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Work Cited Zhang, Michael. ““A Month and a Half Til’ No Bio” (Meiosis, Disease & Viruses Test).” Google Docs, Bergen County Academies, 10 May 2026, docs.google.com/document/d/1PJauKA8Ki5RPk6Z8DPdx5y8lV8eN6n3dbXKdamvMqT0/edit?tab=t.4h5k67shgyed. Accessed 10 May 2026.
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Cancer
A disease caused by an uncontrolled division of abnormal cells in a part of the body
Tumor
Swelling in the body as a result of an abnormal growth of tissue
Benign Tumor
Uncancerous cell growth, stays at the original site
Malignant Tumor
Cancerous cells that grow uncontrollably, spreading from the original site
Metastasis
The development of secondary malignant growths at a distance from a primary site of cancer.
Angiogenesis
The development of new blood vessels
Tumor Suppressor Genes
Genes which prevent cancer by controlling the cell cycle through inhibition.
Proto-oncogenes
Genes that code for proteins that stimulate normal cell growth and division
Oncogenes
Proto-oncogenes which are permanently activated, causing cancer by excessively stimulating the cell cycle.
Division: Normal vs. Cancerous
Cancerous cells are always stimulated, and thus continue dividing at an incredibly fast rate compared to normal cells
Size/Shape: Normal vs. Cancerous
Cancerous cells vary from each other, while normal cells are all ordered and similar
Nucleus: Normal vs. Cancerous
Cancerous cells have larger and darker nuclei than normal cells
Chromosomes: Normal vs. Cancerous
Cancerous cells have an abnormal number of chromosomes, not arranged in any particular way
Arrangement: Normal vs. Cancerous
Cancerous cells cluster together without boundary, while normal cells use contact inhibition
Contact inhibition
Cells stopping growth once touching another cell, stops excessive growth
Function: Normal vs. Cancerous
Cancerous cells either cannot carry out their function properly or lose the ability to completely
Repair: Normal vs. Cancerous
Cancerous cells do not undergo any repair or apoptosis when damaged
Apoptosis
Cell death, used to manage cells damaged beyond repair
Why do cancer cells induce angiogenesis?
Cancerous tumors require great amounts of nutrients, so they grow more blood cells to receive what they need
Mitosis use
Growth and repair
How does cancer develop?
Uncontrolled division, resulting from mutations permanently enabling stimulatory parts of the cell cycle or disabling inhibiting parts of the cell cycle
Oncogene mutations
Dominant
Tumor suppressor gene mutations
Recessive
Carcinogens
Substances that increase mutation rate or are toxic to cells, causing the development of cancer
Senescence
A cell that has passed the hayflick limit and can no longer divide (aging)
Causes of senescence
Telomere shortening (main one), DNA damage, oxidative stress, oncogene activation
Telomeres
Telomeres at the end of chromosomes get shorter and shorter after each division, with the cell entering senescence when it doesn't have enough telomeres to keep dividing
Telomerase
An enzyme in stem and cancerous cells that repairs telomeres, preventing it from reaching senescence
Oxidative Stress
Presence of free radicals and/or reactive oxygen species which damage DNA
Free radicals
Substances with unpaired electrons
Cell Cycle
Stages that cells go through as they grow and divide
Interphase
The phase of the cell cycle where it is preparing for division
G1
Cell grows in size
G0
A resting stage of the cell cycle in which DNA replication and cell division stop, can be entered from G1
Checkpoint at the end of G1
Checks for adequate cell growth, nutrients, and any DNA damage
S
Chromosomes divide
G2
Cell continues to grow
Checkpoint at the end of G2
Checks for the correct amount of chromosomes and any DNA damage
M
Mitosis, the phase where the cell divides
Prophase
Nuclear envelope breaks down, exposing the DNA to the cell, as the centrioles go to either side of the cell and the spindle forms
Metaphase
Chromosomes line up in the middle of the cell as the spindle attaches to their centromere
Checkpoint at the end of metaphase
Checks for spindle being attached to chromosome
Anaphase
Spindle drags chromosomes to either side of the cell
Telophase
Chromosomes become chromatin, as two nuclear envelopes form and cytokinesis occurs
Cytokinesis
Cell pinched in two to become two distinct daughter cells
CDKs
Cyclin-dependent kinases, proteins that phosphorylate others to make them carry out functions
Cyclin
Proteins which activate CDKs by binding and forming CDK complexes
Phosphorylation
The adding of a phosphate group to a molecule
Hayflick Limit
The maximum amount of divisions a cell can have, being ~50, a limit put in place by telomeres
Cancer in Tasmanian Devils
Have a unique contagious cancer known as Devil Facial Tumor Disease. Usually spreads through bites during mating or fights from cancer cells in oral cavities
Cancer in Sealions
Common urogenital cancer. Not contagious, but the sexually transmitted herpesvirus increases risk. Pollution also increases risk
Cancer in Elephants
They should have high rates of cancer, since they have so many cells dividing at the same time, with each division being a chance to develop cancer. However, they have 20 copies of p53, making cells undergo apoptosis and prevent cancer whenever stressors are present
Cancer in Naked Mole Rats
Have low rates of cancer because of p16, a protein that causes contact inhibition earlier
Cancer in Axolotls
Not elaborated on properly in class, but they basically just have really strong immune systems and anti-cancerous mucus (i doubt this info will matter much but js in case)
Topoisomerase
An enzyme which cuts and unwinds DNA, preventing tangling
Helicase
An enzyme which splits the two strands of dsDNA into single stranded DNA
RNA Primase
An enzyme which can assemble RNA primers, short segments of RNA
RNA Primer
Short segments of complementary RNA attached to DNA, 7-12 nucleotides long
DNA Polymerase
An enzyme which assembles dsDNA from ssDNA (by adding nucleotides) that can only form DNA in the 5' - 3' direction, building off of the 3' - 5' template
DNA Ligase
An enzyme which serves as "DNA glue", attaches gaps in the DNA backbone
Single Strand Binding Proteins
Proteins which stabilize ssDNA during replication.
