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Neoplasia > Neoplasia IV > Flashcards

Neoplasia IV Flashcards

1
Q

carcinoma in situ invade beyond basement membrane. True/False

A

False.
All layers of the epithelium show features of neoplasia.
It does not invade beyond the basement membrane, therefore, any access to lymphatics or blood vessels

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2
Q

carcinoma in situ can metastasize. T/F

A

False.
– No metastatic potential at this stage but if not removed is “capable” of metastasis
– Cancers are curable at this stage

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3
Q

Why carcinoma in situ is called malignant if it does not metastasize?

A

They have potential to metastasize but are only physically limited not biologically limited

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4
Q

what is defined by a neoplastic change in epithelium which shows some of the microscopic features of malignancy but does not involve the full thickness of the epithelium, can progress to cancer

A

dysplasia

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5
Q

the architectural organization is preserved in dysplasia.True/False.

A

False.

disordered growth- loss of cellular uniformity and architectural organization

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6
Q

dysplasia necessarily will progress into malignancy. True/False

A

False.

Dysplasia doesn’t equate malignancy and dysplastic cells don’t necessarily progress to cancer

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7
Q

dysplasia is irreversible. True/False

A

False.
Removal of inciting stimulus from dysplastic epithelium can result in reversal to complete normalcy. When dysplastic changes are marked and involve the entire thickness of an epithelium –lesion considered pre-invasive neoplasm – carcinoma in situ.

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8
Q

when dysplastic changes are called precancerous?

A

. When dysplastic changes are marked and involve the entire thickness of an epithelium — lesion considered pre-invasive neoplasm — carcinoma in situ.

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9
Q

grade the dysplasia

A

– MILD
– MODERATE
– SEVERE

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10
Q

what is the term used for dysplasia in cytological preparations (abnormal nucleus) since there is no architecture?

A

DYSKARYOSIS

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11
Q

why dysplasia of cervix is called intraepithelial neoplasia?

A

In the cervix, the term intraepithelial neoplasia has been introduced to highlight the fact that dysplasia is neoplastic. If not treated always will progress to neoplasia, Detected on Pap smear.

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12
Q

describe cervical intraepithelial neoplasia (CIN) 1,2 and 3

A

o CIN1- mild dysplasia which shows disorderly maturation limited to the basal and parabasal layers
Upper 2/3 stratified
Basal 1/3 high nucleo-cytoplasmic ratio + pleomorphic ratio
o CIN2- moderate dysplasia
Superficial stratification
Cellular abnormalities extending up into basal 2/3
o CIN3- sever dysplasia + carcinoma in situ
atypical cells through the entire thickness of epithelium (carcinoma in situ)
may have 1 or 2 layers of stratified squamous epithelium (remainder: immature, large nuclei, mitoses)

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13
Q

CIN 3 is the same as carcinoma in situ.True/False

A

True.

Involve entire layer of epithelium

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14
Q

CIN 1 vs 2

A

Confined to the basal 1/3 of the epithelium vs confined to the basal 2/3 of the epithelium

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15
Q

what type of HPV is associated with CIN?

A

oncogenic types 16/18.

6/8 cause condyloma

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16
Q

SIL vs CIN

A

Both terms are used to describe changes in the cervix. However, they are used in different situations. “Squamous intraepithelial lesion (SIL) is used to describe Pap test results. “Squamous” refers to the type of cells that make up the tissue that covers the cervix. SIL is not a diagnosis of precancer or cancer. The Pap test is a screening test. It cannot tell exactly how severe the changes are in cervical cells. A cervical biopsy is needed to find out whether precancer or cancer actually is present.

Cervical intraepithelial lesion (CIN) is used to report cervical biopsy results. CIN describes the actual changes in cervical cells. CIN is graded as 1, 2, or 3. CIN 1 is used for mild (low-grade) changes in the cells that usually go away on their own without treatment. CIN 2 is used for moderate changes. CIN 3 is used for more severe (high-grade) changes. Moderate and high-grade changes can progress to cancer. For this reason, they may be described as “precancer

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17
Q

LSIL vs HSIL?

A

Low-grade SIL- 80% associated with a high risk of HPV
High-grade SIL – 100% associated with a high risk of HPV
differentiated by cytology

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18
Q

what is actinic keratosis

A

dysplastic lesion of skin squamous cells

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19
Q

what is the reason for screening for cancers?

A

to catch dysplasia (precancerous stage) before it becomes carcinoma or before clinical symptoms arise. The efficacy of screening requires a decrease in cancer-specific mortality.
Common screening methods:
• Pap smear
• Mammography
• PSA and digital rectal exam (PSA is not useful now, mainly used to assess treatment response**)
• Hemoccult test and colonoscopy

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20
Q

what are the hematological effects of cancers?

A

1) anemia
2) hypercoagulable state-thrombosis (DVT/PE)
3) polycythemia

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21
Q

what is the mechanism of anemia due to malignancy?

A

1)Iron deficiency anaemia (commonest)
– Blood loss
2)Megaloblastic anaemia
– Cytotoxic drugs interfering with DNA synthesis
3)Hypoplastic anaemia
– Marrow infiltration by tumour
– or chemotherapy destruction of haemopoietic cells
– or radiotherapy destruction of haemopoietic cells
4)Haemolytic anaemia
– Immune-mediated - the destruction of RBC’s
5) more importantly: AOCD (anaemia of chronic disease). Long-standing inflammatory state leads to increased production of hepcidin which interferes iron usage from storage

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22
Q

why megaloblastic anemia is seen with cancer?

A

some cytotoxic drugs interfering with DNA synthesis, the cell grows but does not divide-so megaloblasts

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23
Q

why malignancy increases the risk of clotting?

