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Pathological Basis of Disease I > Neoplasia - SRS, RM, KS and anyone else willing to pitch in. Currently done through slide 97/129 > Flashcards

Neoplasia - SRS, RM, KS and anyone else willing to pitch in. Currently done through slide 97/129 Flashcards

1
Q

Give 2 definitions of tumor.

A
  1. a swollen part; swelling; protuberance
  2. an uncontrolled, abnormal, circumscribed growth of cells in any animal or plant tissue; neoplasm
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2
Q

What is a benign tumor?

A

One that does not typically kill. Usually the name ends in -oma

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3
Q

What do we call a tumor with the potential to kill?

A

Malignant

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4
Q

What two components do all tumors have?

A

Parenchyma - made up of neoplasm arises from one genetically altered cell.

Stroma - host derived, non-neoplastic supporting tissue

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5
Q

Characterize the origin of the parenchyma of a tumor.

A

Clonal: entire parenchyma arises from one genetically altered cell.

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6
Q

What term would be applied to a “rock hard stroma” of a tumor?

A

Scirrhous desmoplastic reaction

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7
Q

What is a carcinoma?

A

epithelial malignant neoplasm

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8
Q

How does a carcinoma in situ cause metastasis?

A

It does not.

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9
Q

What is a sarcoma?

A

mesenchymal malignant neoplasm

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10
Q

What is a mass producing malignancy formed by lymphoid cells called?

A

Lymphoma

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11
Q

What is a non-mass producing malignancy of hematopoetic cells called?

A

Leukemia

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12
Q

What would you call a combined mesenchymal and epithelial malignancy?

A

carcinosarcoma

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13
Q

What is the name for a melanocytic malignant neoplasm?

A

Melanoma

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14
Q

Walk through the stepwise development of a cancer.

A
  1. Normal cell suffers initiating mutation
  2. Initiated precursor suffers additional mutation impacting genomic integrity
  3. Precursor with mutator phenotype accumulates additional driver mutations
  4. Founding cancer cell accumulates further mutations and clones emerge
  5. Genetically heterogeneous cancer arises
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15
Q

What are the benign and malignant types of stratified squamous tumors?

A
  1. Squamous cell papilloma
  2. Squamous cell carcinoma
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16
Q

What are the benign and malignant types of basal cells of skin or adnexa tumors?

A
  1. Benign - None
  2. Malignant - Basal cell carcinoma
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17
Q

What are the benign tumor types arising from epithelial lining of glands or ducts?

A
  1. Adenoma
  2. Papilloma
  3. Cystadenoma
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18
Q

What are the malignant types that arise from epithelial lining of glands or ducts?

A
  1. Adenocarcinoma
  2. papillary carcinomas
  3. cystadenocarcinoma
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19
Q

What are the benign and malignant types of tumors that arise from respiratory passages?

A

Benign - Bronchial adenoma

Malignant - Bronchiogenic carcinoma

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20
Q

What are the benign and malignant types of tumors that arise from renal epithelium?

A

Benign - Renal tubular adenoma

Malignant - Renal cell carcinoma

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21
Q

What are the benign and malingnant types of tumors that arise from liver cells?

A

Hepatic adenoma

Hepatocellular carcinoma (Hepatoma)

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22
Q

What are the benign and malignant types of tumors that arise from urinary tract epithelium (transitional)?

A

Bening - Transitional cell papilloma

Malignant - Transitional cell carcinoma

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23
Q

What are the bening and malignant types of tumors that arise from placental epithelium?

A

Benign - Hydatidiform mole

Malignant - Choriocarcinoma

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24
Q

What are the benign and malignant types of tumors that arise from testicular epithelium (germ cells)?

A

Benign - none

Malignant - Seminoma or Embryonal carcinoma

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25
Q

What are the benign and malignant types of tumors of melanocytes?

A

Benign - melanocytic nevus

malignant - malignant melanoma

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26
Q

What are the benign types of connective tissue and derivative tumors?

A

Fibroma

Lipoma

Chondroma

Osteoma

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27
Q

What are the malignant tumors of connective tissues and derivatives?

A

Fibrosarcoma

Liposarcoma

Chondrosarcoma

Osteogenic sarcoma

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28
Q

What are the benign and malignant cancer types that arise from blood vessels?

A

Benign: Hemangioma

Malignant: Angiosarcoma

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29
Q

What are the benign and malignant cancers that arise from lymph vessels?

A

Benign: Lymphangioma

Malignant: Lymphangiosarcoma

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30
Q

What are the benign and malignant cancers that arise from mesothelium?

A

Benign: Benign Fibrous tumor

Malignant: Mesothelioma

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31
Q

benign and malignant from hematopoietic cells

A

Benign: none

Malignant: Leukemias

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32
Q

What are the benign and malignant cancers that can arise from lymphoid tissue?

A

Benign: none

Malignant: Lymphomas

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33
Q

What are the benign and malignant tumors that can arise from smooth muscle?

A

Benign: Leiomyoma

Malignant: Leiomyosarcoma

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34
Q

What are the benign and malignant cancers that can arise from striated muscle?

A

Benign: Rhabdomyoma

Malignant: Rhabdomyosarcoma

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35
Q

What is a polyp?

A

When a neoplasm - either benign or malignant - produces a macroscopically visibile projection above a mucosal surface and projects into the lumen.

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36
Q

What histological findings would you expect to find with a leiomyoma of the uterus?

A

Leiomyoma “FIBROID” - benign tumor of smooth muscle

Tumor should be well-differentiated bundles of smooth muscle that are almost identical in appearance to normal smooth muscle cells in myometrium

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37
Q

What should an adenoma of the thyroid look like?

A

Adenoma = benign tumor

Well -differentiated colloid-filled thyroid follicles

Benign tumors are generally well-differentiated

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38
Q

What would an adenocarcinoma of the colon look like, histologically?

A

Adenocarcinoma = Malignant tumor

Glands that are irregular in shap and size, do not resemble normal glands

Tumor is considered differentiated due to presence of glands

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39
Q

Is a well-differentiated tumor malignant?

