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Hematology/Oncology > General Introduction (1) > Flashcards

General Introduction (1) Flashcards

1
Q

What is the most common cancer?

A

Prostate cancer in men and breast cancer in women

skin cancer most common in the US
Lung cancer most common worldwide

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2
Q

Lifetime probability of developing cancer

A

1 in 2 risk for men
1 in 3 risk for women

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3
Q

Age and cancer incidence

A

Disease of aging - incidence increases w/ age

Exposure to a carcinogen (e.g. asbestos, smoking, sunlight, polluted air, etc.) - age no longer plays role, incidence increases regardless of how old you are

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4
Q

Which cancer is most lethal?

A

Lung cancer

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5
Q

Trends of cancer death/survival rates

A

Cancer death rate decreasing

5 year survival rate is used to indicate efficacy and lethality of disease - this has been increasing (indicating advancements in treatment)

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6
Q

Tumor vs cancer

A

A tumor can be benign or malignant
If its cancer - its malignant (meaning it will spread) (there is no such thing as a benign cancer)

Benign = local disease

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7
Q

Metaplasia

A

Change in cell morphology or phenotype (pre cancer indicator, e.g. Barret’s esophagus)

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8
Q

Anaplasia

A

Failure to differentiate to adult phenotype

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9
Q

Dysplasia

A

Failure to differentiate completely/normally

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10
Q

Hyperplasia

A

Increase in cell number

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11
Q

Hypertrophy

A

Increase in cell size

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12
Q

Atrophy

A

Decrease in cell size (does not apply to cancer)

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13
Q

Lymphoma/Leukemia

A

-2nd most common
-Cancer of the lymphocytes (lymphoma) or white blood cells (leukemia)
-Difference between these is that lymphoma involves a solid tumor, leukemia does not (liquid tumor)

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14
Q

Sarcoma

A

Cancer of mesenchymal cells (muscle, bone, cartilage, fat, and fibroblasts)

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15
Q

Carcinoma

A

-Cancer derived from epithelial cells (cells that cover surfaces, e.g. skin, lung, colon, breast cancer)
-Most common

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16
Q

3 types of cancer classifications

A

Carcinoma
Lymphoma/Leukemia
Sarcoma

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17
Q

Nomenclature of neoplasms

A

Prefix - indicates tissue origin

Suffix - indicates malignancy
-benign ends with -oma
-malignant ends with -carcinoma or -sarcoma
exceptions to this are: melanoma, glioma, and astrocytoma which end in -oma, but are malignant

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18
Q

what does the adeno prefix mean

A

origin = glandular cells/tissues

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19
Q

what does the fibro prefix mean

A

origin = fibroblasts

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20
Q

what does the chondra prefix mean

A

origin = cartilage

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21
Q

what does the osteo prefix mean

A

origin = osteoblasts

22
Q

what does the leiomyo prefix mean

A

origin = smooth muscle cells

23
Q

what does the rhabdomyo prefix mean

A

origin = striated muscle cells (skeletal and cardiac)

24
Q

what does the lipo prefix mean

A

origin = adipose cells

25
Q

Methods for tumor detection/diagnosis

A

Gross examination
-feeling/seeing lump/bump/ulcer

Imaging
-x-ray, CT scan, ultrasound, PET scan
-for detecting tumors inside the body

Blood sampling
-Some tumors release certain proteins into circulation, the levels of these in blood can indicate the tumor load (e.g. PSA with prostate cancer)
-liquid biopsy - tumors shed DNA into blood, we can extract DNA from blood samples to determine what kind of tumor it is

Gold standard - histological examination (get a piece of the tumor)
-brush cytology (if on the surface, e.g. pap smear)
-needle biopsy (use needle to grab a piece of tissue, e.g. breast and prostate cancer)
-incisional/disectional biopsy (surgical for other non accessible tissues)

26
Q

How does PET scan work?

A

Cancer cells need a lot of nutrients, they over express glucose transporters to take in more glucose
We can label glucose with a radioactive nucleotide and perform PET imaging to see which cells take up more glucose - which will show where metastasis has occurred throughout the body

27
Q

What are the 2 main things that we can determine from a biopsy?

