Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
93 Cards in this Set
- Front
- Back
Reversible change that most often leads to malignancy. Includes pleomorphism and often abnormal mitosis
|
Dysplasia
|
|
Example of dysplasia, found by Pap smear, caused by HPV 16, and 18 most often
|
Cervical squamous epithelium dysplasia
|
|
Invasion and metastasis are characteristics of this type of neoplasm
|
malignant neoplasm
|
|
Most important defining characteristic of Malignancy
|
metastasis
|
|
Common features of Malignant tumors
|
poor differentiation, pleomorphism, hyperchromatism, increased nuclear/cytoplasmic ration, abnormal mytoses, cellular dyspolarity, and prominant nuclei
|
|
Highly anaplastic tumors are what, and how do they respond to chemo/radiation?
|
very aggressive, respond well to chemo/radiation, due to turnover rate
|
|
Type of cancer seen in stratified squamous epithelium, IE skin, mouth, esophagus, vagina, bronchi, and cervix
|
squamous cell carcinoma
|
|
Paraneoplastic syndrome seen with squamous cell carcinoma of the lung
|
hypercalcemia, due to parathormone production by the (S-100+) tumor. Is of neurendrocrine origin.
|
|
Type of cancer seen in the transitional cells of the urinary tract
|
transitional cell carcinoma
|
|
Type of cancer seen in glandular epithelium, IE: GI mucosa, endometrium, pancreas, breast, and prostrate. Associated with desmoplasia.
|
Adenocarcinoma
|
|
Malignant tumor of mesenchymal origin. Named for tissue of origin.
|
Sarcoma, IE osteosarcoma, rhabdomyosarcoma, leiomyosarcoma, and Lyposarcoma
|
|
Eponymically named tumors:
|
Burkitt Lymphoma, Hodgkin Lymphoma, Wilms Tumor
|
|
Neoplasm (benign or malignant) derived from all three germ cell layers. Can contain bone, skin, hair, and teeth. Most often seen in ovaries or testis
|
Teratoma
|
|
Well differentiated, slow growing, non metastasizing neoplasms:
|
Benign neoplasms
|
|
Benign tumors usually end in OMA, name 4 malignant tumors that also end in OMA:
|
Melanoma, Lymphoma, hepatoma, mesothelioma
|
|
Benign neoplasm that arises from surface epithelium, or transitional epithelium: IE skin, or bladder
|
Papilloma: consists of delicate finger like epithelial processes surrounding a connective tissue stroma
|
|
Benign neoplasm of glandular epithelium, what are the two types?
|
Adenoma: Papillary cystadenoma (cystadenoma of the ovary) extends into cystic spaces. Fibroadenoma: lots of connective tissue surrounding glandular epithelium (breast fibroadenoma)
|
|
5 most common benign tumors of mesenchymal origin:
|
Leiomyoma, rhabdomyoma, Lipoma, fibroma, chondroma
|
|
Most common neoplasm in women:
|
Uterine leiomyoma: (uterine fibroid) is benign, does not become leiomyosarcomas.
|
|
Small area of non neoplastic tissue displaced in another organ:
|
Choristoma, also called a heterotropic rest. like gastric or pancreatic cells in the intestine. can be seen with a Meckel's Diverticulum
|
|
Non-neoplastic overgrowth of local tissue of the affected organ
|
Hamartoma or hemangioma
|
|
Most common marker used to determine clonality:
|
HUMARA: human androgen receptor gene
|
|
Infective infiltration of adjacent tissue by a malignant tumor:
|
Invasion: must penetrate basement membrane, can invade adjacent blood vessels or lymph nodes.