A 
-Tumour activates
    Clotting factors
    Platelets
    Endothelial cells
-Tumour inhibits
    Fibrinolysis
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24
Q

what is the Trousseau sign?

A

The Trousseau sign of malignancy or Trousseau’s syndrome is a medical sign involving episodes of vessel inflammation due to blood clots (thrombophlebitis) which are recurrent or appearing in different locations over time (thrombophlebitis migrans or migratory thrombophlebitis). Commonly seen with pancreatic cancer.

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25
Q

what is the mechanism or polycythemia due to cancer

A

some cancer (eg Renal cell carcinoma) produce erythropoietin which triggers RBC production

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26
Q

define ectopic hormone

A

A hormone is ectopic if it is produced by cells which do not normally produce that hormone

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27
Q

list some hormonal effects of malignancies

A
  1. Cushing’s Syndrome (ACTH)
  2. Excess ADH-SIADH: syndrome of inappropriate ADH production: hypoosmolar serum, hyperosmolar urine
  3. Gynaecomastia - Oestrogen
  4. Hypercalcemia- Squamous cell carcinoma lung
  5. Insulin XSS- Insulinomas of the pancreas
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28
Q

what is PTHrp

A

parathyroid hormone-related peptide produced by lung SCC leads to severe hypercalcemia (dehydration, QT prolongation—arrhythmia)
hypercalcemia can also occur due to bone osteolytic metastasis

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29
Q

list some paraneoplastic syndromes

A

1) Peripheral Neuropathy
2) Myopathy
3) Dermatomyositis (common with ovarian carcinoma)
4) Cerebellar Degeneration (small cell cancer)
5) P.U.O (Pyrexia of Unknown Origin)
6) Night sweats

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30
Q

what is the probable explanation of paraneoplastic syndromes?

A
  • The most likely cause is an immune or cytokine-mediated response.
  • E.g. anti cerebellar antibodies have been secreted by some tumors.
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31
Q

melanoma arise from what cells?

A

melanocytes (in basal layer of epidermis)

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32
Q

what is the ABCD of melanoma?

A
  • A- asymmetry
  • B – border irregular/bleeding
  • C – Colour
  • D – Diameter
  • E- Elevation/Evolution
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33
Q

melanoma can occur in the eye.True/False

A

True.

There are melanocytes in the retina

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34
Q

what is the most important risk factor for melanoma?

A

Sunlight (sun-exposed areas in which lightly pigmented are at more danger) – severe sunburns early in life a risk factor

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35
Q

what gene mutations predispose to melanoma?

A

10-15% are familial mutations (increase RAS and PI3K/AKT associated with sporadic melanomas. BRAF mutations occur in 40-50% of melanomas)

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36
Q

prognosis of melanoma depends on?

A

the thickness of the skin involved.
> 2mm -very poor prognosis (<0.76mm (98% cure).
Clarke’s level of invasion assesses level into different parts of the dermis.

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37
Q

schwannoma is a type of sarcoma. True False

A

True.

Malignant neoplasm arising from Schwann cells which cover nerve cells protecting them from losing action potential

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38
Q

what is the significance of Herpes Virus 8?

A

leads to Kaposi sarcoma in AIDS patients (purple nodules on the skin, in the GI tract)

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39
Q

what factors predispose to sarcoma development?

A 
–	Radiotherapy < 1% post-therapy. Mean latency 10 years
–	Chemicals
–	Herbicides
–	Pesticides
–	Asbestos
–	Genetic
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40
Q

what is the Li Fraumeni syndrome

A

cancers arising in different organs due to germline mutation of the P53 tumor suppressor gene. Li–Fraumeni syndrome is a rare, autosomal dominant, hereditary disorder that predisposes carriers to cancer. This syndrome is also known as the sarcoma, breast, leukemia and adrenal gland (SBLA) syndrome.

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41
Q

name 2 genetic causes of sarcomas.

A

– Li Fraumeni Syndrome - P53 germline DEFECT

– Von Recklinghausen disease 3% - neurofibrosarcomas (neurofibromatosis 1).

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42
Q

chemotherapy is the most important way to treat sarcomas. True/False.

A 
False. Weakly chemosensitive.
–	Wide local excision
–	Radiotherapy
–	+/- chemotherapy
–	Only a limited role for chemotherapy
–	Targeted Tx Imatinib for GIST
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43
Q

mutations in genes RAS and PI3K/AKT are associated with which cancer?

A

sporadic melanomas

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44
Q

sarcoma, breast, leukemia and adrenal gland (SBLA) syndrome, what is this?

A

Li–Fraumeni syndrome is a rare, autosomal dominant, hereditary disorder that predisposes carriers to cancer.
Due to germline mutation of the P53 tumor suppressor gene

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45
Q

what are neuroendocrine tumors?

A

Neoplasms with endocrine function and neural features

Tumors showing differentiation of neural cells and endocrine cells

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46
Q

name 2 highly and low aggressive neuroendocrine tumors

A
  • highly aggressive and lethal (Small cell carcinoma)

* low aggression (carcinoid tumor)

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47
Q

what is chromogranin?