A

It can be, morphological distinction between normal parenchymal cells and neoplastic cells can be subtle

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40
Q

What is anaplasia?

A

Lack of differentiation between normal parenchymal cells and neoplastic parenchymal cells

  • in other words, neoplastic cells and normal cells will be different morphologically and functionally
  • often considered a hallmark of malignancy
  • Implies “dedifferentiation”, or loss of the structural and functional differentiation of normal cells
  • Tissues are very poorly-differentiated
  • Cells appear more bizarre
  • Almost always indicative of malignancy
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41
Q

What does the term “mixed tumors” refer to?

What is this?

A

More than one neoplastic cell type

  • usually derived from one germ cell layer
  • PIC: Mixed Tumor Parotid Gland- epithelial cells forming ducts (central glandular structures) and myxoid stroma that resembles cartilage (Top Left: white)
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42
Q

What types of mixed tumors can grow from the salivary glands?

A

Pleomorphic adenoma

  • benign mixed tumor salivary origins

Malignant mixed tumor of salivary gland origin

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43
Q

What is a Wilm’s tumor?

A

Malignant mixed tumor of renal anlage

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44
Q

What does the term “teratogenous” refer to?

A

Derived from more than one germ cell layer, more than one neoplastic cell type

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45
Q

What type of teratogenous tumors can grow in totipotential cells in gonads or in embryonic rests?

A

Benign: Mature cystic teratoma - dermoid cyst

Malignant: Immature teratoma, teratocarcinoma

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46
Q

A histological slide of a mixed tumor of the parotid gland was shown. Why was it considered a mixed tumor?

A

Contained epithelials forming ducts and myxoid stroma that looked like cartilage

Mixed because it was derived from more than one germ cell layer

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47
Q

What is a teratoma?

A

Tumor arising from totipotential germ cells which have the capacity to differentiate along the three germ layers: endoderm, ectoderm and mesoderm

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48
Q

A teratoma that contains a single tissue type is called a …?

A

Monodermal teratoma

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49
Q

An immature teratoma is generally regarded as benign or malignant? How many immature tissue types can it contain?

A

Considered malignant

Can only be one immature element - immature cartilage, neural tissue, etc.

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50
Q

What is a malignant teratoma?

A

Malignancy/carcinoma arising within mature teratoma

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51
Q

Endoderm gives rise to what structures in the embryo, and in adults?

A

Embryo: embyronic gut

Adults:

inner linings of respiratory & digestive tracts

glands - liver and pancreas

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52
Q

What does mesoderm give rise to in embryos and in adults?

A

Embryos:

Somites

Mesenchyme

Notochord

Adults:

Somites create muscle, outer coverings of internal organs, gonads and excretory system

Mesenchyme creates bones and cartilage, circulatory system, dermis

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53
Q

What does ectoderm give rise to in adults?

A

Epidermis

Brain and nervous system

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54
Q

Where are some common sites for teratomas?

A

1, Ovary and testis

  1. Midline of body
    - pineal body
    - base of skull
    - mediastinum (anterior)
    - retroperitoneal
    - sacrococcygeal
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55
Q

An immature teratoma includes what type of tissue elements?

A

Immature mesenchyme, neural and/or blastemal elements

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56
Q

What is a hamartoma?

A

A benign non-neoplastic tumorlike malformation resulting from faulty development in an organ and composed of abnormally arranged tissue elements normally present in that organ

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57
Q

What is a choristoma?

A

•congenital heterotopic (ectopic) rest of cells (tissue)

Not a neoplasm

Normal tissue, abnormal location

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58
Q

What is Cowden Syndrome?

Mode of transmission/inheritance?

Symptoms?

Morbidity?

A

Part of the PTEN hamartoma tumor syndrome (PTHS) (Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Proteus-like syndrome)

Autosomal dominant genetic disorder

Multiple hamartomas

  • Usually skin and thyroid gland hamartomas
  • May cause symptoms or even death

Additional growths in many parts of the body (mucosa, the GI tract, bones, CNS, eyes, and the genitourinary tract).

Morbidity - associated with ↑ occurrence of malignancies, usually in the breast, endometrium or thyroid.

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59
Q

What is the difference between hyperplasia, metaplasia, and dysplasia?

A

Hyperplasia - same tissue type, more of it

Metaplasia - growth of different tissue or cell type

Dysplasia - growth of abnormal tissue, or abnormally developed tissue

  • expansion of immature cells
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60
Q

What happens in eosinophilic esophagitis?

A

Basal cell hyperplasia

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61
Q

What happens in Barrett esophagus?

A

Metaplasia, change from squamous to glandular tissue secondary to chronic irritation from acid reflux

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62
Q

What is the progression seen in squamous epithelial dysplasia?

A

Normal

Low grade/mild - koilocytic atypia

High grade/moderate - progressive atypia and expansion of immature basal cells above the lower third of epthelial thickness

High grade/severe - diffuse atypia, loss of maturation, expansion of the immature basal cells to the epithelial surface

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63
Q

Where can squamous epithelial dysplasia occur?

A

This can occur in any normal or metaplastic squamous epithelium at any body site

e.g. cervix, anus, oral cavity, skin, bronchus, etc.

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64
Q

What sorts of histological findings would you associate with a carcinoma in situ?

A

Epithelium entirely replaced by atypical dysplastic cells

No orderly differentiation of squamous cells

Basement membrane intact

no tumor in subepithelial stroma

Failure of normal differentiation

Marked nuclear and cellular pleomorphism

Numerous mitotic figures

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65
Q

With what test is squamous epithelial dysplasia of the cervix diagnosed?

A

Via cervical cytology, with a pap smear

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66
Q

What should you see, histologically, on a normal cervical cytology versus an abnormal?

A

Normal

large, flattened squamous cells and groups of metaplastic cells

neutrophils interspersed

Abnormal

numerous malignant cells with pleomorphic, hyperchromatic nuclei

normal PMNs interspersed

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67
Q

What are some characteristics of malignant neoplasia?

