Cancer researchers and clinicians often speak a different language. Here are a few useful terms and definitions.
Adverse Event (AE)
Any undesirable experience associated with the use of a drug.
Blood vessel formation. Because tumors grow fast, they need to generate blood vessels to supply oxygen and nutrition and remove waste. See Avastin.
See Monoclonal Antibodies
Antibody Drug Conjugates (ADCs)
These drugs use antibodies to target cancer cells and precisely deliver an attached drug.
These drugs reduce cell proliferation by interfering with folate function. Folates, also called folic acid, are important nutrients that support red blood cell production and other functions. Anti-folate drugs include methotrexate, pyrimethamine and sulfamethoxazole. For schematic of how it works, please click here.
Abdominal fluid buildup that can appear in late-stage ovarian cancer.
An angiogenesis inhibitor, Avastin (bevacizumab) is a monoclonal antibody drug used to treat recurring ovarian epithelial, fallopian tube, and primary peritoneal cancer
Molecules, such as DNA, RNA or proteins, that provide information about a tumor. For example, a mutated gene may indicate whether the tumor will respond to a specific treatment or be more aggressive.
BRCA1 & BRCA2
These genes work to suppress cell growth. They may be mutated in some breast and ovarian cancers, opening the door for rampant growth. BRCA mutations can also influence the efficacy of certain anti-cancer drugs.
Cancer Antigen 125 protein is a biomarker that may be elevated in the blood of ovarian cancer patients. Sometimes, the level of CA125 is monitored to help determine if a patient improves, stabilizes or worsens during and after treatment.
A chemotherapy drug that is often used to treat advanced ovarian cancer. For schematic of how it works, please click here.
A tumor that is both epithelial (tissue that lines internal organs) and connective tissue (bone, cartilage).
Cancerous cells have uncontrolled growth, invade other tissues and spread throughout the body (metastasis).
Treatments designed to stop cancer by destroying rapidly dividing cells or by preventing the cells from dividing.
Clear Cell Carcinoma
A rare cancer, in which the insides of the cells look clear when viewed under a microscope.
These research studies test whether new medical interventions, such as anti-cancer drugs or combinations of therapies, are safe and effective.
The Clinical Laboratory Improvement Amendments (CLIA) govern laboratory testing on humans. Clearity uses CLIA-certified labs for our Tumor Blueprints.
Complete Response (CR)
Term used in clinical trials. The disappearance of all signs of cancer in response to treatment.
The surgical removal of as much of the bulk of the tumor as possible.
Deoxyribonucleic acid contains our genetic code and is mutated in cancer. See Genes.
These tumors resemble the endometrium, which lines the uterus.
Proteins that catalyze a biochemical reaction, making them extremely important for most cellular functions.
The path eggs take from the ovaries to the uterus.
Therapy given to patients after initial diagnosis of disease. It is often part of a standard set of treatments, such as surgery followed by chemotherapy.
These drugs work against chemicals called metabolites to restrict cell growth and division. Examples include capecitabine, floxuridine and fluorouracil (5-FU). For schematic of how it works, please click here.
Like the fluoropyrimidines Gemzar is an anti-metabolite. For schematic of how it works, please click here.
DNA segments that contain the codes for specific proteins.
Testing to look for inherited changes in genes found in all cells (cancer and non-cancer cells).
These treatments usually block or eliminate hormones to control tumor growth. Examples are anti-estrogens, like Tamoxifen or aromatase inhibitors, like Arimidex and Femara. For a schematic of how they work, please click here.
Homologous Recombination Deficient (HRD)
Tumor with impaired Homologous Recombination Repair. HRD is associated with high genomic instability and may be due to a mutated BRCA gene, absence of BRCA protein, or be BRCA-independent.
Homologous Recombination Proficient (HRP)
Tumor that has functional Homologous Recombination Repair.
Homologous Recombination Repair (HRR)
DNA repair process used by dividing cells to repair double stranded DNA breaks.
Tumor with a positive Homologous Recombination Deficiency test, indicating that the tumor has a high degree of genomic instability.
Tumor with a negative Homologous Recombination Deficiency test indicating that the tumor has a low degree of genomic instability.
Test that estimates the presence of Homologous Recombination Deficiency in the tumor. May include testing for presence of alterations in BRCA and other Homologous Recombination Repair genes as well as the degree of genomic instability of the tumor (the increased tendency for mutations or alterations to occur during cell division).
Mutations in genes involved in Homologous Recombination Repair.
These treatments stimulate the immune system to fight cancer.