A

tumor marker detected by immunohistochemistry, present in neuroendocrine tumors

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48
Q

other tumor markers:

1) vimentin
2) desmin
3) cytokeratin
4) neurofilaments
5) synaptophysin
6) S-100
7) TRAP
8) GFAP

A

1) mesenchymal cells (macrophage, fibroblast, endothelial cell-osteosarcoma, chondrosarcoma, liposarcoma, etc
2) smooth and skeletal muscle-rhabdomyosarcoma, leiomyosarcoma
3) epithelial cells-SCC, BCC
4) neurons-neuroblastoma, neuroendocrine tumors
5) neuroendocrine tumors
6) neural crest cells-schwannoma, melanoma, Langerhans cell histiocytosis
7) Hairy Cell leukemia
8) neuroglia-glioblastoma, astrocytoma

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49
Q

list few benign neuroendocrine tumors

A
  • Insulinoma

* Parathyroid Adenoma

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50
Q

list few malignant neuroendocrine tumors

A
  • Carcinoid tumor
  • Small cell ca lung
  • Pancreatic islet cell neoplasms (some only, 10%)
  • Parathyroid carcinoma
  • Phaeochromocytoma
  • Medullary carcinoma thyroid
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51
Q

papillary thyroid carcinoma is a neuroendocrine tumor. True/False

A

False.

Medullary thyroid carcinoma is a neuroendocrine tumor

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52
Q

name neuroendocrine tumor that causes episodic headaches, tremor, sweating, and high blood pressure

A

phaeochromocytoma

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53
Q

carcinoid tumors are low or high-grade neuroendocrine tumors?

A

low (well-differentiated)

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54
Q

what tumor markers contain carcinoid tumors?

A

chromogranin and synaptophysin

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55
Q

what is the most common site of carcinoid tumor

A

appendix (but rarely metastasize so does not cause carcinoid syndrome, to cause carcinoid syndrome tumor must metastasize to the liver so the biological products will bypass liver detoxifying ability)

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56
Q

what are the sites of carcinoid tumor?

A
  • Appendix (appendiceal carcinoids are found at tip, less than 2cm, usually benign)
  • Ileum
  • Bronchus
  • Anywhere
  • All are capable of metastasis but may not do so for many years. They are less aggressive than the usual carcinoma.
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57
Q

carcinoid tumor can cause acute appendicitis. True/False

A

True

If located on appendix

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58
Q

what is the most common presentation of bronchial carcinoid?

A

hemoptysis. Can block the bronchus leading to atelectasis and recurrent pneumonia

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59
Q

what is carcinoid syndrome?

A

These tumors may secrete a variety of neuroendocrine and paraendocrine substances, in many cases without any clinical functional effects. BUT ileal carcinoids tend to produce peptides (5-HT) which are normally destroyed in the lung and liver. When metastatic deposits are present in the liver,
they may enter the general circulation and produce carcinoid syndrome.
– Carcinoid syndrome develops due to the effects of serotonin
– Serotonin regulates intestinal movement and also causes bronchospasm
– Serotonin is detoxified in the liver and to a lesser extent in the lung.
– Syndrome develops when the liver is bypassed or when the ability of the liver to detoxify is overwhelmed by tumor

Carcinoid Syndrome Effects of Serotonin
– Facial flushing (due to vasodilation)
– Diarrhea (due to hypertrophy of intestinal muscle and fibrosis and obstructive symptoms like diarrhea)
– Bronchospasm
– Pulmonary stenosis
Why pulmonary stenosis and not mitral stenosis? Fibrin formation deposits on valves on the right side of the heart so fibrosis leads to stenosis of the pulmonary valve and tricuspid valve.

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60
Q

which carcinoids commonly produce carcinoid syndrome?

A

ileal, which will metastasize to the liver

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61
Q

which substance is responsible for carcinoid syndrome?

A

serotonin

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62
Q

what are the effects of serotonin?

A

Facial flushing (due to vasodilation)
– Diarrhea (due to hypertrophy of intestinal muscle and fibrosis and obstructive symptoms like diarrhea)
– Bronchospasm
– Pulmonary stenosis

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63
Q

what are multiple endocrine neoplasms? (MEN)

A

• Clustering of more than 1 neuroendocrine neoplasm in the one patient
• Autosomal dominant inheritance
• Types 1 and 2(A and B)
MEN1
- due to the MEN1 gene on chromosome 11 -menin protein
- eg. Parathyroid adenoma

MEN2 due to mutations activating RET oncogene (neural growth factor receptor) on chromosome 10 (point mutation)
MEN 2A
- eg. Parathyroid adenoma
MEN2B
- eg. mucosal neuroma

• Why is it important to know this?
Because they occur as a cluster (so need to be aware that their organs need to be checked). Family screening may pick up tumors at an early age as well.

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64
Q

what tumors are seen with MEN1?

A

parathyroid hyperplasia–hyperparathyroidism
gastrinoma
pituitary adenoma
3 P’s: parathyroid, pancreas, pituitary

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65
Q

describe MEN 2A and 2B

A

Medullary thyroid carcinoma and pheochromocytoma in both

parathyroid adenoma in 2A and mucosal neuromas in 2B

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66
Q

MEN 1 vs MEN 2

A

due to suppression of tumor suppressor gene vs activation of RET protooncogene

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67
Q

what is menin?

A

Menin is a tumor suppressor gene deactivated in MEN1

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68
Q

how carcinoid tumor is diagnosed biochemically?

A

Increased urinary 5 HIAA’s (5-Hydroxyindoleacetic acid)

–These are a breakdown product of serotonin.

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69
Q

in what organs germ cell tumors arise?

A
  1. Testis
  2. Ovary
  3. Thymus
  4. Pineal
  5. Retroperitoneum
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70
Q

name tumor that arises from all 3 layers: endoderm/mesoderm/ectoderm

A

germ cell tumors (so can contain tissues derived from all 3 layers )

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71
Q

list common germ cell tumors?

A
  • Seminoma (Testis) / Dysgerminoma (Ovary)
  • Teratoma
  • Choriocarcinoma
  • Yolk sac Tumour
  • Embryonal Carcinoma
  • Mixed Tumours
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72
Q

what is the most common testicular tumor?