A
  • Differentiation and anaplasia
  • Rate of growth
  • Local invasion
  • Metastasis
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68
Q

How is differentiation/anaplasia different between benign and malignant tumors?

A

Benign:

Well differentiated; structure sometimes typical of tissue of origin

Malignant:

Some lack of differentiation with anaplasia; structure often atypical

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69
Q

How is the rate of growth different between benign and malignant tumors?

A

Benign:

Usually progressive and slow; may come to a standstill or regress; mitotic figures rare and normal

Malignant:

Erratic and may be slow to rapid; mitotic figures may be numerous and abnormal

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70
Q

How is local invasion different between benign and malignant tumors?

A

Benign:

Usually cohesive expansile well-demarcated masses that usually do not invade or infiltrate surrounding normal tissues

Malignant:

Locally invasive, infiltrating surrounding tissue; sometimes may be misleadingly cohesive and expansile

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71
Q

How is metastasis different between benign and malignant tumors?

A

Benign:

absent

Malignant:

Frequent, more likely with large undifferentiated tumors

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72
Q

What are the exceptions that benign tumors can have to the ‘rules’ of differentiation, rate of growth, local invasion, and metastasis?

A

Differentiation/anaplasia:

Premalignant cytologic changes are anaplastic (cervical dysplasia)

Rate of growth:
Benign conditions can grow rapidly (inflammatory pseudotumors)

Local Invasion:
Benign conditions can be infiltrative (fibromatoses)

Metastasis:
Benign conditions can spread (endometriosis)
some relatively normal looking neoplasms can metastasize and cause death (well-differentiated leiomyosarcoma)

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73
Q

How do we determine when there is a malignancy/cancer?

A

“When the lesion has the potential to metastasize and cause death”

i.e. When the characteristics of the lesion are similar to those of other lesions previously noted to have metastasized and caused death!

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74
Q

What is differentiation?

A

how closely the tumor cells resemble the corresponding normal parenchymal cells

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75
Q

What is the difference between well-differentiated, moderately-differentiated, poorly-differentiated, and undifferentiated tumor cells?

A
  • Well-differentiated – closely resembles normal
  • Moderately-differentiated – sort of resembles normal
  • Poorly-differentiated – does not resemble normal
  • Undifferentiated - The tissue of origin cannot be determined based on the histopathologic appearance of the neoplasm
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76
Q

What level of differentation do malignant tumors have? Benign?

A
  • Benign tumors are usually well-differentiated
  • Malignant tumors can have any level of differentiation
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77
Q

What histological findings are found with anaplastic cells?

A
  • Pleomorphism - marked variation in size and shape of the cells and/or nuclei.
  • Abnormal nuclear morphology -hyperchromatic, large nuclei, bizarre nuclear shapes, prominent nucleoli
  • Increased mitotic activity, and atypical mitoses
  • Loss of polarity - orientation is markedly disturbed
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78
Q

What are some differences between benign and malignant tumors in terms of cell size?

A

Benign: 2-5x normal

Malignant: 2-100x normal

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79
Q

What are some differences between benign and malignant tumors in terms of mitotic rate?

A

Benign:

normal or up to 2-3x increase

Malignant:

2-20x increase, with atypical mitoses

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80
Q

What are some differences between benign and malignant tumors in terms of symmetry?

A

Benign:

symmetric

Malignant:

asymmetric

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81
Q

What are some differences between benign and malignant tumors in terms of margins?

A

Benign:

circumscribed

Malignant:

indistinct

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82
Q

What are some differences between benign and malignant tumors in terms of necrosis?

A

Benign:

uncommon

Malignant:

common

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83
Q

What are 3 common features of malignancy?

A

Hyperchromaticity

Desmoplasia

Angiogenesis

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84
Q

What is hyperchromaticity?

A
  • marked increase in DNA content per nucleus (more intense staining by Hematoxylin (H of H&E)
  • A disproportionate increase in DNA density is seen even when there is no significant enlargement of the nucleus
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85
Q

What is desmoplasia?

A

Increased fibrous tissue

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86
Q

What is angiogenesis? What happens to tumors without it?

A
  • increased blood vessels
  • Ischemic tumor necrosis occurs with insufficient angiogenesis
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87
Q

What are the 2 types of angiogenesis?

A

Neo-angiogenesis
- vessels sprout from existing capillaries

Vasculogenesis
- endothelial cells are recruited from the bone marrow

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88
Q

What findings are associated with a gross specimen of a fibroadenoma of the breast? Histological findings?

A

Tan color

Encapsulated small tumor

sharply demarcated from breast tissue

Fibrous capsule delimits tumor from surrounding tissue

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89
Q

What findings are associated with a gross specimen of an invasive ductal carcinoma of the breast? Histological findings?

A

Lesion is retracted

Infiltrating the surrounding breast tissue

Stony hard on palpation

Histology:

invasion of breast stroma and fat be nests and cords of tumor cells

absence of well-defined capsule

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90
Q

A benign tumor of the smooth muscle of the uterus would be called what? What 6 characteristics would you expect?

A

Leiomyoma

  • small
  • well-demarcated
  • slow growing
  • noninvasive
  • nonmetastatic
  • well differentiated
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91
Q

A malignant tumor of the smooth muscle of the uterus would be called what? What 6 characteristics would you expect?

A

Leiomyosarcoma

  • large
  • poorly differentiated
  • rapidly growing with hemorrhage and necrosis
  • locally invasive
  • metastatic
  • poorly differentiated
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92
Q

Grading neoplasms is done with what 2 scales?

A

Histological

  • essentially grades differentiation

Nuclear grade:

  • essentially grades bizarreness/pleomorphisms
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93
Q

What is the gleason scale?

A

Grading scale for adenocarcinomas of the prostate

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5
Perfectly
94
Q

Explain the steps of the Gleason Scale, from 1-5.

A

Well Differentiated

  1. Small, uniform glands
  2. More space (stroma) between glands

Moderately differentiated

  1. Distinct infiltation of cells from glands at margins

Poorly differentiated, anaplastic

  1. Irregular masses of neoplastic cells with a few glands
  2. Lack of or occasional glands, sheets of cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What 9 changes would you expect to see with malignant transformation?