|
|
Implantation in distal sites of tumor emboli:
|
Metastasis
|
|
Steps of successful metastasis:
|
1) growth and vascularization of tumor. 2) penetration into adjacent lymph or blood vessels. 3) transport and survival of tumor cells in the circulation. 4) implantion and invasion of tumor emboli in target tissue
|
|
Preferential route of carcinomas to metastasize, and exceptions
|
Lymphatics, but renal cell carcinoma and hepatocellular carcinoma both invade the veins, and go straight to hematogenous spread
|
|
Preferential route of Sarcomas to metastasize:
|
hematogenous
|
|
Preferential rout of ovarian cancer to spread:
|
Via seeding to the peritoneal cavity
|
|
Primary cancer usually associated with metastatic adrenal, liver, and brain cancer
|
Lung cancer
|
|
Primary cancer in women associated with metastatic lung and bone cancer
|
Breast
|
|
Primary cancer in men causing osteoblastic metastatic cancer of the vertebra
|
Prostate cancer
|
|
Primary cancer causing osteolytic metastatic cancer:
|
multiple myeloma. causes punched out lesions
|
|
Cause of cachexia and wasting seen in the later stages of cancer
|
Cachetin (Tumor Necrosis Factor alpha) a product of macrophages that promotes catabolism of fatty tissue
|
|
Functional pituitary tumor causing amenorrhea, infertility, and sometimes galactoria
|
Prolactinoma
|
|
Functional pituitary tumor causing gigantism in kids or acromegaly in adults:
|
Somatotropic (acidophilic) adenoma
|
|
Functional pituitary tumor causing Cushing Disease (adrenal hypercorticism)
|
Corticotropic (basophilic) adenoma
|
|
Tumors, that based on their functionality, can cause either adrenogenital, Conn, or Cushing Syndrome
|
Adrenocortical tumors
|
|
Ovarian tumor that can cause hyperestrinism:
|
Granulosa-theca cell tumor
|
|
Ovarian tumor that can cause excess androgen production:
|
Sertoli-Leydig cell tumor
|
|
These tumors can cause elevated levels of HCG or Human Placental Lactogen in women
|
Hydatididiform moles and choriocarcinoma
|
|
Paraneoplastic syndrome causing Cushing syndrome:
|
production of ACTH-like substance by small cell carcinoma of the lung
|
|
Paraneoplastic syndrome causing SIADH:
|
release of ADH-like hormone from most often small cell carcinoma of the lung
|
|
Paraneoplastic syndrome causing Hypercalcemia:
|
release of parathormone-like substance from squamous cell bronchogenic carcinoma of lung, or secretion of osteoclast activating factor-like hormone from multiple myeloma
|
|
Paraneoplastic syndrome causing Hypoglycemia:
|
secretion of insulin like substances by: hepatocellular carcinomas, mesotheliomas, and some sarcomas
|
|
Paraneoplastic syndrome causing Hypothyroidism:
|
production of TSH by hyditidiform moles, choriocarcinomas, and some lung tumors
|
|
Oncofetal antigen associated with Colon cancer
|
Carcinoembryonic antigen (CEA)
|
|
Oncofetal protein associated with hepatocellular carcinomas and germ cell tumors:
|
Alpha fetoprotein (AFP)
|
|
Stages of carcinogenesis
|
1) initiation (mutation) 2) promotion (division/replication) 3) progression (specialization of cancer cells)
|
|
Three main causes of carcinogesis:
|
1) Chemical (IE carcinogens in cigarette smoke) 2) Ionizing Radiation or UV radiation 3) Viral infection (HBV)
|
|
Cause of skin cancer in autosomal recessive disorder Xeroderma pigmentosum:
|
failure of DNA repair mechanisms to repair pyrmidine/thymine dymers caused by UV radiation damage
|
|
Virus definitively implicated in adult T cell leukemia and lymphoma
|
HTLV-1
|
|
Virus implicated in genital tract neoplasms, as well as cervical, vulvar, and esophageal cancers.
|
HPV mostly 16 and 18, but any number above 16 can cause neoplasms.
|
|
Suppressor genes knocked out by HPV 16 and HPV 18
|
HPV 16, has E6, which knocks out P-53, HPV 18 has E7, which knocks out the RB gene
|
|
Virus that is associated with Burkitt's Lymphoma:
|
EBV
|
|
Mechanism of EBV caused Burkitts lymphoma
|
EBV attaches to CD 21, causing proliferation of B cells, increasing opportunity for translocation. eventually the C-MYC gene on chrom 8 translocates next to the 14 Ig heavy chain gene, causing increased expression
|
|
Virus associated with Kaposi Sarcoma, mostly seen in immunocompromised patients
|
HHV-8. usually seen in AIDS patients
|
|
Virus known to cause increased rates of CNS Lymphomas
|
HIV, also seen in other immunocompromised individuals
|
|
Only Bacteria known to cause Cancer
|
Helicobacter Pylori, causes adenocarcinomas, B cell lymphomas, and gastric (MALTomas)
|
|
Mutation of the RAS gene occurs at which location, and causes what?
|
Codon 12, causes abherrant P21 protein with intact GTP binding, but no GTP-ase activity. this means they can be activated by GTP binding, but cant be inactivated
|
|
What gene is mutated in 25-30% of all malignancies
|
RAS gene
|
|
Proto-ncogenes are what?