Leading Strand
The strand which is synthesized from 5' - 3'
Lagging Strand
The strand which is synthesized from 3' - 5', uses Okazaki fragments
Okazaki Fragment
Short, discontinuous fragments of DNA, 100-200 nucleotides long
Exonuclease
An enzyme which removes RNA primers from synthesized DNA
Replication Fork
A Y-shaped region where the two strands were separated by helicase
Template DNA
Stand of original DNA that is replicated
p53
The guardian of the genome! It is a tumor suppressor gene that prevents the continuation of the cell cycle if it detects DNA damage
Activation of p53
Phosphorylated by kinases
MDM2
Controls p53 by promoting the ubiquitination of it, or degradation. Since MDM2 controls p53, and increased p53 causes increased MDM2, it displays a negative feedback loop.
Stem cells
Undifferentiated cells that can form other cells with specialization
Differentiation
The process through which a cell undergoes a change in size, shape, and function in order to be capable of carrying out a certain task and becoming specialized
Totipotent stem cells
Can differentiate into any cell in the body
Totipotent cells in humans
Fertilized egg cells
Pluripotent stem cells
Can differentiate into any cell other then placenta and extraembryonic tissue
Placenta tissue
Assists in pregnancy from within the uterus
Extraembryonic tissue
Forms things needed for pregnancy outside the uterus (Ex: Umbilical cord)
Multipotent stem cells
Can differentiate into cells relating to a certain tissue
Multipotent cells in humans
Found in small amounts in the organs (Ex: hematopoietic cells are found in bone marrow and form red blood cells, white blood cells, and platelets, but cannot form anything else anywhere else in the body, like nerves, muscles, etc.)
Unipotent stem cells
Can only differentiate into one type of cell
Unipotent cells in humans
Found in all tissue and organs (Ex: Muscle satellite cells repairing muscle tissue)
Meiosis Interphase
Same as mitosis interphase
Prophase I
Chromosomes condense, form a tetrad, and cross over as the nuclear envelope breaks down and the spindle begins to form
Tetrad
Sister chromatids attaching at the centromere in two chromosomes
Crossing Over
Homologous chromosomes swap parts of their chromatids with each other
Metaphase I
Tetrads line up at the metaphase plate and attach to centrioles
Independent Assortment
The order of tetrads in metaphase I is completely random
Anaphase I
The spindle separates the tetrads into the homologous chromosomes and brings them to opposite sides of the cell
Telophase I
Nuclear envelopes reform and cell pinches to form new cells
What does meiosis I end with?
Two haploid cells
Prophase II
DNA condenses and spindle reforms
Metaphase II
Chromosomes line up on the metaphase plate as centrioles attach
Anaphase II
Sister chromatids pulled to opposite sides of the cell by the spindle
Telophase II
Chromosomes recondense and nuclear envelopes reform, with the cell pinching it into two new ones
What does meiosis II end with?
4 haploid cells (all genetically different from each other)
Types of meiosis
Oogenesis and spermatogenesis
Spermatogenesis
Meiosis in males, forms four sperm cells
Oogenesis
Meiosis in females, produces one ovum and three polar bodies
Ovum
An egg cell
Polar bodies
Eliminate extra genetic information (prevents things like nondisjunction) and ensure that the ovum receives extra nutrients and cytoplasm