A

seminoma
– 50% of testicular tumors
– All are malignant
– Age 20-40 (rare before puberty) – seminoma spreads via lymphatics
– Have a characteristic lymphocytic response and host response
– Usually do not need chemotherapy unless late-stage

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73
Q

seminoma present most commonly at what age?

A

20-40

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74
Q

what is the treatment of seminoma

A

orchiectomy (no chemotherapy)

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75
Q

what is the common site of metastasization of germ cell tumors?

A

lungs

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76
Q

teratomas in testis vs ovary

A

mostly malignant vs benign

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77
Q

origin of teratoma?

A

Originates from totipotent germ cells capable of differentiating into derivatives of ectoderm, endoderm, and mesoderm, so frequently contain hair, teeth and other tissues

78
Q

what does it mean totipotent germ cell?

A

capable of differentiating into derivatives of ectoderm, endoderm, and mesoderm

79
Q

malignant tumor derived from the trophoblast is called?

A

choriocarcinoma. The trophoblast is composed of cytotrophoblast and syncytiotrophoblast

80
Q

choriocarcinoma usually arises after?

A

hydatidiform mole

81
Q

what is the most important feature of choriocarcinoma?

A

is aggressive and cause early lung metastases

82
Q

what hormone is secreted by choriocarcinoma?

A

beta-HCG which is normally secreted by the syncytiotrophoblast, used to monitor disease and treatment

83
Q

Yolk sac tumors produce what tumor marker?

A

Alpha-fetoprotein

84
Q

what is the best treatment option for germ cell tumors?

A

chemotherapy

85
Q

describe embryonic tumors

A
  • Occur in children
  • Aggressive tumours
  • Consist of one embryonal-like cell
  • Neuroblastoma - neural tissue
  • Nephroblastoma - kidney
  • Retinoblastoma - retina
  • Medullablastoma - cerebellum
86
Q

list few borderline tumors

A
  • This categorization is most commonly ascribed to ovarian serous and mucinous tumors.
  • Examples- Kaposi sarcoma and hemangioendothelioma (borderline vascular tumors)
87
Q

why the incidence of cancers increases at old age?

A
  • Carcinogens have sufficient time to cause multiple genetic alterations.
  • Immunosuppression - elderly people have mild immunosuppression.
  • Less lymphoid tissue (regresses and atrophies the older you get)
88
Q

why do cancers occur in childhood?

A

•Often found an inherited loss of one allele on an important gene
– e.g. retinoblastoma
•Subsequent acquired loss of the second allele of retinoblastoma.

89
Q

what is hamartoma?

A

A benign mass composed of mature cells that are native to the tissue of origin but have abnormal tissue organization. Has a low potential to undergo malignant transformation.
example: capillary angioma

90
Q

hamartoma is present at birth.true/False

A

True.

Enlargement continues until physiological growth ceases (reach adulthood)

91
Q

what is tumor marker?

A

– The term is used for the antigen or antibody which is specific to a tumor.
– These are either antigen-specific to certain cell types that are recognized by antibodies.

92
Q

what is the role of tumor markers?

A

– They can be used in the diagnosis, follow up and screening of tumors.
– Useful in determining therapeutic responses or tumor recurrence

93
Q

list a few examples of tumor markers

A

– HCG
• Choriocarcinoma

– AFP - Alpha-fetoprotein
• Hepatocellular carcinoma
• Yolk sac tumor

– Prostatic specific antigen (not used for screening)
• Prostatic carcinoma

94
Q

AF is seen in what tumors?

A

Hepatocellular carcinoma

Yolk sac tumor

95
Q

Where Are Tumour Markers Detected?

A

Blood/Serum
Urine
Tissue section

96
Q

list tumor markers commonly used on tissue sections on histopathology

A 
–	Carcinoma-Cytokeratin
–	Sarcoma-Vimentin (found in mesenchyme)
–	Lymphoma- CD45
–	Melanoma-S100 P or Melan A
–	Prostate-PSA
–	Thyroid-Thyroglobulin
–	Yolk Sac tumor-AFP
–	Choriocarcinoma-HCG
97
Q

how tumor markers on tissue sections are detected?

A

– An antibody detects the antigen on the cell by a process called immunohistochemistry
– A colored dye (usually brown dye) is attached to an antibody.
– The antibody is poured on to the tissue
– If the antibody finds its antigen, it binds to it and cannot be washed off
– After washing the section, the antibody, which is bound to the antigen, is recognized by its attached dye

98
Q

tumor markers are used for the diagnosis of both primary tumor and metastasis.True/False

A

True
e.g. a node which contains a tumor which reacts with thyroglobulin can be definitively diagnosed as a metastasis from thyroid carcinoma

99
Q

what is a magic bullet?

A

Magic bullet: Or, sometimes, silver bullet. The perfect drug to cure a disease with no danger of side effects

100
Q

what is the cell cycle?

A

a sequence of events that take place to enable DNA replication and cell division.
The cell cycle is first divided into two phases: interphase and mitosis.
Interphase is further divided into the G1 (gap 1), S (synthesis), and G2 (gap 2) phases, which prepare the cell for division.
Billions of cells are replaced in the body every day in a carefully controlled manner through the influence of factors on the cell cycle. These include proteins with different functions e.g. growth factors, growth factor receptors, enzymes, and signal transducers. Such cell replacement is essential to replace cells lost every day through natural wastage and injury

101
Q

controlled vs uncontrolled cell proliferation?

A 
-Controlled
   Hyperplasia and Hypoplasia
- Uncontrolled
   Neoplasia
   Benign
   Malignant
102
Q

what is the clinical significance of the cell cycle?

