Cell growth and neoplasia Flashcards
What is development?
From the perspective of the cell: dramatic changes in …
- Cell proliferation
- Cell death (apoptosis)
- Cell differentiation
- Cell migration
- Cell-cell interactions

For an adult organism with normal homeostasis:
From the perspective of the organism:
•Cell regulation is a highly orchestrated, more static program resulting in optimal function of specialized tissues/ organs/ organ systems.

What are some examples of tissues constantly dividing?
What are quienscent tissues/cells?
What are examples of non-dividing cells?
Continuously dividing tissues/cells
**Mostly in S phase of cell cycle
–eg: skin, gut epithelium, hematopoietic system
–Constant turnover
•Quiescent tissues/cells (normaly don’t proliferate but can under certain stimuli?
-Can be in S phase (dividing) or G<u>0</u> phase (non-dividing)
–eg: hepatocytes
–Normally little to no turnover
–Capacity for proliferation if needed
•Non-dividing tissues/ cells
**mostly in GO (not dividing)
–eg: CNS neurons
–Little to no capacity for proliferation

Hypertrophy and hyperplasia:
What are they?

What are some physiologic examples of hypertrophy?
What are some pathologic examples of hypertrophy?

Examples:
–Physiologic: uterus in pregnancy (actually combination of hypertrophy AND hyperplasia)
–Pathologic: heart in hypertension (high blood pressure)

What is hyperplasia?
It may be associated with what?
What are some physiologic examples?
What are some pathologic examples?

-Increase in cell number
–Often driven by hormones/ growth factors
–May be associated with an increased risk of neoplasia
–Physiologic
–>mammary gland during puberty and pregnancy
–Pathologic:
–>endometrium (since it is constantly renewing itself).
•known risk factor for endometrial neoplasia

What is metaplasia?
What are some examples?
Give an example from columnar to squamous epithelium change?
Metaplasia
–Change from one benign, differentiated cell type to another, usually in response to injury (eg: inflammation)
–May be associated with an increased risk of neoplasia
•Examples:
–Bronchus
–>Columnar (Pseudostratified) of the mainsteam bronchus epithelium changes to squamous metaplasia in response to smoking.
- cause: smoking
- known risk factor for bronchopulmonary neoplasia (or squamous cancer cancer in the mainstem bronchus).
–Esophagus
- squamous to columnar (glandular) metaplasia (“Barrett esophagus”)
- cause: acid reflux (from the stomach into the distal esophagus)
- known risk factor for esophageal neoplasia

Neoplasia
What is it?
What is it origin usually?
How is it different from tumor?
- “new formation”
- Progressive, unchecked increase in cell number (-/+ invasion/metastasis)
- Clonal process
- Generally pathologic and irreversible
“tumor”
Original meaning (latin) = swelling
In current usage, generally synonymous with neoplasm
Neoplasia, what are some global mechanistic hallmarks:
What cell’s autonomous mechanism are disrupted?
What non-autonomous mechanisms are altered?
Disruption of normal homeostatic mechanisms
–Altered cell-autonomous mechanisms
- Activation of oncogenes (induce cell proliferation)
- inactivation of tumor suppressors (which normaly suppress cell division)
–Cell-nonautonomous mechanisms
•Altered microenvironment
–surrounding tissue, including stroma, blood vessels, immune cells
•Altered macroenvironment
–Circulating cells (eg: immune cells) and factors (eg: hormones, cytokines)
Benign neoplasms
Malignant neoplasm, how is it different than benign neoplasms?
–Do not invade or metastasize (unregulated proliferation of cells that does not invade or spread to other sites)
–Cause injury largely by compression/ interference in function of adjacent structures
Malignant neoplasms
–Invade and metastasize to other sites
–“CANCER”
–Cause injury both by local tissue destruction and distant dissemination and tissue destruction
What are some pathologic differences between benign and malignant neoplasia?
Which one is circumscrived or encapsulated?
Necrosis is common in which one?

Microscopic pathologic features
which one is well differentiated?
Which one has a high rate of cell turnover?
Which one show cytologic pleomorphism?
in which one is the boundary between tumor and adjacent tissue is maintained?

General classification: *don’t pay too much attention



For benign neoplasms:
What is a way to treat?
Does it reccur?
Does it progress to malignant neoplasm?

What are some non-genetic factors that may lead to cancer?

What are some genetic factors that may lead to cancer?

Dysplasia
What are some histologic characteristics?

- “Disordered growth”
- In epithelia, hallmark of early premalignant neoplasia
- Characteristic histologic features
–Loss of cytologic uniformity
–Loss of normal histologic maturation
–Loss of architectural orientation
•Usually assigned histologic “grade” (low versus high; marked/extensive dysplasia = “carcinoma in-situ”)
Histologic grade:
Low grade means more or less resemblance to normal tissue?
What about high grade?

Degree of tumor histologic differentiation (ie: resemblance of normal tissue counterpart).
–Low grade: more differentiation/ greater resemblance to normal
–High grade: less differentiation/ resemblance to normal (poorly differentiated)
- Grading schemes vary by tumor type
- Some schemes also take into account mitotic activity and tumor architectural features (eg: extent of gland formation in an adenocarcinoma)
- Can be predictive of biologic behavior (tumor dependent), but overall less reliable than disease stage

Multistep pathway to breat cancer:

Colon cancer

Most important parameter is disease STAGE


What is special about pediatric neoplasms?