A
  1. The origin
  2. If it is benign/malignant
28
Q

Hematoxylin and eosin (H & E) staining

A

Most common staining done to show cell morphology

H (hematoxylin) stains the nuclei blue
E (eosin) stains the cytoplasm pink

The bigger the blue (nuclei) - the more DNA replication is occurring
And the smaller the pink (cytoplasm) - the less cell differentiation

This happens with cancer as it progresses -> cells become smaller (bigger nuclei but smaller cytoplasm) and they are poorly differentiated (look different from their normal counterpart, only focused on replicating)

29
Q

Grade vs stage

A

Grade is a prediction indicates degree of differentiation (the similarity of the cell to its normal corresponding cell - if it has less differentiation, that means it is further from the normal cell, i.e. the further from the normal cell, the less differentiation, the higher the grade)
-this is a prediction - not very reliable

Stage is an evaluation - indicates the extent of tumor invasion and metastases
- this is a more accurate estimate than the grade

30
Q

Grade

A

Indicates degree of tumor cell differentiation to predict tumor cell behavior
Grade 1 (low)- well differentiated
Grade 2 (intermediate) - moderately differentiated
Grade 3 (high) - poorly differentiated
Grade 4 (anaplastic) - almost no differentiation

As you go up in grade, nucleus becomes bigger, cytoplasm becomes smaller

Used to make a prediction (not as reliable as staging)…
Lower grade indicates slower growth and suggests longer patient survival

31
Q

Stage

A

Assess the current disease situation
-assigned at time of diagnosis, may be updated as disease progresses

Staging is done based on TNM staging protocal
-T (tumor) = the size of the primary tumor
-N (nodes) = metastasis to lymph nodes
-M (metastasis) = metastasis to distant organs

Stage 0 - pre cancer (on going disease but not full blown cancer yet)

Stage 1-2 - local or regional spread

Stage 3-4 - distant spread

(specific definition depends on the type of cancer)

32
Q

What are the 4 hallmark characteristics of malignant tumors

A
  1. Lack of differentiation (i.e. look different from normal counterpart)
  2. Enhanced cell proliferation and/or reduced cell death
    (once we are matured, this ratio should be 1:1, in cancer, this is changes, which is why a mass develops)
  3. Local invasion
  4. Metastasis
33
Q

Tumor growth

A

Every round of mitosis, the number of cells doubles

From 1 transformed cell…
-Tumor becomes detectable (with imaging) after 27 doublings (5 mm)
-Tumor becomes palpable after 30 doublings (10 mm)
-Tumor becomes lethal after 40 doublings (100 mm)

So there is not much time from the point where it is detectable to the point when it becomes lethal (which is why early detection and treatment are important)

Most benign tumors grow slowly, whereas most cancers grow rapidly

34
Q

How does tumor invasion of surrounding tissue occur?

A

Benign tumors grow within a boundary set by the basement membrane
-this makes them easy to remove surgically

In cancerous tumors - the boundary is unclear - the basement membrane is broken
-usually the epithelial cells will grow inside the lumen, but if they are malignant they will invade the basement membrane and grow out
-this is how they invade surrounding tissue - then they can get into circulation and disseminate throughout the body (metastasize)

35
Q

How do tumors metastasize? (3)

A

Metastasis is the spread of malignant cells to distant sites - this is how cancer kills people

There are 3 routes of metastasis:
1. Direct seeding of body cavities
-cancer breaks wall and disseminates inside the entire cavity (especially peritoneal cavity - then it can spread to other GI organs)

  1. Lymphatic channels
  2. Blood vessels
36
Q

Which sites do cancers usually metastasize to? (4)

A

Places rich in capillaries
-brain, lungs, liver, bone marrow

37
Q

Breast and prostate cancer tend to metastasize to which area?

