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Pathology - Exam 1 > Neoplasia III > Flashcards

Neoplasia III Flashcards

1
Q

BCL2. What is it and how is it activated?

A

The prototypic anti-apoptosis gene

Can be activated by translocation from chromosome 18 to the Ig heavy chain locus on chromosome 14

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2
Q

What happens when BCL2 is over-expressed?

A

Protects cells from apoptosis, allowing them to survive for prolonged periods
Results in steady accumulation of cells - often seen in “low-grade” lymphomas
Tumors grow slowly not because cells are proliferating, they just aren’t dying

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3
Q

Sustained Angiogenesis

A

Even with multiple genetic abnormalities, tumors cannot exceed 1-2 mm in diameter unless they are vascularized
Angiogenesis facilitates metastases - provides access to the vasculature

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4
Q

T/F - all cells are capable of metastasizing

A

False - Only certain subclones may be capable of metastasizing

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5
Q

What are the two phases of Invasion and Metastasis?

A

1) Invasion of ECM

2) Vascular dissemination and adhesion/homing of tumor cells

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6
Q

Steps of Invasion of ECM

A

1) Tumor cells detach from one another
2) They attach to ECM components (collagens, glycoproteins, and proteoglycans)
3) They degrade matrix components
4) Migration of tumor cells

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7
Q

Once in circulation, tumor cells are vulnerable to what?

A

Destruction by the host immune cells

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8
Q

How can the distribution of tumor metastases be predicted?

A

Based of the location of the primary tumor and its vascular and/or lymphatic drainage

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9
Q

Organ tropism

A

Sometimes seen in metastases

a. Organ-specific endothelial adhesion molecules bind tumor cell ligands
b. Chemokine receptors on tumor cells home to tumor cells home to sites where specific ligands are readily produces

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10
Q

What is critical to integrity of genome and control of cellular growth?

A

DNA repair

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11
Q

Patients with inherited defects in DNA repair have what?

A

Increased risk for cancer

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12
Q

If errors in DNA replication occur naturally, why isn’t cancer more common?

A

DNA repair genes - they’re pretty reliable

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13
Q

Hereditary nonpolyposis colon cancer sydrome

A

Familial cancers of the colon resulting from defective genes involved in DNA mismatch repair and evidence of microsatellite instability

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14
Q

Xeroderma pigmentosum

A

Defective nucleotide excision repair system
Sunlight (UV light) causes pyrimidine cross-linking in DNA, halting replication
Lacking ability to excise and repair their altered residues leads XP patients at risk for cancer

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15
Q

Bloom Syndrome, Ataxia telangiectasia, Fanconi anemia

A

Disorders characterized by hypersensitivity to DNA damage

Patients have increased cancer risk and other health problems

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16
Q

BRCA1 and BRCA2

A

Genes involved with repair of dsDNA breaks, may also have tumor suppressor roles
Patients are at risk for other forms of cancer besides breast cancer

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17
Q

Multistep carcinogenesis

A

No single mutation results in cancer
Cancers typically exhibit multiple genetic alterations including activation of several oncogenes and two or more cancer suppressor genes

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18
Q

What is the epidemiological evidence for multiple step carcinogenesis?

A

Cancer is more likely to occur in older people

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19
Q

Tumor Progression and Heterogeneity

A

Tumors begin as a monoclonal proliferation of one transformed cell. As daughter cells divide, they tend to develop more and more mutations
By the time a tumor mass is formed, the cells may be quite heterogeneous in many lesions
The subclones may be able to survive certain therapies, invade certain host tissue, or metastasize with greater efficiency

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20
Q

What are the different Karyotypic Changes in Tumors?

A

Balanced Translocations
Deletions
Gene amplifications

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21
Q

Balanced translocations

A

Extremely common, especially in hematopoeitic neoplasms

example: CML (philladelphia chromosomes) - translocation between chromosomes 9 and 22, causing 22 to become shorter

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22
Q

Deletions

A

Second most prevalent form of karyotypic abnormalitites in tumores
example: 3p, 9p, and 17p are common areas of loss in oral cancers

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23
Q

Gene amplifications

A

Seen in neuroblastoma and some breast cancers

24
Q

What are the three major classes of carcinogenic agents?

A

Chemicals
Radiant energy
Oncogenic viruses

25
Q

Sir Percival Pott

A

200 yrs ago described scrotal skin cancer in chimney sweeps and attributed it to chronic exposure to soot

26
Q

Procarcinogens

A

Most carcinogens are indirect and require some metabolic conversion
Procarcinogens are before the conversion

27
Q

What are the end products of procarcinogens?

A

Ultimate carcinogens

28
Q

All carcinogens are what? How do they cause damage?