A

Neoplasms occur when cell cycle is not normally controlled

103
Q

list 3 types of cell (based on cell proliferation)

A 
•	Labile (rapid turnover)
o	e.g. skin, GIT
•	Stable (low turnover)
o	Liver
•	Permanent (no turnover)
o	Neurons and cardiac muscles and skeletal muscles
104
Q

liver cells are stable or permanent?

A

stable

In some situations, they can proliferate

105
Q

name few permanent cells

A

Neurons and cardiac muscles and skeletal muscles

– This explains the relentless loss of cerebral function in Alzheimer’s disease.

106
Q

what is a stem cell?

A

Stem cells are cells capable of self-renewal and differentiation into specialized cells.
Cell division
-Symmetric division: self-replication → both daughter cells possess the stem cell properties.
-Asymmetric division: differentiation → one stem cell is a copy of the mother stem cell and the other daughter cell is a precursor cell with differentiated properties.
Characteristics
Totipotent (omnipotent): the ability of a cell to differentiate into all cell types
Pluripotent: the ability of a cell to differentiate into nearly all cell types
Multipotent: the ability of a cell to differentiate into more than one cell type, but not all cell types
Classification
Embryonic stem cells (ESCs)
Origin: from the inner cell mass in the blastocyte stage
Degree of differentiation: pluripotent cells that can only develop into embryonic cells, but not trophoblastic cells
Adult stem cells
Origin: differentiated tissue with high potency (e.g., bone marrow)
Degree of differentiation: pluripotent cells that provide a supply of cells for regenerative tissue

107
Q

what is the role of telomere?

A

The distal end of a chromosome that contains a non-coding, repetitive base sequence (TTAAGGG in humans). A chromosome is shortened with every successive cycle of DNA replication because the enzymes that replicate DNA cannot proceed all the way to the end of a DNA sequence. The presence of expendable, non-coding telomeres at the end of a chromosome ensures that important genetic information is not lost with every cycle of cell division.
–When the telomere runs out, cell replication is no longer possible.

108
Q

list phases of the cell cycle

A
  • G0 = resting phase
  • G1 - M = cells becoming altered in preparation for cell division i.e. mitosis
  • M - Cell division (mitosis)
    Interphase
    Definition: The interval between cell divisions in which the cell prepares for the next division. The duration of interphase varies and contains three phases (excluding the G0 phase):
    G1 phase : synthesis of RNA, proteins, and cell organelles
    Occurs after mitosis
    There is one chromatid present per chromosome
    The cell grows during this phase
    Nucleotide excision repair takes place.
    G1 checkpoint before entering S phase
    S phase
    DNA replication → results in two sister chromatids per chromosome
    Synthesis of proteins required for DNA packaging (especially histones)
    Most mismatch repair takes place during the S phase.
    Once the S phase is initiated, the cell cycle must be completed.
    G2 phase :
    Further synthesis of proteins required for mitosis
    Repair of DNA replication errors
    G2 checkpoint before entering mitosis
    G0 phase (Resting phase)
    Resting period of a cell after exiting the cell cycle.
    Cell is differentiated and has a specific respective function but is no longer undergoing cell division.
    Only proliferating cells pass through the cell cycle. Most mature tissue cells are in the G0 phase.
    Certain cell types can enter the G1 phase from the G0 phase if stimulated
    Mitosis
    Definition: the process of cell division from the distribution of DNA to budding of the cellular body
    Duration: ∼1 h
    Mitotic index: the ratio of the number of cells undergoing mitosis to the total number of cells in the given population (e.g., per 1,000 cells or per microscopic area in the specimen)
    Phases of mitosis
    –Prophase
    Chromosome condensation begins
    Centrosome separation
    –Centrosome
    Point of origin of the mitotic spindle
    Composed of two centrioles and a surrounding matrix, from which the microtubules can emerge
    Formation of the mitotic spindle begins
    –Prometaphase
    Degradation of the nuclear membrane into small vesicles and intercellular vesicle storage
    Completion of the mitotic spindle
    –Metaphase
    Maximal condensation of the chromosomes, which are aligned in the equatorial plane of the cell
    –Anaphase
    Separation of sister chromatids due to cohesion dissolution at the centromere by the enzyme separase
    The cell becomes elongated.
    –Telophase
    Decondensation of the chromosomes
    Disintegration of the mitotic spindle
    Formation of a new nuclear membrane
    Cell bodies divide at the equatorial plane
    Ribosomal RNA (rRNA) synthesis begins

few things from me to better understand cell cycle**

109
Q

what is a mitotic index

A

the ratio of the number of cells undergoing mitosis to the total number of cells in the given population (e.g., per 1,000 cells or per microscopic area in the specimen)
• A high mitotic rate is seen in especially aggressive tumours.
• A high mitotic index is seen in tumours that progress rapidly through the cell cycle.
The apoptotic index is a reflection of the loss of tumor cells by apoptosis

110
Q

what are the factors that control cell proliferation?

A 
•	Signaling from cell membrane → nucleus
•	Growth factors
–	(k-ras)
•	Growth factor receptors
–	(c-erbB-2)
•	Signal transducers
–	(k-ras)
–	e.g. protein kinases
–	G Proteins
•	Transcription factors
–	(c-myc)
111
Q

what is PDGFB?

A

Platelet-derived growth factor, overexpressed in astrocytomas

112
Q

what is ERBB2

A

epidermal growth factor receptor, amplified in breast carcinomas (Her2)

113
Q

what is RET?

A

neural growth factor receptor, point mutation in MEN 2A and 2B, medullary thyroid cancer

114
Q

what is kIT

A

stem cell growth factor receptor, point mutation in gastrointestinal stromal tumor

115
Q

what is RAS?