A

Self-sufficiency in growth signals
Insensitivity to growth-inhibitory signals

Evasion of apoptosis
Limitless replicative potential
Sustained angiogenesis
Ability to invade and metastasize
Defects in DNA repair
Alterations in cell metabolism (e.g. Warburg effect)
Ability to evade host immune response

96
Q

With alterations in malignant transformation, what does self-sufficiency in growth signals mean?

A

capacity to proliferate without external stimuli

oncogene activation with oncoprotein production (gain of function)

97
Q

With alterations in malignant transformation, what does insensitivity to growth-inhibitory signals mean?

A

May not respond to molecules that are inhibitory to the proliferation

  • TGF-β dysfunction
  • cyclin-dependent kinase inhibitor dysfunction
98
Q

With alterations in malignant transformation, what does evasion of apoptosis mean?

A

May be resistant to programmed cell death

  • p53 and other tumor suppressor gene inactivation (loss of function)
  • activation of anti-apoptotic genes (gain of function)
  • inactivation of apoptotic genes (loss of function)
99
Q

With alterations in malignant transformation, what does limitless replicative potential mean?

A

•unrestricted proliferative capacity avoiding cellular senescence

100
Q

With alterations in malignant transformation, what defects in DNA repair are expected?

A

May fail to repair DNA damage (loss of function)

  • genomic instability
  • mutations in proto-oncogenes and tumor suppressor genes
101
Q

What are the 10 hallmarks of cancer?

A
  1. Evading growth suppressors
  2. Enabling replicative immortality
  3. Tumor-promoting inflammation
  4. Activating invasion and metastasis
  5. Genomic instability
  6. Inducing Angiogenesis
  7. Resisting cell death
  8. Deregulating cellular energetics
  9. sustaining proliferative signaling
  10. avoiding immune destruction
102
Q

What gives it away?

A

Immature Teratoma

Immature mesenchyme, neural and/or blastemal elements

**Dark banding areas=undifferentiated cells–>might be malignant***

103
Q

Who am I?!

A
  • Well-differentiated squamous cell carcinoma of the skin
  • The tumor cells similar to normal squamous epithelial cells
  • with intercellular bridges and nests of keratin pearls (arrow)
  • growing all over the place.
104
Q

Why? Most worrisome aspect?

A

Malignant Teratoma

-Carcinoma, sarcoma and/or germ cell malignancy in teratoma

***Bottom Left: If Brusk Carcinoma? Glandular tissue àwould give chemo

105
Q

What do you see here?

A

R side: thickening, loss of maturation= cells at top look like bottom.

DYSPLASIA

  1. lack maturation
  2. nuclear enlargement
  3. loss of normal arrangment (nuclear)
106
Q

What defines each type? Rank?

A
  • This can occur in any normal or metaplastic squamous epithelium at any body site
  • cervix, anus, oral cavity, skin, bronchus, etc.
  • CIN I-Mild halos at top L from HPV
  • CINII – Moderate Lower 2/3 involved
  • CIN III/CIS Severe Dysplasia
  • CIS- Carcinoma In Situ- immaturity Full thickness of epitelium

In this example BM is intact- until there is invasion it will kill the patient

107
Q

What are the 3 main factors for determining the rate of cancer growth?

A
  1. Doubling time of tumor cells
  2. Fraction of tumor cells in the replicative pool
  3. Rate at which cells are shed/die
108
Q

Solid tumors that are detected clinically have….?

A

already completed a major portion of its life span

109
Q

In addition to doubling time, fraction of cells in replicative pool, and rate of death, what other factors influence tumor growth?

A

Blood supply - think angiogenesis inhibitors for treatment

Hormonal factors - estrogen/testosterone blockers for Tx

emergence of aggressive sub-clones

110
Q

What is the smallest clinically detectable tumor mass? How many cells is this? Doubling times?

A

smallest mass = 1 gram

30 doublings

10^9 cells

111
Q

What class of immune cells recognizes tumor cells?

A

CD8+ T cells

112
Q

Normal host cells will display what type of antigens, leading to a what type of response in what type of immune cell?

A

Normal cells display multiple MHC-associated self antigens

CD8+ T cells will have no response

113
Q

What sorts of ‘clues’ are expressed by tumor cells that lead to recognition by the host’s immune system?

A

Tumor cells will express different types of tumor antigens

For example:

oncogene or mutated suppressor gene products

mutated self proteins

Overexpressed or aberrantly expressed self proteins

oncogenic virus

114
Q

What are 3 mechanisms by which tumor cells evade host immunity?

A
  1. Failure to produce tumor antigen, antigen-loss variant of tumor cell
    - leads to lack of T-cell recognition of tumor
  2. Mutations in MHC gene or genes needed for antigen processing, class I MHC deficient tumor cell
    - leads to lack of t-cell recognition of tumor
  3. Production of immunosuppressive proteins or expression of inhibitory cell surface proteins
    - leads to inhibition of t-cell activation
115
Q

What is the Warburg Effect?

A

Metabolic alteration in tumor cells - switch to aerobic glycolysis

Tumor cells will shift their glucose metabolism away from O2-hungry mitochondria to aerobic glycolysis leading to lactose fermentation

116
Q

In addition to tumor cells, what other types of tissues do you see the Warburg Effect in?

A

embryonic tissues

117
Q

What is the advantage of the Warburg Effect for tumor cells?

A

•Provides metabolic intermediates used in synthesis of cellular components

118
Q

How can clinicians exploit the Warburg Effect for better patient outcomes?

A

Aerobic glycolysis leading to lactose fermentation allows visualization of tumors via positron emission tomography (PET)

119
Q

In normal non-proliferative tissues, how do cells react to normal and low concentrations of oxygen?

A

In normal ppO2:

oxidative phosporylation happens

glucose → pyruvate

pyruvate oxidized in mitochondria

In low ppO2:

anaerobic glycolysis happens:

glucose → pyruvate

pyruvate → lactate, not into mitochondria

120
Q

How do cancer cells respond to different levels of O2?

