Cancer Flashcards

(44 cards)

1
Q

G1

A

G1 phase: cell grows larger, organelles duplicated

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2
Q

S phase

A

DNA and centrosome (microtubule- organizing structure) copied in nucleus

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3
Q

G2 phase

A

growth, proteins and organelles are made, preparation for mitosis

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4
Q

M phase

A

cell divides copied DNA and cytoplasm to make two new cells

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5
Q

Late g2

A

DNA is copied, so chromosomes in nucleus are two connected copies: sister chromatids
Two centrioles

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6
Q

prophase

A

Chromosomes begin to condense
Mitotic spindle forms (made of microtubules)
Nucleolus (where ribosomes are made) disappears

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7
Q

prometaphase

A

Mitotic spindle begins to organize chromosomes

Nuclear envelope breaks down

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8
Q

spindle anatomy

A

Microtubules bind to chromosomes at the kinetochore
Centromere is where the sister chromatids join together
Aster: structure of microtubules bound to chromosomes

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9
Q

metaphase

A

All chromosomes aligned at the metaphase plate
Two kinetochores of each chromosome should be attached to microtubules from opposite spindle poles
Spindle checkpoint: cell checks that sister chromatids will separate evenly

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10
Q

anaphase

A

Sister chromatids split - this is driven by motor proteins that “walk” along the microtubule tracks

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11
Q

telophase

A

Mitotic spindle is broken down
Two new nuclei form, nuclear membranes reappear
Chromosomes decondense

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12
Q

cytokinesis

A

Starts in anaphase/telophase
Separation of the cytoplasm
An actin ring forms a cleavage furrow

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13
Q

how cyclins work

A
Cyclin dependent kinases (CDK)
- when bound to cyclin its active
(phosphorylates targets)
Kinase: adds a phosphate group
CDK default function is to be inactive
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14
Q

G1 regulation

A

cycD, cycE

Phosphorylates Rb protein→ can’t inhibit DNA replication

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15
Q

s regulation

A

cycA

Activates DNA replication

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16
Q

G2 regulation

A

Cyc B

Activates mitosis/cell division

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17
Q

oncogenes

A

Cancer is a disease of uncontrolled cell division: cyclins expressed at high levels or overactive growth factor receptor
Proto-oncogene (normal cell growth) → oncogene (overactive, cancer-promoting) gene

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18
Q

how gene can mutate

A

AA mutation, amplification (cell gains extra copies of a gene), error in DNA repair where a proto-oncogene is attached to a different gene. This then makes an unregulated, new protein

oncogenes result from the activation (turning on) of proto-oncogenes

19
Q

tumor suppressor genes

A

Genes that normally block cell cycle progression: tumor suppressors
Tumor protein p53 is involved in cellular response to DNA damage
Primarily acts at G1 checkpoint where it blocks progression in response to damaged DNA

tumor suppressor genes cause cancer when they are inactivated (turned off)

20
Q

normal p53 protein

A

detects and binds damaged DNA. halts cell at g1 checkpoint, repairs it or apoptosis

21
Q

what causes cancerous cell 4

A

Mutation that turns proto-oncogenes into oncogenes
- Change in AA sequence, Amplification, DNA repair error

Mutation causes a change in Ras and Raf structure
- Ras is a G protein - Switches between active and inactive forms
Ras protein is stuck in “active” form, unable to switch to “inactive” form
- Prompts cell division even in absence of growth factor
- missing or bad p53 (no stopping the mutations)

22
Q

benign vs malignant

A
  • Benign Tumor - Mass of cells that divide excessively but don’t have potential to invade other tissues
    Is not considered cancerous yet
  • Malignant Tumor - Mass of cells that divide excessively and can invade other tissues (Metastasis)
  • Offspring from original mutated cell may have enough mutations to become cancerous
23
Q

causes of cancer 6

A
  • smoking and tobaccco (radioactive)
  • diet and physical activity (18% of cancer is due to fatness)
  • UV rays, or xray and gamma ray
  • radon
  • viruses (15-20%) since they can insert genes OR alter cell behaviour
  • HIV/AIDS are more likely to get kaposi sarcoma, non-hodgkin lymphoma, cervical cancer
24
Q