A

GTP-binding protein (signal transudcer), point mutation in carcinomas/ melanoma

116
Q

what is ABL

A

Tyrosine kinase (signal transducer), translocation with BCR in CML t(9;22)

117
Q

what are C-MYC, L-MYC, and N-MYC?

A

transcription factors, C-MYC is translocated (8;14) in Burkit Lymphoma, L-MYC and N-MYC are amplified small cell lung cancer and neuroblastoma

118
Q

what is CCND1 (cyclin D1)

A

cyclin, translocated (11;14) in mantle cell lymphoma

119
Q

what is CDK4?

A

cyclin-dependent kinase, amplified in melanoma

120
Q

what is hyperplasia?

A

increase in organ or tissue size due to increase cell number,

121
Q

hyperplasia is controlled or uncontrolled?

A

controlled

– Increased cell proliferation due to increased controlled proliferation, in response to a stimulus

122
Q

what type of cells can undergo hyperplasia?

A

– It can only occur in labile or stable cells as permanent cells cannot divide e.g.left ventricle.

123
Q

list few clinically significant hyperplasia examples

A
  • Breast(Physiological)
  • Endometrium(Physiological)
  • Thyrotoxicosis(Due to increased TSH)
  • Lymphadenopathy(Viral infection)
  • Marrow hyperplasia(After blood loss)
  • Skin in wound(Healing)
124
Q

how heart increase in size if myocardial cells cannot undergo hyperplasia

A

due to hypertrophy (increase in individual cell size not a number)

125
Q

how permanent cells increase their workload?

A

by hypertrophy, eg cardiac hypertrophy in response to long-standing hypertension, bodybuilding, If one limb is in a plaster other limb hypertrophies.

126
Q

reduction in the size of organ or tissue is called?

A

ATROPHY

  • Thymus in adults
  • Breasts after pregnancy
  • Salivary gland in duct obstruction.
127
Q

Failure of the organ to reach expected size is called?

A

hypoplasia (underdevelopment of an organ, with a decreased number of cells)
lung hypoplasia of the fetus

128
Q

Failure of an organ to develop is called?

A

Agenesis (complete absence of an organ and its associated primordium)
e.g. renal agenesis

129
Q

what is metaplasia?

A
  • Abnormality of cellular differentiation.

- Change from 1 adult type of epithelium to another adult type.

130
Q

what is Barret esophagus?

A
  • e.g. Barrett’s esophagus (acid reflux); squamous metaplasia of lung due to smoking(lung is usually pseudostratified squamous epithelium).
  • Barrett’s esophagus is the finding of gastric type epithelium rather than squamous epithelium in the esophagus.
131
Q

is metaplasia protective?

A

Yes
-Metaplasia is a protective mechanism
e.g. in reflux oesophagitis (Barrett’s esophagus)
squamous epithelium changes to gastric epithelium to withstand the acid environment due to the reflux of acid contents into the oesophagus.

132
Q

does metaplasia have malignant potential?

A

YES!
It had been previously thought that metaplasia is not neoplastic but we now find that similar genetic changes occur both in metaplasia and neoplasia.
This suggests that metaplasia is a neoplastic process in some instances, eg Barret metaplasia can transform in adenocarcinoma

133
Q

what are the events causing cancer?

A
  • Environmental factors
  • Inherited genetic factors (Seed & Soil!!!!)
  • Role of the immune system
  • 100 times incidence of carcinoma of the skin in renal transplant recipients who have been immunosuppressed
134
Q

does immunosuppression increase the risk of cancer?

A

Yes

100 times incidence of carcinoma of the skin in renal transplant recipients who have been immunosuppressed

135
Q

give examples of evidence that inherited factors cause cancer

A
  1. Familial Adenomatous polyposis coli → colonic carcinoma
  2. Retinoblastomas occur in families
  3. Breast carcinoma (5%) have an FH
  4. Melanoma (2% FH)
  5. Medullary carcinoma of the thyroid (30% of cases have FH)
136
Q

what are BRCA 1 and 2?

A

An autosomal-dominant inherited gene mutation (BRCA1 or BRCA2) of a tumor suppressor gene that codes for a DNA repair protein. Associated with an increased risk of breast cancer (∼ 70%) and ovarian cancer as well as, to a lesser extent, colon, pancreas, stomach and prostate cancer. BRCA is an abbreviation for BReast CAncer.

  • 60% lifetime risk of breast cancer
  • 40% lifetime risk of ovarian cancer
  • Probably 100 different mutations involved so it is difficult to screen for them all.
137
Q

list a few environmental carcinogens?

A
  • Chemicals
  • Radiation (UV & Ionizing)
  • Hormones
  • Viruses
  • Chronic Inflammation
  • Parasites and other organisms

80% of cancers are caused by environmental factors

138
Q

how chemical carcinogens cause cancer?

A 
1)Genotoxic (initiator)
–	Interfere with DNA binding
–	Impede DNA repair
2)Non genotoxic (promoter)
–	Non genotoxic chemical carcinogens act as promoters eg. Hormones, oestrogens
139
Q

list genotoxic vs nongenotixic chemical carcinogens

A

1) genotoxic:
- Polycyclic hydrocarbons (lung)
- Nickel& chromate (nose)
- Aniline dye (bladder)
- Alkylating agents (leukemia)
2) Hormones e.g. estrogen

140
Q

aniline dyes cause what cancer

A

bladder cancer

141
Q

nickel cause what type of cancer

A

nose (head and neck)

142
Q

what cancer is caused by polycyclic hydrocarbons?

A

lung

143
Q

alkylating agents?

