neoplasia nad tumor markers

[LO1: Cell cycle] What are the four main cell-cycle phases, in order?

G1 → S → G2 → M.

[LO1: Cell cycle] Which phases make up interphase?

G1, S, and G2.

[LO1: Cell cycle] What happens during G1?

Cell growth, RNA and protein synthesis, and preparation for DNA replication; organelles and cytoskeletal components increase.

[LO1: Cell cycle] During which phase is nuclear DNA replicated?

S phase.

[LO1: Cell cycle] What happens during G2?

Premitotic preparation: RNA and protein synthesis continue, and proteins needed for division are produced and positioned.

[LO1: Cell cycle] What happens during M phase?

Mitotic spindle formation, nuclear division, and cytoplasmic division produce two daughter cells.

[LO1: Cell cycle] What is G0?

A quiescent state outside the active cell cycle; some cells can reenter the cycle, while terminally differentiated cells may remain there.

[LO1: Cell cycle] What can cause cells to enter or leave G0?

Nutrient/growth-factor shortage or specialisation can favour entry; nutrients, growth factors, hormones, tissue injury, or cell loss can stimulate reentry in capable cells.

[LO1: Cell cycle] Compare labile, stable, and permanent cells using the lecture's examples.

Labile: continuously cycling cell populations, such as GI lining cells. Stable: hepatocytes that can leave G0 when stimulated. Permanent: terminally differentiated neurons that remain outside the cycle.

[LO1: Cell cycle] What does the G1/S checkpoint assess?

Whether DNA is damaged before replication proceeds.

[LO1: Cell cycle] What does the G2/M checkpoint prevent?

Entry into mitosis before DNA replication is complete.

[LO1: Cell cycle] How do cyclins regulate the cell cycle?

They bind cyclin-dependent kinases (CDKs); different cyclin–CDK complexes control different stages.

[LO1: Cell cycle] Which cyclin–CDK complex regulates early G1?

D-type cyclins with CDK4/6.

[LO1: Cell cycle] Which cyclin–CDK complex triggers entry into S phase?

Cyclin E–CDK2.

[LO1: Cell cycle] Which complexes regulate completion of S phase in the slides?

Cyclin A–CDK2 and cyclin A–CDK1.

[LO1: Cell cycle] Which cyclin–CDK complex controls mitosis?

Cyclin B–CDK1.

[LO1: Cell cycle] What do CDK inhibitors (CKIs) do?

They inhibit cyclin–CDK complexes and help enforce checkpoints, allowing repair of DNA replication errors.

[LO2: Neoplasia mechanisms] What does neoplasia mean, and what defines a neoplasm?

New growth: an abnormal tissue mass whose growth is excessive and poorly coordinated with normal tissue.

[LO2: Neoplasia mechanisms] Which three processes maintain normal tissue renewal and repair?

Proliferation, differentiation, and apoptosis.

[LO2: Neoplasia mechanisms] Distinguish proliferation, differentiation, and apoptosis.

Proliferation produces additional cells; differentiation produces specialised cells; apoptosis removes unwanted, senescent, or DNA-damaged cells.

[LO2: Neoplasia mechanisms] Does the word tumor always mean cancer?

No. It can describe swelling from inflammation or trauma, or a mass caused by cellular overgrowth.

[LO2: Neoplasia mechanisms] How do benign and malignant neoplasms differ?

Benign tumors are usually well differentiated and localised; malignant tumors are often less differentiated, invade surrounding tissue, and can metastasise.

[LO2: Neoplasia mechanisms] How can a benign tumor cause serious harm?

Its size or location can interfere with vital functions.

[LO2: Neoplasia mechanisms] What is metastasis?

Spread from a primary tumor through invasion and blood or lymphatic routes, producing secondary tumors at distant sites.

[LO2: Neoplasia mechanisms] How do solid tumors and hematologic cancers differ in their initial distribution?

Solid tumors start in a particular organ or tissue; hematologic cancers involve blood/lymph cells and may be disseminated from the beginning.

[LO2: Neoplasia mechanisms] What is metaplasia?

Replacement of one cell type by another, often associated with tissue damage, repair, and regeneration.

[LO2: Neoplasia mechanisms] What is dysplasia?

Disordered growth, particularly in epithelium, with abnormal cellular morphology.

[LO2: Neoplasia mechanisms] What distinguishes carcinoma in situ from invasive carcinoma?

Carcinoma in situ involves severe full-thickness epithelial dysplasia without penetration of the basement membrane.

[LO2: Neoplasia mechanisms] Which sites of carcinoma in situ are listed?

Skin, breast, bladder, and uterine cervix.

[LO2: Neoplasia mechanisms] What molecular capabilities facilitate cancer development in the slides?

Defective DNA repair, abnormal growth signalling, evasion of apoptosis and senescence, sustained angiogenesis, invasion, and metastasis.

[LO2: Neoplasia mechanisms] What categories of cancer risk factors are listed?