A

Cancer cells will convert most glucose to lactate regardless of ppO2.

  • also seen in normal proliferative tissues
121
Q

What is metastasis? What type of tumor metastasizes?

A

Metastasis is the spread ot a tumor to sites that are physically discontinuous with the primary tumor

Metastasis = malignant

122
Q

What is local invasion?

A

Growth of cancers is accompanied by progressive infiltration, invasion, and destruction of the surrounding tissue.

Benign tissues will grow as expanding, cohesive masses and remain localized to point of origin.

  • often lack capacity to infiltrate, invade, or metastasize to distant sites
123
Q

What is the general sequence of events in the sequence of events leading to invasion of the epithelial basement membrane by tumor cells?

A

Tumor cells detach from each other due to reduced adhesiveness and attract inflammatory cells. Intercellular junctions are loosened.

Proteases secreted from tumor cells and inflammatory cells degrade the basement membrane, ECM.

Binding of tumor cells to proteolytically generated binding sites and tumor cell migration and invasion follow.

124
Q

What characteristics of a tumor make it more likely to metastasize?

A

Rapidly growing

larger

more aggressive

125
Q

What percent of new cancer diagnosis will be metastatic?

A

30%

126
Q

What are the patterns of metastasis?

A

Direct seeding of body cavities or surfaces

Lymphatic spread

Hematogenous spread

127
Q

What happens with hematogenous spread of metastatic cancers?

A

Venous invasion with tumor cells into capillary bed

direct transplantation by surgical intervention

128
Q

What types of cancers or venous systems make for hematogenous spread?

A

Portal blood supply from gut into liver

Caval blood supply traveling to lungs

Hepatic, renal and adrenocortical cancers propagate in veins

129
Q

What is the proto-oncogene associated with Adenocarcinoma of the lung? Give both names

A

ERBB1 (EGFR)

130
Q

What is the proto-oncogene associated with breast carcinoma? Give both names.

A

ERRB2 (HER)

131
Q

In adenocarcinoma (ERBB1/EGFR) and Breast carcinoma (ERRB2/HER) What is the mode of activation?

A

Mutation amplification

132
Q

What conditions does a point mutation in the RET gene lead to?

(3)

A
  1. Multiple endocrine neoplasia Type 2A
  2. Multiple endocrine neoplasia Type 2B
  3. Familial Medullary thyroid carcinoma
133
Q

If the ALK gene undergoes translocation, fusion, or point mutation, what conditions may arise?

(3)

A
  1. Adenocarcinoma
  2. Certain lymphomas
  3. Neuroblastoma
134
Q

A point mutation in the KRAS gene which encodes a GTP-Binding protien is associated with what tumors? (3)

A
  1. Colon
  2. Lung
  3. Pancreatic

He indicated this was a pretty important one…

135
Q

What would a point mutation in the GNAS gene lead to? (2 - kinda)

A
  1. Pituitary adenoma
  2. Other endocrine tumors
136
Q

What does an NRAS mutation lead to potentially?

A

Melanomas

Hematologic malignancies

(Think he said this one was more of a later on type information)

137
Q

If point mutation affected the ABL gene, what conditions could arise?

A
  1. Chronic myeloid leukemia
  2. acute lymphoblastic leukemia (don’t really need to focus on this now)
138
Q

A translocation event occurs that leads to the patient having chronic myelogenous leukemia… what genes are involved, and what is the end product of the translocation?

A

Translocation: (9;22)(q34;q11)

Affects: ABL 9q34 and BCR 22q11

139
Q

What does a point mutation or translocation involving the BRAF gene lead to?

(3)

A
  1. Melanomas
  2. Leukemias
  3. Colon carcinoma
140
Q

What could a translocation involving C-MYC lead to?

A

Burkitt lymphoma

141
Q

What could an amplification of N-MYC lead to?

A

Neuroblastoma

Small cell carcinoma of the lung

142
Q

What could an amplification of the L-MYC gene lead to?

A

Small cell carcinoma of the lung

143
Q

What could arise d/t a translocation event involving CCND1 (Cyclin D)?

A

Mantle cell lymphoma

Multiple myeloma

144
Q

What genes are affected in chronic myelogenous lymphoma translocations?

A

ABL 9q34/BCR 22q11

145
Q

What genes are involved in the translocation event that leads to Burkitt lymphoma?

A

c-MYC 8q24

IGH 14q32

146
Q

What is the translocation that you end up with in Burkett’s lymphoma?

A

(8;14)(q24;q32)

147
Q

What genes are involved in Ewings Sarcoma?

A

FLI1 11q24

EWSR1 22q12

148
Q

What is the translocation result you get in cases of Ewing Sarcoma?

A

(11;22)(q24;q12)

149
Q

What are the four cell cycle components and inhibitors that he told us we need to know that are frequently mutated in cancer?

A
  1. CDK4; D cyclins
  2. INK4/ARF Family (CDKN2A-C)
  3. RB
  4. P53
150
Q

What is the normal role of CDK4; D cyclins?

A

Form a complex that phosphorylates RB, allowing the cell to progress through the G1 restriction point

151
Q

What is the role of INK4/ARF family (CDKN2A-C)?

A
  1. p16/INK4a binds to cyclin D-CDK4 and promotes the inhibitory effects of RB
  2. p14/ARF increases p53 levels by inhibiting MDM2 activity
152
Q

What is the role of RB in the cell?

A

Tumor suppressive “pocket” protein that binds E2F transcription factors in its hypophosphorylated state, preventing G1/S transition; also interacts with several transcription factors that regulate differentiation

153
Q

What is the normal role of P53 in the cell cycle?

A
  • Tumor suppressor
    • causes cell cycle arrest and apoptosis
    • requird for G1/S checkpoint and is a main component of the G2/M checkpoint
154
Q

In cancers why might you see increased levels of P53 or RB?

A

The proteins are present, just mutated to the point where they do not function. Thus, produced and present just not working.