A

leukemias

144
Q

what cancers are caused by UV radiation?

A

– Squamous cell carcinoma of skin
– Basal cell carcinoma of skin
– Malignant melanoma of skin

145
Q

what are the sources of ionizing radiation?

A

– HIROSHIMA
– CHERNOBYL
– Therapeutic radiotherapy
– Diagnostic Radiotherapy

146
Q

ionizing radiation causes what cancers?

A

– Cause leukemias and sarcomas

147
Q

the risk of what cancers are increased due to exposure to asbestosis?

A
  1. Mesothelioma
  2. Lung cancer
    (SCC of lung>mesothelioma)
148
Q

list a few examples of hormones causing cancer

A
  • Breast carcinoma -e.g. HRT
  • Endometrial carcinoma - e.g. Tamoxifen (it is an antagonist of estrogen receptor in the breast, but agonist in endometrium!!!!!)
  • Prostatic carcinoma - Androgens
149
Q

risk of what cancers increased due to EBV?

A
  • Nasopharyngeal carcinoma

- Some of Hodgkin’s Disease

150
Q

list a few viruses that cause cancer

A 
•Epstein Barr
-Nasopharyngeal carcinoma
-Burkitt’s lymphoma
-Some Hodgkin’s Disease
•HPV (some types)
-Cervical carcinoma and anal carcinoma
•Hepatitis B&amp;C Viruses
-Hepatocellular carcinoma
•Herpes-type 8-Kaposi’s sarcoma
•HPV 16 oropharyngeal carcinoma
151
Q

schistosomiasis can cause what cancer?

A

bladder cancer

152
Q

what cancer can be caused by parasite Clonorchis Sinensis

A

cholangiocarcinoma

153
Q

what bacteria is oncogenic?

A

helicobacter Pylori

Carcinoma and lymphoma of stomach (MALToma)

154
Q

what genes can be altered to cause cancer?

A
  • Proto-oncogenes
  • Tumor suppressor genes
  • Repair genes
  • Anti Apoptotic genes
  • Methylation of genes hyper or hypomethylation affect DNA function
155
Q

what is proto-oncogene?

A

Genes that encode proteins that are important in normal cell division and cell differentiation. Cause cancer when activated!!! Examples include:
Protein kinases, e.g., protein kinase B (PKB)
PKB activates and inhibits various substrates and therefore suppresses, e.g., apoptosis, and activates translation and, indirectly, cell division.
PKB is activated by phosphatidylinositide 3-kinase (PI3K).
Ligand-directed transcription factors (intracellular hormone receptors)
GTP-binding proteins
G protein-coupled receptors
Small G-proteins such as Ras
Tyrosine kinase receptors
Growth factors and cytokines

156
Q

what is the tumor suppressor gene?

A

A gene that normally controls and suppresses cell proliferation. Loss of function or inactivation leads to an increased risk of developing cancer. Both alleles need to be mutated in order for complete loss of function of the gene.

157
Q

list few proto-oncogenes

A
  • Growth factors (C-sis)
  • Growth factor receptors (c-erbB-2)-breast cancer
  • Signal transducers (c-ras)-colorectal cancer
  • Nuclear regulation (c-myc)-Burkitt lymphoma
  • Mitochondrial (Bcl-2)-Follicular lymphoma
158
Q

what genetic changes are the reasons of proto-oncogene activation?

A 
-Mutation
     •e.g. radiation
-Amplification
-Translocation
     •e.g. EB virus
-Insertional Mutagenesis
     •e.g. viral insertion
-Methylation
159
Q

why genetic changes occur to activate proto-oncogenes?

A

1) Environmental agents – carcinogens
2) Inherited susceptibility to mutation or amplification.
3) *These genetic changes are caused by environmental agents often at the site of a proto-oncogene or of a promoter.
4) e.g. EB Virus

160
Q

viruses can cause activation of proto-oncogenes.

True/False

A

True, eg EBV, HHV-8, HPV

161
Q

c-myc oncogene is activated by?

A

EBV virus causing translocation, result in Burkitt lymphoma

162
Q

how tumor-suppressor genes are affected?

A 
•	Alteration by:
-	Deletion (usually)
-	Mutation
•	Translocation by:
-	Environmental agents.
163
Q

give examples of tumor suppressor genes

A
  • P53 (wild type and mutant type)
  • APC
  • Retinoblastoma
164
Q

what is P53

A

p53 protein
Causes cell apoptosis (by activating proapoptotic gene such as BAX) and cell cycle arrest at the G1 phase (by activating p21)
Inhibits entry in the S phase via inhibition of pRb phosphorylation
Mutated in Most human cancers, LiFraumeni syndrome

165
Q

what is the guardian of the genome

A

P53
• It detects DNA damage and stops cell progressing through the cell cycle to give cell repair enzymes time to repair before they divide.
• Therefore, they maintain the integrity of the DNA of the cell.
UV causes mutation in p53 which causes skin cancer.
• P53 is mutated in 50% of carcinomas
• Mutated P53 does not act as a guardian of the genome and does not act as a tumour suppressor gene.

166
Q

what is Adenomatous Polyposis Coli gene (APC)

A

APC is a protein that prevents unregulated cell proliferation by inhibiting β-catenin synthesis

167
Q

the risk of what tumor is increased due to loss of APC gene

A

Lost in colon cancer, mainly familial, but also some sporadic.
Also lost in some gastric cancers.

168
Q

what is the retinoblastoma gene and its product?

A

Retinoblastoma protein (Rb protein): causes cell cycle arrest at the G1 phase by inhibiting E2F transcription factor

  • Function is deleted in retinoblastoma which is an aggressive tumor of the eye in neonates or infants.
  • Replacement of the Rb gene to cultured cells from a retinoblastoma tumor causes the cells to become non- neoplastic.
  • can also cause osteosarcoma
169
Q

what is mismatch repair gene?