inherited cancer

A
  • 5-10%
  • breast and ovarian
  • lynch, colorectal, li fraumeni syndrome (see card)
25
breast anatomy
- Each female breast contains 15-20 sections called lobes - Each lobe contains smaller sacs called lobules - Lobules/glandular tissue produce breast milk - Ducts carry milk to the nipple - Connect the lobes and lobules to the nipple - Fatty adipose tissue and connective fibrous tissue which surrounds the lobules and ducts
26
lymph and breast
- Lymphatic System: Part of immune system that protects the body from disease and infection - Made from lymph vessels found throughout body - Vessels carry lymph/clear fluid to lymph nodes to trap or remove harmful substances from body Ex. Cancer cells, bacteria - Axillary nodes are closest nodes to breast, found in armpit; Internal mammary nodes under breastbone - In case of breast cancer, cancer cells can enter lymph vessels and grow in lymph nodes - Vessels carry lymph away from breast
27
signs of breast cancer 7
``` New lump in breast or underarm Thickening or swelling of breast Irritation or dimpling Redness or flaky skin in nipple area Nipple discharge other than breast milk (ex. blood) Size or shape change Pain ```
28
BRCA genes
5-10% of breast cancers are hereditary and involve mutations in BRCA1 or BRCA2 genes BRCA genes function to repair cell damage and keep breast, ovarian, and other cells growing normally Everyone has two copies of the BRCA1 and BRCA2 genes passed from their mother and father Cancer occurs when both copies are mutated Mutations are inherited through generations Linked to a strong history of breast and ovarian cancer
29
invasive breast cancer, 3
Begins when cells in the breast such as those lining the ducts and lobules grow abnormally, growing out of control and invading surrounding tissue Invasive Ductal Carcinoma (IDC): Starts in ducts and accounts for 80% of breast cancers Invasive Lobular Carcinoma (ILC): Starts in lobules and accounts for 10% of breast cancers
30
Major molecular subtypes
Depend on presence of estrogen-receptor (ER), progesterone-receptor (PR), and human epidermal growth factor receptor-2 (HER2) Estrogen and progesterone are needed for normal breast development HER2 deals with cell growth and repair in healthy breast cells Luminal A: ER/PR positive, HER2 negative, slow-growing, have best prognosis Luminal B: ER/PR positive, HER2 positive, fast-growing, aggressive Triple-negative: Negative/No receptors, most common with BRCA1 mutation HER2-positive: ER/PR negative, HER2 positive, energizes cell growth, worse prognosis Normal-like: ER/PR positive, HER2 negative, slightly worse prognosis than luminal A
31
metastasis
Invasion: Cancer cells from the primary tumor escape and spread in surrounding connective tissues of the organ Intravasation: Cells cross vessel wall of organ and enter bloodstream or lymphatic system Survival: Cells survive in circulation Extravasation: Cells leave bloodstream and enter another organ through endothelial barrier Colonization: Secondary tumor develops in target organ
32
detection and diagnosis of breast cancer 6
Breast Screening: Process of checking a woman’s breasts for cancer before there are signs or symptoms of disease Clinical Breast Exam (CBE): Exam by doctor or nurse; using hands to feel for lumps or abnormalities Mammogram: Place breast on plastic plate and take an X-ray; best option for early detection; encouraged for women to get them annually starting at age 45, every 2 years for 55 years and older Breast MRI: Uses magnets and radio waves to take pictures of the breast; may appear abnormal even without the presence of cancer; used only for high-risk patients Breast Ultrasound: Uses soundwaves to take images of the breast tissue Biopsy: Removal of tissue or fluid from breast to be tested for cancer presence
33
stages of breast cancer
Stage 0: Abnormal cells with potential to become cancerous Stage I: Early-stage; cancer cells break through a small part of tissue Invasive breast cancer Stage II: Cancer is beginning to spread to nearby tissues and lymph nodes First area of spread outside of breast tissue is axillary node Stage III: Continuous growth; larger infected areas Stage IV: Metastatic cancer; spread to other areas of the body
34
cancer treatment
Surgery: Make an incision in the breast tissue and remove the tumor cells, remove most if tumor is too large Chemotherapy: Cytotoxic drugs to kill and slow cancer cell growth Radiation Therapy: High doses of radiation to kill and slow cancer cell growth by damaging their DNA Targeted Therapy: Use of drugs to target proteins that control how cancer cells divide, grow, and spread Immunotherapy: Inhibit immune system checkpoints for stimulation or injection of immune-like substances to make the immune system work harder to find tumor cells
35
most common treatments