An experimental drug that has not been approved by the Food & Drug Administration, often in clinical trials.
Loss of Heterozygosity (LOH)
Cells have two copies of all genes, one from each parent, allowing for possible variation (heterozygosity). LOH is when one parental copy of a region on a chromosome is lost and only a single copy of the region is left.
Tumor with high levels of loss of heterozygosity indicating that the tumor has a high degree of genomic instability.
Tumor with low levels of loss of heterozygosity indicating that the tumor has a low degree of genomic instability.
Therapy given to patients to help keep cancer from coming back after it has responded to therapy.
Tumor cells break away, travel through the blood stream and form other tumors throughout the body.
Medical tests that look at DNA, RNA and/or proteins to learn more about a tumor and which drugs might be most effective against it. See Tumor Blueprint.
These proteins, which are produced in the laboratory, can be made to bind with cancer cells, making them useful for therapies.
Genetic alterations. In some cases, these variations can lead to diseases, such as cancer.
These drugs inhibit cell division by blocking DNA synthesis. An example is Gemcitabine — click here for a schematic of how it works.
Treatment before surgery to shrink a tumor; often used to make surgery more effective.
Objective Response Rate (ORR)
Term used in clinical trials. The proportion of patients in a clinical trial whose tumors shrink after treatment.
With no residual tumor mass greater than 1.0 cm after surgery.
Cancer that forms in the ovary. Most ovarian cancers are ovarian epithelial, which begins in ovarian surface cells, or malignant germ cell tumors, which begin in egg cells. Fallopian tube and primary peritoneal cancers are similar to ovarian epithelial.
The female glands that produce eggs.
Overall Survival (OS)
Term used in clinical trials. The length of time after a patient is diagnosed or has started treatment that they are still alive.
These drugs block Poly-ADP ribose polymerase (PARP), an enzyme that repairs DNA damage. In some cases, blocking PARP can generate enough damage to kill cancer cells. PARP inhibitors include Lynparza, Rubraca and Zejula. For a schematic of how it works, please click here.
Partial Response (PR)
Term used in clinical trials. A decrease in the size of a tumor, or in the extent of cancer in the body, in response to treatment.
Groups of molecules, generally proteins, that work in concert to control cellular function. For example, a growth pathways modulates the cell’s ability to grow and divide and is often corrupted in cancer.
The space within the abdomen that contains the intestines, the stomach, and the liver. It is bound by thin membranes.
Pharmacodynamics and Pharmacokinetics
Pharmacodynamics describes how a drug affects the body, for example, its mechanism of action. Pharmacokinetics describes how the body affects the drug, for example, how rapidly it metabolizes that molecule.
Inert substance given to clinical trial participants. Researchers compare results from the placebo against the group that receives the active agent.
These chemotherapy drugs damage DNA, leading to cell death. Platinum drugs include: carboplatin, cisplatin, oxaliplatin. Whether a patient is platinum-sensitive or platinum-resistant can have a profound impact on their care plan. For a schematic of how it works, please click here.
Progression Free Survival (PFS)
The length of time a patient lives with cancer without the disease getting worse
These molecules perform much of the work in cells and form much of the tissue in the body. They are created from gene templates. Certain protein mutations can drive cancer or lead to treatment resistance. See enzymes.
Directed x-ray radiation is used to treat a variety of cancers. Radiation damages DNA, killing tumor cells.
Randomized Clinical Trial
A clinical study in which patients are randomly assigned certain groups, such as a treatment group or a placebo (control) group.
RECIST: Response Evaluation Criteria in Solid Tumors
Set of rules, based on measurements of the change in tumor size that define when cancer patients improve, stabilize, or worsen during a treatment regimen.
Cancer that has come back after initially successful treatment.
Cancer that does not respond to treatment.
Stable Disease Response (SD)
Term used in clinical trials. Cancer that is neither decreasing nor increasing in extent or severity.
With residual tumor mass greater than 1.0 cm after surgery.
These drugs target specific molecules and mutations that may drive cancer.
These drugs block cell division to inhibit cancer growth and kill cancer cells. Examples include: paclitaxel (Taxol) and docetaxel. For a schematic of how it works, please click here.
Topo I & II Inhibitors
These drugs inhibit DNA synthesis and RNA transcription by blocking topoisomerase I or II enzymes. Topo I Inhibitors include: topotecan, irinotecan, camptothecin. Topo II Inhibitors include doxorubicin, etoposide, epirubicin.
A sophisticated tumor biomarker test that examines the molecules in a tumor to determine what kinds of mutations it has and which treatments might be most effective.