Lsu Pa Intro To Oncology Csm

Front 1

Define cancer.

Back 1

Cancer is a group of diseases with uncontrolled growth and spread.

-Cancer is caused by both external and internal factors. This initiates carcinogenesis.

-10 or more years may pass between exposure and detectable cancer.

Front 2

Define Neoplasm

Back 2

Abnormal mass of tissue with excessive growth due to loss of responsiveness to normal growth controls

Front 3

What is a benign tumor?

Back 3

Not malignant,end in suffix “oma”; adenoma – derived from glands, fibroma – fibrous tissue, lipoma – fatty tissue, chondroma – cartilage origin

Front 4

Define sarcoma.

Back 4

malignant mass arising from mesenchymal tissue; fibrosarcoma – malignant fibrous tissue, chondrosarcoma – malignancy from chondrocytes, osteosarcoma


*LOTS of terminology exceptions: lymphoma, melanoma, mesothelioma all malignant

Front 5

Define carcinoma.

Back 5

malignancy arising from epithelial cells
squamous cell carcinoma – appearance similar to squamous epithelium
adenocarcinoma – appearance of glandular pattern
poorly differentiated carcinoma – undifferentiated, features of either none or both adeno and squamous cell carcinoma neuroendocrine carcinoma - forms from cells that release hormones

Front 6

Define lymphoma

Back 6

– malignancy arising from lymph tissue

Front 7

Identify the three most common types of Cancer for males and females in the United States

Back 7

Men:
1. lung and brunchus (30%)
2. prostate (9%)
3. colon and rectum (9%)

Women:
1. lung and broncus (26%)
2. breast (15%)
3. colon and rectum (9%)

Front 8

Describe the function and result of malfunction of tumor suppressor genes.

Back 8

Tumor-suppressor genes are recessive genes that keep cellular growth in check. When tumor-suppressor genes undergo mutation or deletion, the rate of neoplastic transformation is significantly higher. Tumor-suppressor genes are targeted in a different way than oncogenes: mutations in these genes result in a decreased activity of the gene product. One of the best-known tumor-suppressor genes is p53. This gene deletion can also be inherited, and progeny have a much higher rate of a variety of cancers, including breast and brain tumors, leukemia, and sarcoma, a pattern termed the Li-Fraumeni syndrome. If a loss of function of the remaining normal copy of p53 occurs through mutation or deletion in a specific organ through an acquired insult, tumors then may occur in that organ, such as in the breast, bladder, and colon. The most commonly mutated gene in sporadic human cancers is p53. Suppressor-gene mutations are also the most common cause of hereditary cancer. Unlike oncogene activation, mutations in both alleles of a tumor-suppressor gene are required to induce tumorigenesis. For instance, a germline (inherited) mutation in a single retinoblastoma gene (RB1, a tumor-suppressor gene) may not by itself cause retinoblastoma in a young child. However, if that child's genome suffers a second hit after birth (i.e., an RB1 somatic mutation), multiple tumors including bilateral retinoblastomas may occur. Single mutations in the RB1 tumor-suppressor gene may predispose an individual to osteosarcoma, soft tissue sarcoma, melanoma, and brain tumors later in life.

Front 9

Describe the function and result of malfunction of oncogenes.

Back 9

Oncogenes are evolutionarily conserved genes that play an important role in normal cellular proliferation. Oncogene activation can result from chromosomal translocations, gene amplifications, or intragenic mutations. Activation of an oncogene leads to an increased amount of the gene product. For example, chronic myelogenous leukemia (CML) occurs when the proto-oncogene, abl, from chromosome 9 translocates to the bcr gene on chromosome 22. The new protein formed by the union of the bcr and abl oncogenes, called BCR-ABL, plays a role in coupling cell-surface receptors to the signal transduction pathway with resulting unchecked growth-promoting signals to the nucleus. An activating mutation in one allele of an oncogene is generally sufficient for enhancing tumorigenesis. Oncogene research has led to the use of oncogenes as targets of specifically designed drugs. Oncogenes are also used as biomarkers to predict prognosis and select therapy. The presence of t(8;21) or inv(16) translocations in patients with acute myeloid leukemia (AML) is usually predictive of a good response to standard antileukemic therapy. In patients with breast cancer, overamplification of HER-2 is a poor prognostic marker overall, but it is a predictor of response to the anti-HER-2 monoclonal antibody, trastuzumab.

Front 10

Describe the function and result of malfunction of DNA damage response genes.

Back 10

Accumulating evidence suggests that in addition to oncogenes and tumor-suppressor genes, mutations in a third class of genes called stability or caretaker genes can also promote tumorigenesis. Stability genes are responsible for the repair of errors in normal DNA replication and include mismatch repair genes, base-excision repair genes, and nucleotide-excision repair genes. Mutations in stability genes lead to increased errors in replication. Eventually, mutations in oncogenes and tumor-suppressor genes occur and this drives malignant transformation. The Lynch syndrome, or hereditary nonpolyposis colon cancer, is an example of an inherited syndrome of defects in DNA mismatch repair genes. Colon and endometrial cancers are two of the most commonly observed cancers in families afflicted by the Lynch syndrome. Somatic mutations in these genes are responsible for 10% to 15% of sporadic colon cancers as well. Similar to tumor-suppressor genes, both alleles of stability genes must be inactivated for tumorigenesis to occur.
-The repair mechanics for DNA
-Cancer arises when both genes fail, speeding the accumulation of mutations in other critical genes

Front 11

List the ways by which a cancer can metastasis.

Back 11

Direct tumor invasion to nearby tissues

Lymphatic spread – through lymphatic vessels

Hematogenous spread – through blood vessels

Front 12

List factors that can effect the location to which a cancer will metastisis.

Back 12

Sites depend on:
Vascularity
Immune defense
Hormonal environment
Tissue structure and function

Front 13

Tumor marker for colon CA

Back 13

CEA – colon CA

Front 14

Tumor marker for hepatoma, germ cell CA

Back 14

AFP – hepatoma, germ cell CA

Front 15

Tumor marker for germ cell CA, testicular CA

Back 15

Beta HCG – germ cell CA, testicular CA

Front 16

Tumor marker for prostate CA

Back 16

Prostatic specific antigen(PSA) – prostate CA

Front 17

Tumor marker for ovarian CA

Back 17

CA-125 – Ovarian CA

Front 18

Tumor marker for pancreatic CA

Back 18

CA-19-9 – Pancreatic CA

Front 19

Describe the TNM system for staging cancers.

Back 19

T = size and location of primary tumor

N = lymph node involvement

M = distant metastasis

Front 20

List three cancers that the ACS strongly recommends to screen for.

Back 20

Breast, colon, and cervical.