T2 - Neoplasia 1 And 2 - Robichaux Intro

Front 1

Define atrophy, hypertrophy, hyperplasia, neoplasia, and tumor (objective)

Back 1

Neoplasia - new growth that happens without regard to regulatory input - independent cell that divides on its own. Can be benign or malignant (not completely true, as some depend on hormones and can be treated as such).

Tumor - any swelling, whether inflammatory or by neoplasia.

Hypertrophy - growth in the size of cells.
Atrophy - decrease in the size of cells.
Hyperplasia - increase in the number of cells (think of uterus during monthly cycle).

Front 2

define hamartoma, choristoma, and teratoma (objective)

Back 2

teratoma:
teratomas come from totipotent stem cells and can represent all 3 types of embryonic tissue, so have bones/teeth/hair/epithelium/fat/nerve/everything else. neoplasm = yes.

HAMARTOMA:
not technically a neoplas, as it's growing at the same rate as the surrounding tissue. This is disorganized tissue typical for the site it's found - as in a weird clump ducts/hepatocytes in the liver, etc. These are mature cells.

Choristoma - this is like a hamartoma, except the normal tissue is found in the wrong place (pancreatic tissue in the stomach). again, probably not a neoplasm.

Front 3

define hyperplasia, metaplasia, dysplasia, carcina in situ, and invasive carconima (microinvasive carcinoma too) - objective

Back 3

Dysplasia = early on is NOT necessarily a neoplasia. Refers to LOSS IN UNIFORMITY of individual cells, weird architecture. In epithelial cells. See cancerous-like changes (hyperchromatic nuclei, mitotic cells where they shouldn't be, High nuclear to cytoplasm ratios.

once the full thickness of the epithelim has become dysplastic, this is CARCINOMA IN SITU and is considered pre-invasive stage of cancer. Dysplasia doesn't automatically mean cancer or future cancer.

Metaplasia - change in cell type. In the esophagus, barrett's = change from squamous epi to columnar epithelium, better able to withstand acid. Lungs, see replacement of cilia with squamous. Pre-cancerous.

microinvasive - malignant cancers can invade local tissue, especially at the microscopic level (hence wide margins).

Front 4

what's the terminology used for malignant tumors?
compare sarcoma vs. carcinoma. go over the terminology for benign tumors - which are badly named? (objective)

Back 4

sarcomas vs. carcinomas.

sarcomas come from MESENCHYMAL tissues - like fibroblasts (fibro-sarcoma), or cartilege (chondro-sarcoma), or bones (osteo-sarcoma).

epithelial-derived malignancies = CARCINOMAS. remember that the parenchyma of organs = epithelial. if it makes glandular-looking structure, it's an ADENO-CARCINOMA.

if it makes squamous looking things, it's SQUAMOUS CELL CARCINOMA.

BADLY NAMED:
lymphoma
mesothelioma
melanoma
seminoma
all these are MALIGNANT, but have benign names.

Front 5

characteristics of benign neopalsms? talk about the major different ones.

Back 5

benign tumors sit still, don't invade.

add "oma" to the original = benign name.


fibrous tissue = FIBROMA
either from a gland, or makes glandular like tissues = ADENOMA.

papillomas are from/make little epithelial fingers

polyp - extends past a mucosal surface, like into the gut.

cystadenoma - hollow, cyst-like masses - they're usually on the ovaries.

Front 6

what are some basic cytologic changes seen in malignant tumors? growth patterns? metatstatic patterns?

Back 6

Malignant tumors can be either differentiated or anaplastic.

anaplastic cells are pleomorphic, with lots of variability. see HYPERCHROMATIC CELLS, and LARGE.
Big old nucleoli. Giant cells. Weird mytocies (merceds sign).

Front 7

basic comparison of benign vs. malignant tumors? 4 things. How do differentiation and speed of growth relate?

Back 7

benign tumors stay put - microscopically, you can tell if it's going to remain local, not invade, not metastasize, easy to remove surgically. Note however that "benign" tumors can kill (grow in the brain, up ICP, etc).

malignant: spread to adjacent and distant sites, doesn't stay confined. destroy tissue/structures.

Malignant tumors generally grow faster than benign tumors, but not always. With malignant tumors, generally the faster it grows, the LESS DIFFERENTIATED (more anaplastic) the tumor.

Benign = no invasion, no metastasis. Some even have capsules around them for easy removal/ID.

Front 8

let's practice some names: talk about the benign and malignant names of muscle tumors, lymph node tumors, blood vessels,

Back 8

lymph nodes: benign = Lymphangioma.
Malignant = LymphangioSarcoma.

smooth muscle - benign: Leiomyoma.
Malignant = LeioMyoSarcoma

striated muscle = benign = Rhabdomyoma
malignant = RhabdoMyoSarcoma

blood vessels: benign = Hemangioma
malignant = AngioSarcoma

Front 9

Talk about the four basic characteristics of tumors and how malignant and benign tumors vary:

Back 9

Differentiation/Anaplasia.
Benign tumors are WELL DEFERENTIATED (look like their parent cells).