|
normal genes that code for proteins that play essential roles in DNA replication and transcription
|
|
Oncogenes are what
|
abnormal genes that have been permanently activated by carcinogenesis (chemical, radiation, or infection) that cause unchecked replication of their counterpart DNA
|
|
Growth factor associated with the v-sis oncogene
|
B chain of platelet derived growth factor
|
|
Growth factor associated with the v-erb oncogene
|
epidermal growth factor (EGF) receptor
|
|
Growth factor associated with the v-fms oncogene
|
colony stimulating factor 1 receptor
|
|
Growth factor associated with the c-neu oncogene
|
gene for the EGF receptor
|
|
Four ways by which cancer oncogenes become tumorigenic
|
1) promoter insertion (insertional mutagenesis) 2) point mutation 3) translocation 4) gene amplification
|
|
MOA of promoter insertion in causing tumorgenesis:
|
inserts retroviral promoter or enhancer sequences in host genome, leading to increased expression of a nearby oncogene
|
|
MOA of point mutation in tumorgenesis:
|
Single nucleotide change in codon 12 of RAS gene, causing many human tumors
|
|
MOA of chromosomal translocation in tumorgenesis:
|
breaks and then rearrangements of certain genes next to other genes have been associated with many different cancers
|
|
Cause of Burkitts Lymphoma, and associated oncogenes
|
c-myc protooncogene on chrom 8 is translocated next to the Ig heavy chain locus on chrom 14, increasing expression of c-myc
|
|
Cause of B-Cell follicular lymphoma, and associated oncogenes
|
Ig heavy chain on chrom 14 is translocated next to the bcl-2 oncogene on chrom 18, enhancing the expression of bcl-2, which inhibits apoptosis
|
|
Role of BCL-2 oncogene
|
inhibits apoptosis, when over expressed in a cell, causes that cell to be immortal
|
|
Cause of Chronic Myeloid Leukemia (CML) and associated oncogenes
|
C-abl proto-oncogene on chrom 9 is translocated next to the bcr (breakpoint cluster) region on chrom 22. Fusion of bcr-abl codes for a protein that increases tyrosene kinase activity. is called philadelphia chromosome
|
|
Cause of Acute promyelocytic Leukemia (AML) and oncogene involved
|
PML gene on chrom 15 is moved next to the retinoic acid receptor a (rar-a) gene on chrom 17. causing proliferation of immature promyelocytes
|
|
Treatment for AML
|
all trans retinoic acid. matures these cells, and allows them to die
|
|
Cancer caused by amplification of the n-myc gene:
|
Neuroblastoma. this cancer correlates inversely with the degree of differentiation of the cells
|
|
Type of cancer caused by amplification of the HER-2/neu (c-erbB2) oncogene
|
Breast cancer
|
|
MOA of cancer suppressor genes. (anti-oncogenes)
|
Stops the cell cycle in G1 phase if there are any defects so that it can be repaired, if it cannot be repaired, these genes will signal caspases to initiate apoptosis
|
|
Knudson two hit hypothesis:
|
states that it requires both copies of a cancer suppressor to be knocked out for the suppressor not to work
|
|
Two most important cancer suppressor genes:
|
P-53 and RB genes, P53 signals the RB gene to stop the cell cycle at G1 until it can be repaired. the RB gene actually stops the cycle.
|
|
Syndrome caused by heredetary inactivation of 1 P-53 gene
|
Li Fraumeni syndrome, means only 1 more p-53 gene needs to get inactivated to cause cancer in any cell of body. causes breast cancer, sarcomas, brain tumors, and leukemias
|
|
Syndrome caused by hereditary inactivation of 1 RB tumor suppressor gene:
|
causes familial retinoblastoma, only 1 RB gene needs to be knocked out to remove suppression of cell cycle in damaged cells. causes retinoblastoma and osteosarcoma
|
|
Cancer caused by inactivation or deletion of the WT1 or 2 tumor suppressor genes on Chromosome 11
|
Wilms tumor in children
|
|
Cancer caused by inactivation or deletion of the APC tumor suppressor gene
|
Familial polyposis Coli and adenocarcinoma of the colon
|
|
Cancer caused by inactivation or deletion of the BRCA-1 or BRCA-2 tumor suppressor gene
|
BRCA-1 causes breast and ovarian carcinomas, BRCA-2 is only breast cancer
|
|
Mutations in the NF-1 tumor suppressor gene causes what:
|
Von-Recklinghausen Neurofibromatosis type 1: cafe au lait spots, benign neurofibromas, iris hamartomas, and increased risk of fibrosarcomas.
|
|
Cause of Von-Recklinghausen Neurofibromatosis type 1:
|
NF-1 tumor suppressor gene normally functions as a GAP protein that inactivates RAS. when damaged, it cant inactivate RAS
|
|
Cause of Multiple Neuroendocrine Neoplasia (MEN) type 1 and 2B
|
Is caused by a mutation in the RET proto-oncogene transmitted in the germline
|
|
Cancers caused by MEN 1 and MEN 2B
|
medullary thyroid carcinoma, pheochromocytoma, and hyperparathyroidism due to tumor.
|
|
Cause of hereditary non polyposis colon cancer (HNPCC) Lynch Syndrome
|
inherited mutations in certain DNA mismatch repair genes. causes (R) sided colorectal carcinomas
|
|
What is the grade of a tumor
|
it is the degree of differentiation, well differentiated would be low grade, non aggressive, poorly differentiated would be high grade and aggressive.
|
|
What is the stage of a tumor
|
Uses the TNM system, first is the size of the tumor (T), then is whether or not, and how many lymph nodes are involved (N), then is whether or not there is metastases (M). prognosis gets worse as you go from T to N to M.
|