A

A collection of genes that encode proteins that recognize and excise mismatched nucleotides in newly synthesized DNA strands. Essential for the maintenance of genomic stability. Examples include MLH1 and MSH2.

170
Q

mismatch repair is defective in?

A

in patients with hereditary nonpolyposis colorectal cancer (Lynch syndrome).

171
Q

what are the antiapoptotic genes?

A

-These genes impair the process of apoptosis, therefore giving a survival advantage to tumor cells.

172
Q

what is BCL 2

A

An antiapoptotic protein that inhibits the intrinsic pathway of apoptosis by blocking the release of cytochrome C and maintaining the impermeability of the mitochondrial membrane. Translocation t(14,18) can lead to overexpression of Bcl-2, which results in inhibition of apoptosis. Alterations in Bcl-2 are associated with follicular lymphomas and diffuse large B cell lymphoma.

173
Q

t(14;18) translocation cause

A

follicular lymphoma

174
Q

germline vs somatic gene abnormalities

A

–Germline mutation (gametic mutation): mutations in the cells from which egg or sperm cells develop. These mutations can, therefore, be passed on to offspring
–Somatic mutation: acquired mutations that are present only in certain somatic cells
Primarily affect only one allele of a gene
Do not occur in the germline and therefore cannot be passed on to offspring via the ovum or sperm
Almost all malignancies are preceded by a somatic mutation

175
Q

Li-Fraumeni syndrome is due to germline or somatic mutation?

A

germline

An inherited germline loss of one allele and subsequent loss of the second allele is associated with some cancers

176
Q

renal transplant patients have increased risk of what cancer?

A

SCC of the skin due to immunosuppression

177
Q

immunosuppressed patients have an increased risk of what cancers?

A
  • Renal transplant patients on immunosuppression have X 100 incidence of skin carcinoma.
  • Have a higher incidence of malignancies especially lymphomas
  • Older patients also have an increased risk of malignancy which may be partly due to immunosuppression.
178
Q

how tumor cells evade the immune system

A
  • Tolerance
  • Local immune suppression
  • Dysfunction in T cell signaling
  • Activating endogenous immune checkpoints (that terminate immune responses)
179
Q

what is epigenetics?

A

Epigenetics focuses on the heritable chemical modifications of DNA and histone proteins caused by environmental factors. Through these modifications, gene activity can be regulated, i.e., genes can be switched on or off. In contrast to genetic studies, epigenetics is not concerned with the information encoded in the DNA sequence itself.
The epigenetic regulation of genes is all about whether or not genes are transcribed. Classical genetics, on the other hand, is concerned with the presence or absence of a gene. Gene expression or repression is determined by chemical modifications of bases (methylation) and histone proteins (various covalent modifications), which are carried out by specialized enzymes.

180
Q

what is the role of immunotherapy in the treatment of cancers?

A

• Up-regulate or down-regulate immune response

181
Q

give examples of cancer immunotherapy?

A

Vaccination (BCG for in situ bladder ca- as it will lead to stimulation of the immune response and overcoming the cancer cells)

  • Immune checkpoint pathway inhibitors
  • PD1 and CTLA-4 (immune checkpoint inhibitors) dampen down the immune response.
  • Anti-CTLA-4 and anti-PD1 switch on the immune response against the tumour.
182
Q

what is CTLA 4?

A

A protein receptor involved in the regulation of T cell activation. Its expression is upregulated by T cell receptor activation and pro-inflammatory cytokines (e.g., IL-12, IFN-γ). Anti-CTLA-4 antibodies (e.g., ipilimumab) are immune checkpoint inhibitors used in anticancer therapy.

183
Q

what is PD-1?

A

• PD1 is a cell surface receptor expressed on T cells and some B cells
• Functions as an immune checkpoint which regulates (causes) immunosuppression, thus inducing tolerance to the neoplasm, by preventing activation of T cells against the tumor antigens
• It downregulates the immune response against the tumor.
anti-PD-1 antibody drug, nivolumab for non-small-cell lung cancer, melanoma, and renal-cell cancer

184
Q

what is the frozen tissue section?

A

he frozen section procedure is a pathological laboratory procedure to perform rapid microscopic analysis of a specimen. It is used most often in oncological surgery
The principal use of the frozen section procedure is the examination of tissue while surgery is taking place
• Margins of excision assessment (does the surgeon need to cut out more tumor/tissue
• An intra-operative diagnosis that will affect the extent of further surgery e.g. liver lesion is it a metastasis or benign

185
Q

geographical epidemiology of cancer?

A
  • Different malignancies are commoner in different parts of the world.
  • Breast carcinoma - Europe & USA
  • Gastric carcinoma- China & Japan
  • Hepatocellular carcinoma - Middle East
  • Bladder carcinoma - Egypt
  • Nasopharyngeal carcinoma - Asia
  • Burkitt’s lymphoma - Africa
  • Cervical carcinoma - Africa
186
Q

gastric cancer is prevalent in what countries?

A

China & Japan

187
Q

hepatocellular carcinoma is prevalent in what countries?

A

Middle East countries

188
Q

bladder carcinoma is prevalent in whar country?

A

Egypt

189
Q

nasopharyngeal carcinoma is prevalent in?

A

Asia

190
Q

Burkitt lymphoma is prevalent in?

A

Africa

191
Q

cervical carcinoma is prevalent in?

A

Africa

192
Q

Breast carcinoma is prevalent in?

A

Europe and USA

Neoplasia (3 decks)

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