Stem Cell Therapy: Procedure restoring blood-forming cells destroyed by high doses of chemotherapy or radiation therapy Hormone Therapy: Drugs that block body’s ability to make certain hormones to stop or slow cancer growth Ex. Anti-estrogen therapy blocks the production of estrogen in women Ex. Aromatase inhibitors block the production of estrogen in postmenopausal women \
36
oral manifestations
Depending on the type of cancer and treatments, oral manifestations will vary Most common side effects seen in almost all cancers and treatments include: Xerostomia Decreased salivary flow Leads to increased dental caries Mucositis Oral candidiasis Red/white lumps found within the oral cavity Pain Gingival bleeding Oral dysesthesia
37
high risk groups
``` Tobacco and Alcohol Use One of the strongest risk factors for oral cavity and oropharyngeal cancers Human Papillomavirus (HPV) Infection HPV Infection found in 2 out of 3 oropharyngeal cancers Gender Twice as common in men than in women Excess Body Weight/Poor Nutrition Age UV Light Genetic Syndromes Fanconi Anemia Dyskeratosis Congenita ```
38
patient bone thing
Osteochemonecrosis is defined as medicine-induced osteonecrosis, or death of the jawbone Osteochemonecrosis is a form of osteoporosis Osteoporosis: Condition where bones lose strength and thickness (density) Weakens bones, more likely to break/fracture Osteoporosis can occur due to a lack of estrogen levels within the body Estrogen protects against bone loss and helps to keep bones strong Low levels of estrogen are connected to cancer treatments such as chemotherapy and hormone therapies such as anti-estrogen therapies Tamoxifen: Anti-estrogen modulator, blocking the effect of estrogen on cancer cells to stop growth but can increase the risk of osteoporosis in postmenopausal women Bisphosphonates: Taken to stop cancer spread to the bone and reduce risk of fracture Side effect is osteochemonecrosis
39
BP therapy management
Stress the importance of routine dental care to keep a healthy oral cavity and reduce infection Careful management of oral health and relevant dental procedures can decrease risk of osteonecrosis Considering the patient’s cancer status, further consultation with a specialist or oncologist prior to any essential dental treatments is encouraged In non-cancer patients, it is suggested that a patient on bisphosphonate therapy to stop taking the medicine 3 months prior to an invasive dental procedure such as an extraction and to prescribe an antibiotic such as Amoxicillin
40
detecting oral cancer
Dentist will check lips, gingiva, inside of cheeks and roof/floor of mouth Appears as a red/white patch, sore that bleeds easily and doesn’t heal, a thick lump or a rough/crusted area Other signs include numbness, pain, or change in the bite If there are signs of cancer present, refer the patient to an oncologist for a biopsy Dentists can only detect cancer but cannot diagnose it
41
pre chemo
Dental professionals should ensure the patient has all infected teeth removed, gum disease treated, cavities filled and crowns/bridges restored prior to chemotherapy The patient should use extra-soft nylon bristle brushes and gentle flossing to remove plaque 5000 ppm fluoride toothpaste/gel to mitigate risk of caries Topical management of xerostomia and oral lesions if need be
42
during chemo, 4
If patients have a port under skin for medication or feeding, they are often taking anti-blood clotting medications This can increase bleeding during dental procedures and risk of infection Weakened immune system which can have bacteria in mouth spread to the rest of the body easily Infection: Manifests as a sore or sticky, white film. Contact doctor since this can delay cancer treatment. Xerostomia: recommend use of artificial saliva/fluoride rinse to reduce tooth decay Sensitive gums/ gum disease: minor tissue swelling from chemotherapy. Treat by topical anti-inflammatory, steroid/antibacterial/antifungal rinse. Jaw pain: common during radiation therapy near head/neck. Treat using muscle relaxants, exercises and anti-inflammatory medication.
43
mucositis
Mucositis is when your mouth or gut is sore and inflamed Occurs because chemotherapy works to destroy rapid growth cells and some healthy cells are also affected Prevention: Suck on ice chips for 30 minutes before and during chemotherapy to keep oral cavity moist Rinse with alkaline saline mouthwash that includes ½ teaspoon of baking soda and ½ teaspoon salt in 16 ounces of water. Rinse 5 times /day Also can give saliva substitutes, topical anesthetics, cellulose film-forming agents, antacid solution
44
Post- treatment
Patient should visit the dentist regularly, since the effects of cancer treatment can include tooth decay as a result of dry mouth Brush twice a day with fluoride toothpaste + floss Avoid tobacco and alcohol Eat nutritious foods to boost immune system