of BCR-ABL1 and ABL1 mRNA transcripts in peripheral blood specimens of diagnosed t(9;22) positive Chronic Myeloid Leukemia (CML).
BCR-ABL PCR TEST
51
In colorectal cancer, ______ is associated with a distinct subtype of tumors characterized by poor prognosis and resistance to conventional chemotherapy.
In colorectal cancer, BRAF V600E mutation is associated with a distinct subtype of tumors characterized by poor prognosis and resistance to conventional chemotherapy.
52
Targeted therapies, such as _________ have been developed specifically for patients with BRAF-mutant melanoma and have shown significant clinical benefits, including improved survival and tumor regression.
Targeted therapies, such as BRAF inhibitors (e.g., vemurafenib, dabrafenib) and MEK inhibitors (e.g., trametinib), have been developed specifically for patients with BRAF-mutant melanoma and have shown significant clinical benefits, including improved survival and tumor regression.
53
BRCA genes help repair DNA damage via
homologous recombination.
54
is a condition characterized by the accumulation of genetic errors within microsatellites.
Microsatellite instability (MSI)
55
arises from defects in the DNA mismatch repair (MMR) system
MSI
56
When the MMR system is impaired, errors in DNA replication are not properly repaired, leading to the accumulation of mutations and microsatellite instability.
MICROSATTELITE INSTABILITY (MSI)
57
often associated with specific clinicopathological features, including right-sided tumor location, mucinous histology, and a higher frequency in older patients.
often associated with specific clinicopathological features, including right-sided tumor location, mucinous histology, and a higher frequency in older patients.
58
MSI-H tumors
exhibit a high level of microsatellite instability
59
have stable microsatellites.
MSS tumors
60
MICROSATTELITE INSTABILITY (MSI) LAB DETECTION
PCR IDYLLA biocartis
61
gene encodes a protein involved in signaling pathways that regulate blood cell production and differentiation.
the Janus kinase 2 (JAK2) gene.
62
The JAK2 mutation assay is particularly important in the diagnosis and classification of .
MPN