Malignant tumors can be either well differentiated or totally undifferentiated (=anaplastic = undifferentiated).

Note that with either of these, differentiated tumors (malignant and benign) can secrete hormones - and they don't even have to be at the original location (lung tumors make ACTH).

Rate of growth: cancer generally grows faster than benign tumors

Local invasion

Metastatsis:

Front 10

what is anaplasia? Pleomorphism?

what's meant by the nuclear to cytoplasm ratio?

Back 10

it's a hallmark of malignancy. means "to form backwars" = undifferentiated cells. Could be stem cell tumor that never differentiated, or a more mature cell that de-evolved. They have a lot of PLEOMORPHISM - lots of variability in the cells.

nuclear to cytoplasm ratio - recalling that malignant, pleomorphic cells are HYPERCHROMATIC and LARGE, also see that there's not a lot of cytoplasm in the fast dividing cancer cells, and a higher relative concentration of nucleus. Usually 1:4, with cancer it's closer to 1:1.

Front 11

at the time of cancer diagnosis, what percentage have already spread? how many divisions have happened? why is this interesting?

what are some general rules about probability of metastasis?

Back 11

robichaux says 75% to 80%.
Robbins says 50%.

by the time a cancer shows up, it's 75% of the way through its lifespan. Realize that 30 cell doublings is about the number required to make a detectible cancer (1cm cubed, 1 gram).

10 more doublings would make it a kilogram in size and fatal. So, it's most of the way through its development.

more anaplastic, larger primary tumor = more likely to be metastatic.

Front 12

what are the ways a cancer can metastasize, and which favor which?

Back 12

can have seeding through natural compartment...see this with ovarian tumors that spread all over the peritoneum, or CNS tumors that spread over the CNS.

lymphagenous spread - this is favored by the carcinomas

hematogenous spread - favored by the sarcomas.

though these aren't hard and fast rules.

Front 13

Epidemiology, incidence, geographic factors, environmental factors, age, genetic, carcinogens and changing incidence of cancer - objective

where do most cancers come from?

Back 13

men and women most killed by lung cancer. for men, colon/prostate come in second and third.

for women, breast beats colon.

stomach cancers big in japan, small in US. we get more colon cancers. Japanese immigrants to US stop getting stomach cancer, get more colon cancer - so environmental/diet matters big time.

data says that environmental causes of somatic mutations accounts for MOST sporadic cancers.

old people get more cancer, due probably to the accumulation of somatic mutations. worst death rate between 55 and 75, then it drops off.

Front 14

give ideas for the origin of neoplasias. this is going to be long. - objective

Back 14

heredity - there are inherited cancer syndromes (RB, APC). There are familial cancers (most cancers have a familial form), and autosomal recessive diseases of DNA repair (xenoderma pigmentoum). Mostly, you inherit a predisposition to fall victim to an environmentally-derived somatic DNA mutation.

generally, genetic mutation is involved. radiation/chemicals/viruses, etc can all cause this.

Generally, growth promoters (oncogenes), growth inhibitors (tumor suppressors), apoptosis genes, and DNA repair are the targets of mutations that lead to cancer.

Idea is that you acquire more mutations as time goes on. Several required for cancer to develop.

Front 15

talk about the number of necessary mutations in proto-oncogenes vs. tumor suppressors

Back 15

usually, you need only one mutation in a proto-oncogene to get cancer. tumor suppressors require 2.

another way of saying this is that oncogenes are DOMINANT, tumor suppressors are RECESSIVE.

This is because a tumor suppressor should still work if its un-mutated duplicate is still present. Oncogenes overexpress some growth factor - only need one of these to be messed up to get cancer.

Front 16

so tumors are thought to be monoclonal - how does this vary as the disease progresses?

Back 16

start out monoclonal, but accumulate more mutations in more cells as time goes on. this generates subclones - some may be better at invasion, some at metastasis, others at avoiding chemotherapy. so HETEROGENOUS by the time you get to end stage disease.

this also supports the idea of accumulation of multiple mutations - see cancer get worse as time goes on indicating that more dangerous mutations are being acquired as time passes. Those that are LESS antigenic, grow in the ABSENCE of growth factors, etc are SELECTED for.

= TUMOR PROGRESSION.

Front 17

in general, what are 7 great mutations to get that allow a cancer to develop?

Back 17

independence of growth signals

independence of inhibitory signals.

no apoptosis potential

immortality (telomerase, avoid G0 sensencence)

angiogenesis

invasion/metastasis

genomic instability (allows for the accumulation of subspecies, tumor progression, selecting the most virulent cells).