155
Q

What famillial syndrome gives rise to…

  • neuroblastoma
  • juveline myeloid leukemia

and what gene is mutated?

A
  • Neurofibromatosis type 1 (neurofibromas and malignant peripheral nerve sheath tumors)
  • NF1
156
Q

What famillial syndrome gives rise to Schwannomas and meningiomas?

What gene is mutated?

A
  • Neurofibromatosis type 2 (acoustic schwannoma and meningioma)
  • NF2
157
Q

What familial syndrome gives rise to…

  • retinoblastoma
  • osteosarcoma
  • carcinomas of the…
    • breast
    • colon
    • lung

And, what gene is mutated?

A
  • Familial retinoblastoma syndrome (retinoblastoma, osteosarcoma, other sarcomas)
  • RB
158
Q

What familial syndrome commonly leads to renal cell carcinomas?

What gene is mutated?

A
  • Von Hippel Lindau syndrome (cerebellar hemangioblastoma, retinal angioma, renal cell carcinoma)
  • VHL
159
Q

What is Li-Fraumeni syndrome due to?

What does it lead to?

A

D/T loss of P53 from a mutation to TP53 gene.

Leads to development of most human cancers.

160
Q

What are BCRA1 and BCRA2 implicated in?

A

Familial breast and ovarian carcinoma; carcinomas of male breast; chronic lymphocytic leukemia (BRCA2)

161
Q

What does a mutation in MEN1 lead to?

A
  1. Multiple endocrine neoplasia type I (MEN1)
  2. Pituitary adenoma
  3. parathyroid endocrine tumors
  4. pancreatic endocrine tumors
162
Q

What are the 7 steps of the metastatic cascade - hematogenous spread of a tumor?

A

1) Changes (“loosening up”) of tumor cell-cell interactions
2) Degradation of ECM
3) Attachment to ECM components
4) Migration (locomotion ) of tumor cells
5) Clumping in vessels
6) Adhesion to the endothelium
7) Egress through the vascular basement membrane

163
Q

If a person has a problem with E-Cadherin, what would they be predisposed to developing?

A

Increased Risk of GI cancers.

(Though not in slides, he talked about this a couple of times)

164
Q

What is this?

A

Liver studded with metastatic cancer

165
Q

Top right is a normal axillary lymph node.

Bottom left is taken from a patient with metastatic breast carcinoma.

What do you see happening here?

A

Encircled are aggregates of tumor cells metastasizing to the subcapsular sinus.

The subcapsular sinus is the first plase cancer will metastasize to in a lymph node.

166
Q

What is depicted in A - The blue circle, and B- the green circle?

A

A – Micrometastasis

B – Subcapsular histiocytosis - Epitheliod macrophages (he called them this in lecture)

167
Q

What is Cachexia?

Cancer Cachexia is caused by what main process?

A
  1. •Progressive loss of body fat and lean body mass accompanied by profound weakness, anorexia, and anemia
  2. •TNFα and IL-1 produced by macrophages in response to tumor cells or by the tumor cells themselves mediates cachexia
168
Q

What is a paraneoplastic syndrome?

A

•Symptom complexes that cannot readily be explained, either by the local or distant spread of the tumor or by the elaboration of hormones indigenous to the tissue from which the tumor arose, are known as paraneoplastic syndromes.

169
Q

What are the two paraneoplastic syndromes associated with small-cell carcinoma of the lung?

A

Cushing Syndrome

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

170
Q

What paraneoplastic syndrome is associated with squamous cell carcinoma of the lung?

A

Hypercalcemia

171
Q

How does squamous cell carcinoma of the lung cause hypercalcemia?

(4)

A
  1. Parathyroid hormone-related protein (PTHRP),
  2. TGF-α,
  3. TNF,
  4. IL-1
172
Q

Why do paraneoplastic syndromes only occur with malignant tumors?

A

They actually occur with both malignant AND benign tumors. Ha!

173
Q

What paraneoplastic syndrome does renal carcinoma classically present with?

What causes this?

A

Polycythemia

Erythropoietin

174
Q

A patient presents to the clinic with diarrhea, cramps, nausea, vomiting, wheezing, dyspnea and cough.

On physical exam you find hepatomegaly, cutaneous flashes and apparent cyanosis.

The patient if diagnosed with hepatocellular carcinoma. What is the paraneoplastic sydrome this patient has?

What might you see in their heart?

A
  1. Carcinoid syndrome
  2. Heart
    1. Pulmonic and tricuspid thickening and stenosis
    2. endocardial fibrosis
175
Q

What paraneoplastic syndrome is associated with…

  1. hepatocellular carcinoma
  2. bronchial adenoma (carcinoid)
  3. pancreatic carcinoma

What is the causal mechanism?

A

Carcinoid syndrome

Serotonin

Bradykinin

176
Q

What can carcinoid syndrome easily be mistaken for?

A

Type I hypersensitivity

177
Q

Myasthenia gravis is a paraneoplastic syndrome associated with what cancer?

So what should the first thing we look for be when a patient presents with myasthenia gravis?

A
  1. Thymic neoplasms
  2. Bronchogenic carcinoma

Check for thymomas

178
Q

What paraneoplastic syndrome is associated with…

Gastric carcinoma

Lung carcinoma

Uterine carcinoma

and what is a giveaway physical finding you should be aware of?

A

Acanthosis nigricans

Armpits will be much darker than they should be.

179
Q

A patient presents with muscle weakness and a helicotrope rash. They have cancer.

What is the paraneoplastic syndrome?

What is the likely cancer candidate?

A

Dermatomyositis

Bronchogenic Breast Carcinoma

180
Q

You have two patients to see today in your oncology rounds, one has pancreatic carcinoma and the bother has bronchogenic carcinoma. The attending physician asks you what the associated paraneoplastic syndromes are for each.

You answer?

A

Inside your head you again consider what a douche your attending is, while you verbally respond…

Both those cancers are associated with venous thrombosis, (and, showing off, you add) also known as Trousseau phenomenon.

181
Q

What paraneoplastic syndrome is associated with…

Acute promyelocytic leukemia

Prostatic carcinoma

???