A

Bone

38
Q

Metastatic process through blood vessels

A

First the primary tumor invades surrounding tissue

Then intravasation occurs - gets into capillaries, adheres lymphocytes, platelets, and other components

This is how they are transported throughout circulation

Once they get to a certain area, they adhere to the vessel wall and extravasation occurs… they get out grow and disrupt normal organ function
-the more metastases - the more organ function is disrupted (this is how cancer kills … organ failure)

39
Q

Carcinogens

A

Carcinogens are chemical or physical agents that cause cancers

Can be found in lifestyle/environmental factors

3 most prominent ones:
-UV radiation, smoking, charred meats

40
Q

Carcinogenesis

A

process of cancer generation
3 stage model…
1. Initiation
-cell mutation occurs

  1. Promotion
    -expansion of mutated cell population (proliferation)
  2. Progression
    -continued mutation and expansion (with increased capability to survive, grow, and metastisize)
41
Q

Mutations

A

Mutations are the cause of cancer
Mutations involve changes in DNA coding

They can be somatic mutations - meaning they occur after birth, typically due to exposure to mutagen (chemicals that cause mutations) - these drive most carcinogenic processes
Or germline mutations - mutations inherited from parents

4 types of point mutations:
Synonymous - a single nucleotide change does not cause a change in the coded amino acid
^ this one does not cause issues, the other 3 do…
Non-synonymous - a single nucleotide change causes encoding for a different amino acid (effects protein function)
Nonsense - single nucleotide change causes encoding for a stop codon (results in incomplete transcribed genome)
Readthrough - single nucleotide change changes a stop codon to encode for an amino acid (should stop, but keeps going… elongated gene)

42
Q

How does UV radiation cause cancer?

A

Pyrimidines absorb UV light causing covalent bond to form between thiamine’s … form cross linked T-T dimers / pyrimidine dimers (causing mutation)

43
Q

How does smoking cause cancer?

A

Benzopyrene is metabolized in the body by CYP enzymes to an epoxide which is a carcinogen (BPDE)

The epoxide causes DNA adduct formation (the carcinogen binds to the DNA) –> causing DNA damage and mutations

44
Q

How do charred meat products cause mutations?

A

PHIP - metabolized by CYP enzyme converted carcinogen attacks the guanine nucleotide, causing DNA adduct formation

45
Q

Which types of cancers have higher mutation frequencies?

A

All cancers involve meditations
Melanoma has the highest frequency mutation
And that is followed by lung, bladder, and stomach cancers - in general these cancers have more mutations as opposed to other like leukemia because they involve cells that are exposed to the outside (carcinogen exposure = mutation)

46
Q

Cancer is a disease of mutations, but what are the 2 main categories of genes that are mutated?

A

Oncogenes and tumor suppressor genes

Oncogenes
-stimulate cancer cell formation (promote cell growth and migration)
-act dominantly - only 1 copy is needed to be active

Tumor suppressor genes
-genes capable of inhibiting tumor cell growth
-act recessively - both copies need to be inactivated in order for function to be lost

Cancer patients often have both oncogene increase and tumor suppressor gene decrease

47
Q

Activation of oncogenes (3 methods)

A

Non synonymous point mutation (causes coding for a different protein

Gene amplification (normally we have 2 copies of each gene, but genetic mutation can result in multiple copies of the same gene resulting in generation of more oncogene proteins)

Translocations - rearrangements of DNA, caused by swapping chromosomes
e.g. translocation of chromosome 9:22 (creating this mutated Philadelphia chromosome) generates the Bcr-Alb fusion oncoprotein (only exists in patients with leukemia)

48
Q

How do oncogenes cause cell proliferation?

A

activating growth factor signaling pathways

-the problem with cancer is there is a mutation that makes the growth factor receptors much more active … the receptor will keep firing even without the binding of its ligand - causing the continuous growth signal
-for example the EGFR (epidermal growth factor receptor) fires without the binding of EGF (epidermal growth factor)

-so we can use drugs to target these specific mutations

49
Q

Inactivation of tumor suppressor genes

A

This is recessive - both copies need to be turned off in order for function to be gone
-the most common cause of tumor suppressor loss is through gene deletion

50
Q

What was the first tumor suppressor gene discovered?

A

Retinoblastoma (RB) (this is a tumor suppressor gene)

Retinoblastoma (condition) is when there is a tumor in the retina (causes blindness)
It can be familial or sporadic

Familial - typically effects both eyes, happens fast (within 10 years of birth)
Sporadic - only effects one eye

People with familial RB are born with only 1 copy of the RB tumor suppressor gene (one copy is inactivated at birth, but with time the second one is damaged, which is why blindness occurs

People with sporadic RB are born with 2 functional RB tumor suppressor genes , mutations occur after birth - and mutations have to hit both genes (since it is recessive) in order for blindness to occur

Hematology/Oncology (17 decks)

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