Cancer Flashcards
Cachexia
Anorexia anemia, malaise, fatigue. Eight loss, generalized wasting
What causes sx in cachexia?
tNF alpha cytokine
How does sepsis present?
Warm and well perfused caused by massive vasodilated by lipopolysaccarides (cause what?), hypotension also from vasodilatación not from low volume or volume loss,
Acute phase reactants are made by what?
Liver
These are products made by lover in inflammation or infection.Liver goes into overdrive and makes acute reactantas like
Ceruloplasmin, haptoglobin, amiloid, complement, ferritin
What gene causes resistance to chemotherapy.
MDR1
Chemotherapy resistance is caused by what?
Increased flux of drug out of cytosine, reduces influx to cytosine, self heals itself from chemotherapy, amplify resistance genes, mutations
Tumor lysis syndorme
Emergency during chemotherapy. All tumor cells lose at same time because susceptible to the agent and release all potassium that sits inside of their cells. All of this at once gets hyperKalemia. Also hypocalcemia because calcium binds to all the ohospahate to for, the calcium phospahate salts. Hyoerphospahatemia because all of it ha suene released from the cell so it increases in blood.
Nucleotide release by tumor lysis causes
Uriel acid which damages kidney.
Uriel acid precipitates in an
Acidic environment
Hypocalcemia in tumor lysis syndrome gives you
Calcium stones, tetany, seizure y myopathies.
Rasburicase is used for?
Wash out the Uric acid from the kidney. It is approved by FDA for Tumor lysis Syndrome. Does not work for gout.
Turns uric acid into allantoin whcih then gets excreted.
Number three cancer for everything
Colcorectal
Number one killer of man and women
Lung cancer
Number two killer are
Breast and prostate
Number one cancer incidence is
Breast and prostate
Number two cancer in terms of incidence and prevalence
Lung cancer
Number one cancer over all, everything accounted for
.
Breast cancer, estimated 271,000 new cases for 2019
Number three cancer is
Prostate
Number four cancer across the board
Skin cancer
Metaolasia
One type of cell is replaced with another bc new cell can handle better the new hostile environment.
Squamous epithelial replaced by columnar epithelium is an example of a ——— better examples by barrett’s esophagus.
Metaplasia
Why do we worry about Barrett’s?
Structures which could cause dysphasia.
Carcinoma in situ is example of
High grade dysphasia which does not violate the BM.
High grade dysphasia involves
Entire epithelium that doesn’t penetrate Bm
Description of dysplastic cells
Cells pleomorphic so they vary in shape and size, o sea, cells are diff from each other, the stain intensely bc they are replicating, mitifica cells increases so epithelium does not look normal, nucleares to cytoplasm is elevated bc these cells have very little cytoplasm bc they are replicating their DNA
Metastasis
Violation of BM. Then get into vasculature, etc.
How can cancer cells can hide themselves?
Hide by adhering to platelets.
When tumor cells detach what decreases?
There is decrease in e cadherin
Laminin binds to —— in Bm
Enactin
Metástasis steps
- Cells detach from other cells by decrease e cedhering
- Increase expression of laminin and adhesion molecules to adhere to the BM
- Secrets proteolytic enzymes
What do metalloproreinases do?
They degrade both extracellukar Matrix and BM laminin y type 4 y 7 collagen
First step of invasion?
Penetration of BM
First place of breast cancer to go?
Lymphatic, to LN. From lymphatics can drain into circulation through thoracic duct, or from subcutaneous to small blood vessel.
Breast cancer goes to
Bones, brain liver and lungs
Colon cancer goes to
Liver, lungs, bones, and brain
Prostate goes only to
The bones
Melanoma
Bones, brain liver and lungs
MEchanism of cancer
Pre initiation (all healthy), then initiation (exposure to carcinogen which interacts with DNA and this time instead of causing nothing it causes mutation to the DNA), then promotion (mutation to DNA may have been to promoter which turns on transcription of a gene), now one cells is replicating. Then more as more mutations accumulate. that is progression. When cells proliferate, immune system recognizes and No y Cd T cells destroys it or not. But if not, then malignancy.
Anti oncogenes do what?
Protect cells from cancer.
Functions of tumor suppressor genes?
Depress genes that are essential for cell cycle. Programmed cell death, cell adhesion, blocks loss of contact inhibition, inhibit metastasis, repair damaged DNA, stops cell cycle when damaged dna is present arresting in G1 to S transition.
Two hit hypothesis
Both tumor suppressor mutscmjtate before cancer occurs.