A

Disseminated intravascular coagulation

182
Q

Your patient has valve leaflet vegetations d/t hypercoagulative state. They have advanced cancer. What is the paraneoplastic syndrome they are enduring?

A

Nonbacterial thrombotic endocarditis

183
Q

What is the initiator in the 2 hit hypothesis?

A

The thing that does the direct damage to the DNA

184
Q

What is the incidence of a cancer?

A

•probability of being diagnosed with a disease during a given period of time

TQ alert in these

185
Q

How is the incidence of cancer calculated?

Expressed?

A
  • number of new cases of a disease divided by the number of persons at risk
  • usually expressed as new cases/year per 100,000 population
186
Q

What is the prevalence of cancer?

A

•the total number of cases of disease existing in a population

187
Q

How is prevalence calculated?

Expressed?

A
  • total number of cases of a disease existing divided by the total population
  • Usually expressed as total cases per 100,000 persons
188
Q

For women, what cancer has the highest incidence?

Highest mortality?

A

Incidence - Breast

Mortality - Lung

189
Q

For men what cancer has highest incidence?

Mortality?

A

Incidence - prostate

Mortality - Lung

190
Q

This sample showing “small round blue cell tumors” was most likely taken from what age patient?

What are the four common cancers this could be a sample from?

A

Infant or childhood

  1. •Neuroblastoma
  2. •Wilms tumor (nephroblastoma)
  3. •Retinoblastoma
  4. •Acute leukemias
191
Q

In 1775 london, Sir Percival Pott made a connection between chimney sweep’s exposure to soot and a type of cancer. What type of cancer whas it?

A

Squamous cell carcinoma of the scrotum

Sorry for the image… I had to. He said there would be a TQ on this. Now you won’t forget it… EVER.

192
Q

The population of Japan historically has had a higher incidence of gastric cancer than japanese populations that have migrated to the USA. What caused this?

A

Some component of diet, possibly the preservative techniques used.

193
Q

What is the classic example of a chemical carcinogen that contributes to oral cancer?

A

Betel nuts

194
Q

Arsenic is an example of an occupational agent that is carcinogenic. What cancers does this cause?

A
  1. Skin carcinoma
  2. Lung carcinoma
195
Q

What cancers does asbestos lead to?

A
  1. Lung,
  2. esophageal,
  3. gastric, and
  4. colon carcinoma;
  5. mesothelioma
196
Q

Where can mesothelioma arise apart from the lungs?

A

Testes

197
Q

What cancer does benzene lead to?

A

Acute myeloid leukemia

198
Q

What cancer does Radon and its decay products lead to?

What populations are at risk for this?

A

Lung cancer

Workers in quarries and underground mines

199
Q

What cancer does PVC exposure lead to?

A

NONE!!! This is one of his hot buttons. Know that it’s Vinyl Chloride, a component in the manufacture of PVC, that is carcinogenic.

200
Q

Ok, so what does vinyl chloride exposure predispose you to?

A

Hepatic Angiosarcoma

201
Q

What are the oncogenic RNA viruses? What conditions are they associated with?

(2)

A
  1. •HTLV-1 – adult T-cell leukemia/lymphoma
  2. •HCV – hepatocellular carcinoma
202
Q

What are the oncogenic DNA viruses??

(6)

A
  1. HBV
  2. HPV
  3. HHV-8
  4. EBV
  5. CMV
  6. Merkel cell polyomavirus
203
Q

What does infection with HBV predispose one to?

A

Hepatocellular carcinoma

204
Q

What does infection with HPV predispose one to?

(types 1,2,4,6,7,11, 16,18)

(4)

A

carcinomas of…

  1. Cervix
  2. Anus
  3. Penis
  4. Oropharynx​
205
Q

What fungus is associated with cancer? What toxin does it have that is related to this?

Finally what is the cancer?

A
  1. Aspergillus
  2. Aflotoxin B1
  3. hepatocellular carcinoma (P53 mutation)
206
Q

What is infection with HHV-8 associated with? (2)

A
  1. Kaposi sarcoma
  2. Primary effusion lymphoma
207
Q

What three things is EBV associated with?

A
  1. Burkitt lymphoma,
  2. Hodgkin lymphoma
  3. nasopharyngeal carcinoma
208
Q

What cancer is CMV (HHV-5) infection associated with?

A

Mucoepidermal carcinoma

209
Q

What cancer is merkel cell polyomavirus associated with?

A

Merkel cell Carcinoma

210
Q

What are the parasites associated with cancer? (3)

What cancers are each associated with?

A
  • Schistosoma haematobium – bladder cancer
  • Schistosoma japonicum – colon cancer
  • Opisthorchis viverrini – cholangiocarcinoma
211
Q

H. pylori infection predisposes one to develop what two cancers?

A
  1. Extranodal marginal zone (MALT) lymphoma
  2. Gastric adenocarcinoma
212
Q

A large # of cancer types have combined environmental influences and hereditary predispositions. What does this mean in the context of the two hit theory?

A
  • Hit 1 in first mutated gene (abnormal) is inherited
  • Hit 2 in second mutated gene (originally normal) is acquired
213
Q

What are the four identified genetic predispositions to cancer?

A
  1. Defective DNA-Repair Syndromes
  2. Famillial Cancers
  3. Autosomal Dominant Inherited Cancer syndromes
  4. Interactions of genetic and non-genetic factors
214
Q

What are five inherited autosomal recessive syndromes of defective DNA repair that Dr. Gomez put on the slide but didn’t discuss?

A
  1. Xeroderma pigmentosum (nucleotide excision repair of cross-linked pyrimidine dimers)
  2. Hereditary nonpolyposis colon cancer syndrome (DNA mismatch repair)
  3. Ataxia-telangiectasia (DNA repair by homologous recombination)
  4. Bloom syndrome (DNA repair by homologous recombination)
  5. Fanconi anemia (DNA repair by homologous recombination)
215
Q

What are the autosomal recessive Defective DNA repair conditions we covered?