A

Highly reactive electrophiles, interacting with the electron-rich DNA molecule and inducing genetic damage

29
Q

Some carcinogens can be augmented by what? How does this work?

A

Promoters (agents that have little inherent transforming ability)
The carcinogen is thought to serve as the initiator of a mutagenic event, while the promotor drives replication of the damaged cell

30
Q

What are some examples of radiation carcinogenesis?

A

UV - skin cancers
X-rays - early dentists got simp. sqau. cell carcinoma on their fingers from holding films
Radionuclides - miners of radioactive elements and lung cancer
Gamma radiation from nuclear fission - atomic bomb survivors had cancer with 8-12 yr latency

31
Q

What is the latency of radiation and cancer

A

Usually long after exposure (7-12 years)

32
Q

What are the different types of viral oncogene viruses?

A

RNA oncogene viruses

DNA oncogene viruses

33
Q

DNA oncogene viruses

A

Transforming DNA viruses from stable associations with the host genome

34
Q

What are some different DNA oncogene viruses?

A

HPV - leads to benign squamous papillomas or uterine cancers
EBV - implicates several human malignancies
HBV - linked to development of hepatocellular carcinoma

35
Q

Tumor immunity/surveillance

A

The recognition and destruction of non-self tumor cells when they appear
Not a perfect system, otherwise there’d be no cancer

36
Q

What are the different tumor surveillance mechanisms?

A

Tumor antigens
Antitumor effector mechanisms
Immunosurveillance

37
Q

Tumor-specific antigens

A

Only associated with tumor cells

38
Q

Tumor-associated antigens

A

These are antigens that may be found on normal cells, but may be over-expressed or represent a specialized function of the cells (differentiation-specific antigens)

39
Q

Antitumor Effector mechanisms

A

These are ways in which the body kills tumors

  • Cytotoxic T-cells
  • Natural killer cells
  • Macrophages
  • Humoral mechanisms
40
Q

Cytotoxic T lymphocytes (CD8+)

A

Play a role against virus-induced neoplasms

41
Q

Natural killer cells

A

Lymphocytes that kill tumor cells without prior sensitization
May be the first line of defense against tumors

42
Q

Macrophages

A

May collaborate with T cells and NK cells to destroy tumor cells
May act by mechanisms used to destroy microbes or by producing TNF-a

43
Q

Humoral mechanisms

A

Either activation of compliment or induction of antibody-dependent cytotoxicity by NK cells

44
Q

What is the strongest argument for immunosurveilance?

A

Increased frequency of cancer is observed in immunocompromised

45
Q

How can tumors evade the immune system?

A

Selective outgrowth of antigen-negative variants
Loss or reduced expression of histocompatability antigens
Lack of T-cell co-stimulation
Immunosuppression

46
Q

Selective outgrowth of antigen-negative variants

A

Subclones that are most immunogenic to the host are destroyed, leaving the subclones that are relatively antigen-negative

47
Q

Loss of reduced expression of histocompatability antigens

A

Tumor cells not express normal levels of HLA class I, thereby escaping attach by cytotoxic T cells

48
Q

Location effect of tumors on host

A

Eventhough malignancies are of great concern, benign tumors that are located in critical areas can be very serious

49
Q

Tumor effects on hormone production

A

Adenomas and carcinomas arising from the beta cells of the pancreatic islets may produce hyperinsulism, which may be fatal
Hormone production is more frequent with well-differentiated, benign tumors

50
Q

Ulceration of host with tumors

A

When a tumor expands to the point of breaking through an epithelial surface, problems with bleeding and secondary infection can arise

51
Q

Cachexia

A

Seen in cancer patients
Characterized by progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia, and anemia
Usually a terminal event associated with advanced cancer
Process not fully understood

52
Q

Parenoplastic syndromes

A

Occur in 10-15% of cancer patients
May represent and early manifestation of occult disease
May pose significant clinical problems for affected patients
May mimic metatastic disease and thereby confound treatment

53
Q

Grading of cancer

A

Refers to an estimate of the aggressiveness of a cancer

Based on the microscopic appearance

54
Q

Staging of cancer

A

Describes the cancer extent - size of primary lesion, lymph node involvement, metatastic spread
Estimated by clinical exam and imaging

55
Q

What are the types of labratory diagnosis of cancer

A 
Biopsy
Electron microscopy
Frozen section biopsy
Fine-needle aspiration biopsy
Cytologic (Pap) smear
Flow cytometry
Biochemical assays
Molecular diagnoses
56
Q

Incisional biopsy

A

Portion of the lesion is taken for microscopic examination

57
Q

Excisional biopsy

A

Entire lesion is removed for microscopic examination

Pathology - Exam 1 (9 decks)

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