Mutant oncogenes are usually —- and tumor suppressor genes are usually ——.
dominant, recessive
Tumor suppressor
Gene that codes for a protein that could be a relressor protein, for example, that binds to a DNA sequence to prevent transcript of that dna, so that dna that was supposed to to be made gave an advantage, so you stopped that advantage, that is what tumor suppressor does.
Proto oncogene
Codes for cell growth and differentiation. Mutated causes improper growth and differentiation. But normally we need them,
———- of a Protooncogene is when it can get relocated to a new site of more expression leading to fusion between protooncogene and promoter increasing cancerous activity.
Translocation
AKt1 oncogene
Lung, ovarian, colon y wilm’s tumor
AKT1 oncogene
Lung, ovarian, colon y wilm’s tumor
BRAF
Malanoma, lung, colorectal,
BRAF
Malanoma, lung, colorectal, ovary, gist (gastrointestinal stromatolites tumor).
CTNNB1 oncogene
Ovarian, colorectal, liver, thyroid, endometrial, skin, medulloblastoma
FOS
Osteosarcoma, endometrial, cervical
ERBB2 (her-2-new)
Breast, lung, gastric, ovarian, glioma
JUN
Non small cell,
MET
Clear cell of the kidney
MYB
Breast
C-MYC
Burtkitts lymphoma, ovarian, breast, colorectal, pancreas, uterine
L-MYC
Small cell, leukemia
N-MYC
Neuroblastoma
HRAS
Bladder, head and neck
KRAS
Lung, pancreas, colorectal
NRAS
Neuroblastoma
RET
Medullary carcinoma of the thyroid, MEN 2A and MEN 2B
WNT1
Basal cell, colorectal, breast
Translocation for Burkitt
8, 14
T(9:22)
Philadelphia chromosome, CML
Virus activate ——- to cause cancer.
growth promoter, inhibit tumor suppressor,
Human papilloma virus suppresses 2 proteins , —— y ——- which bind and inactivate tumor suppressors —— y ———-.
E6 and E7, p53 y pRB
Translocation for follicular lymphoma
14,18
Translocation for Ewing’s osteosarcoma
11,22
Translocation for AML or Promyeloblastic leukemia
15,17
Burkitts associated with what virus?
EBV
Cervical cancer is associated with virus?
HPV
Hepatocellukar carcinoma is associated with what virus?
Hep B and C
T cell leukemia is associated with virus?
Retroviruses
Genital warts caused HPV strains
6 and 11
HPV cancer (penile, anal, vulvar, throat) is caused by strains
16 and 18
Where is desciment membrane located?
Cornea, between the storm and the epidermal membrane?
Grading is a —- classification
Histologíc. Every cancer has different grading.
Localized cancer to with?
Surgical excision.because it is located to organ it began on and no spread.
Distant metastasis treatment.
Chemotherapy or nothing
What does TNM stand for in tumors?
T tumor
N nodes extent of spread
m metastasis
Stage of carcinoma in situ
0, benign
Stage 1-3 cancer
More extensive disease
Stage 4 cancer
Cancer has spread, metastasis
Gx grade
Inadequate sample, not enough tissue
The higher you go in grade, the ——
The worse the tissue looks.
Benign lesion is
Well circumscribed, freely mobile, encapsulated, doesn’t grow outside of capsule, growth limitation, no metastasize, follows rules of physiology, so makes hormones the tissue was supposed to make.
Malignant lesion is
Not circumscribed, adherent ti surrounding tissue,s outgrows it’s blood supply, not encapsulated, outgrows it’s capsule. Metastasize, does not follow physiological rules
Anaplastic cells
Looks nothing like the cell it was supposed to be, complete lack of differentiation. Worse case scenario, lost cell polarity, no orientation or configuration.
——- are Cells with Large nuclei, hypochromatic nuclei, strains intensely, giant muktunucleated cells, variation in size, and in shape, abnormal mitosesloss of normal architecture.
Anaplastic cells
Angiogenin works with —- in cancer cells.
Works with VEGF in cancer cells.
Required to help cancer cells produce its own blood vessels
Angiogenin
Anti angiogenin interferes with activity of certain growth factors
Endostatin
Side effects of chemotherapy?
Bone marrow suppression so anemia, destroys mucus membranes, hair follicles so alopecia, GI tract so ulcers, and hematopoietic cells so infections bc of suppression of bone marrow.
Hydroxyurea
Blocks ribonuckeotide reductase, prevents converting uranyl to thymine