A
  1. Xeroderma Pigmentosa
  2. Ataxia Telangiectasia
  3. Bloom Syndrome
  4. Fanconi Anemia
216
Q

Name the condition

  • FA process defects associated with aplastic anemia, hypopigmentation, café-au-lait spots, skeletal problems, defects of the genitourinary tract; gastrointestinal tract; heart; eye and ears with hearing loss and acute myeloid leukemia
A

Fanconi anemia

217
Q

Name the condition -

  • Helicase abnormality associated with short stature, sun-sensitive skin changes, an increased risk of cancer, and other health problems
A

Bloom syndrome

218
Q

Name the condition

-
•ATM gene defect (involved in DNA repair) associated with progressive difficulty with coordinating movements, weakened immune system, leukemias and lymphomas

A

Ataxia Telangiectasia

219
Q

Name that condition

-

•Nucleotide excision repair abnormality associated with extreme sensitivity to ultraviolet (UV) rays affects the eyes and skin (cancers), may also have CNS problems (increased pyrimidine dimers)

A

Xeroderma pigmentosa

220
Q

What is the autosomal dominant defective DNA repair condition we were presented with?

A

Hereditary nonpolyposis colorectal cancer (HNPCC) = Lynch syndrome

221
Q

Name that condition!

•DNA mismatch repair abnormality leading to microsatellite instability associated with colorectal, endometrial, gastric, ovarian, ureteral, CNS, small bowel, hepatobiliary tract and skin cancers

A

Hereditary nonpolyposis colorectal cancer (HNPCC) = Lynch syndrome

222
Q

This is an example of defective DNA repair. This condition carries increased risk for skin cancers d/t exposure to UV. UV causes cross-linking of pyrimidine residues which prevents normal DNA replication. What process is impaired in this patient?

A

Nucleotide Excision repair - several proteins are involved in this. Loss of any one can give rise to Xeroderma Pigmentosum

223
Q

Inherited cancer syndromes are usually a point mutation in a single ellele of a tumor supressor gene. The second event that incites tumorigenesis involves a second mutation in the other remaining previously normal allele.

What are three example of this?

What is the age of onset?

What are two other characteristics?

A
  1. •Retinoblastoma
  2. •Familial adenomatous polyposis
  3. •MEN syndromes
  • Early age at onset
  • Tumors arising in ≥2 close relatives of the index case
  • Multiple or bilateral tumors
224
Q

What is the inheritance pattern for each of these conditions?

Retinoblastoma

Li-Fraumeni syndrome (various tumors)

Melanoma

Familial adenomatous polyposis/colon cancer

Neurofibromatosis 1 and 2

Breast and ovarian tumors

Multiple endocrine neoplasia 1 and 2

Hereditary nonpolyposis colon cancer

Nevoid basal cell carcinoma syndrome

Cowden syndrome (epithelial cancers)

Peutz-Jegher syndrome (epithelial cancers)

Renal cell carcinomas

A

Autosomal Dominant

225
Q

For each of these, name the gene associated with them!!!!

Retinoblastoma

Li-Fraumeni syndrome (various tumors)

Melanoma

Familial adenomatous polyposis/colon cancer

Neurofibromatosis 1 and 2

Breast and ovarian tumors

Multiple endocrine neoplasia 1 and 2

Hereditary nonpolyposis colon cancer

Nevoid basal cell carcinoma syndrome

Cowden syndrome (epithelial cancers)

Peutz-Jegher syndrome (epithelial cancers)

Renal cell carcinomas

A

Retinoblastoma - RB

Li-Fraumeni syndrome (various tumors) - P53

Melanoma - P16/INK4A

Familial adenomatous polyposis/colon cancer- APC

Neurofibromatosis 1 and 2 - NF1, NF2

Breast and ovarian tumors - BRCA1, BRCA2

Multiple endocrine neoplasia 1 and 2 - MEN1, RET

Hereditary nonpolyposis colon cancer - MSH2, MLH1, MSH6

Nevoid basal cell carcinoma syndrome - PTCH

Cowden syndrome (epithelial cancers) - PTEN

Peutz-Jegher syndrome (epithelial cancers) - LKB=STK11

Renal cell carcinomas - VHL

226
Q

What is the eponym for MEN1?

What are the three P’s of MEN1?

A

Werner syndrome

  1. Pituitary adenoma
  2. parathyroid hyperplasia
  3. pancreatic tumors
227
Q

What is the common thread between MEN2A, B and FTMC?

A

Medullary Thyroid cancer d/t RET mutation

228
Q

What are the differences between MEN2A and B?

A

MEN2A - has parathyroid hyperplasia

MEN2B - Has marfanoid body habitus and mucosal neuromas

229
Q

What are two examples of nonhereditary predisposing conditions for cancer? What are examples of these?

A

Chronic inflammation

  • Persistent regenerative cell replication (cirrhosis—hepatocellular carcinoma), (chronic skin fistula—SCC)
  • Helicobacter pylori gastritis
  • Viral hepatitis
  • Chronic ulcerative colitis
  • Chronic pancreatitis

Precancerous conditions such as repair followed by dysplasia

  • Leukoplakia of the oral cavity, vulva or penis
  • Villous adenoma of the colon
  • Chronic atrophic gastritis-pernicous anemia
  • Chronic ulcerative colitis
  • Solar keratosis of the skin
230
Q

What neoplasm is associated with asbestosis and silicosis?

What is the etiologic agent?

A
  1. Mesothelioma
  2. Lung Carcinomas

Asbestos fibers and silica particles

231
Q

What neoplasm is associated with IBS?

A

Colorectal cancer

232
Q

What neoplasm is associated with lichen sclerosus et atrophicus?

A

Vulvar squamous cell carcinoma

233
Q

What neoplasm is associated with Sjögren syndrome, Hashimoto thyroiditis?

A

MALT Lymphoma

234
Q

What is Schistomiasis the etiologic agent for?

A

Bladder carcinoma and the associated chronic cystitis

235
Q

What, in the USA, causes bladder cancer?

A

Smoking!

236
Q
A

Pathological Basis of Disease I (11 decks)

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