Heredity, hormonal and immunologic factors, chemicals, radiation, and cancer-causing viruses; obesity is also associated with cancer mortality.

[LO2: Neoplasia mechanisms] What are the three stages of carcinogenesis?

Initiation, promotion, and progression.

[LO2: Neoplasia mechanisms] What happens during initiation, promotion, and progression?

Initiation: carcinogen-associated DNA damage/mutation. Promotion: accelerated expansion of mutated cells. Progression: acquisition of malignant characteristics.

[LO2: Neoplasia mechanisms] How can failed DNA repair lead to malignant growth?

Persistent mutations can activate oncogenes, inactivate tumor suppressors, and alter apoptosis control, allowing unregulated growth and differentiation.

[LO2: Neoplasia mechanisms] What is a proto-oncogene?

A normal regulatory gene involved in cell growth and division.

[LO2: Neoplasia mechanisms] What is an oncogene?

An activated or altered growth-promoting gene that drives excessive growth, potentially without normal external growth signals.

[LO2: Neoplasia mechanisms] What is a tumor suppressor gene?

A growth-inhibiting regulatory gene whose protein helps prevent uncontrolled proliferation; examples include RB and TP53.

[LO2: Neoplasia mechanisms] Which functions are regulated by TP53 in the lecture?

Cell-cycle progression, DNA repair, cellular senescence, and apoptosis.

[LO2: Neoplasia mechanisms] How does p53 arrest the cell cycle after DNA damage?

DNA damage activates p53 → p21 production → inhibition of cyclin–CDK complexes → arrest, usually at G1/S, allowing repair.

[LO2: Neoplasia mechanisms] What does p53 do if DNA damage is too severe to repair?

It activates pro-apoptotic genes and promotes programmed cell death.

[LO2: Neoplasia mechanisms] Which form of RB acts as the cell-cycle brake in the lecture?

Unphosphorylated RB, which binds and inhibits E2F transcription factors.

[LO2: Neoplasia mechanisms] Why does RB binding to E2F prevent S-phase entry?

It blocks expression of genes needed for cell-cycle progression and DNA replication.

[LO2: Neoplasia mechanisms] Connect p53, p21, cyclin–CDK complexes, RB, and E2F after DNA damage.

p53 induces p21 → p21 inhibits cyclin–CDK complexes → RB remains unphosphorylated and active → E2F stays inhibited → proliferation stops.

[LO3: Cancer-cell changes] How does glycolysis change in cancer cells according to the slides?

It increases, including aerobic and anaerobic glycolysis, supporting the demands of proliferating cells.

[LO3: Cancer-cell changes] How do DNA and RNA synthesis change in cancer cells?

Both increase relative to normal cells.

[LO3: Cancer-cell changes] What membrane and surface changes occur in cancer cells?

Altered permeability and surface charge; altered glycoproteins, glycosphingolipids, and oligosaccharides; appearance of new antigens and loss of others.

[LO3: Cancer-cell changes] What fetal patterns can reappear in cancer cells?

Fetal isoenzyme patterns and oncofetal proteins such as AFP and CEA.

[LO3: Cancer-cell changes] How do cancer cells respond to growth-factor deprivation?

They can continue growing without normal mitogenic stimuli.

[LO3: Cancer-cell changes] What does loss of contact inhibition look like in cultured cancer cells?

Cells grow over one another and form multilayers rather than stopping at contact.

[LO3: Cancer-cell changes] What attachment-related change is described in malignant transformation?

Diminished adhesion and growth without attachment to a surface in vitro.

[LO3: Cancer-cell changes] Which morphological changes are listed for transformed cells?

Cellular/nuclear pleomorphism, hyperchromatism, altered nuclear-to-cytoplasmic ratio, abundant mitoses, and sometimes giant tumor cells.

[LO3: Cancer-cell changes] Which nucleotide-metabolism changes are listed in the cancer-cell table?

Increased ribonucleotide reductase activity and decreased pyrimidine catabolism.

[LO3: Cancer-cell changes] How can hormone and growth-factor production change in cancer cells?

Inappropriate hormone/growth-factor synthesis and increased secretion of certain growth factors may occur.

[LO4/6: Marker types and associations] What are tumor markers, and where can they originate?

Measurable substances or cellular features produced by a tumor or by healthy tissue responding to a tumor.

[LO4/6: Marker types and associations] What are the two main location-based categories of tumor markers?

Circulating markers in body fluids and tissue/cell markers measured in tumor samples.

[LO4/6: Marker types and associations] Which biochemical classes of tumor markers are listed?

Enzymes, serum proteins, endocrine markers, oncofetal antigens, and receptors; the tables also include glycoproteins and cell-free DNA markers.

[LO4/6: Marker types and associations] What are oncofetal antigens?

Proteins produced during fetal development that can reappear later with benign or malignant neoplasms; examples are AFP and CEA.

[LO4/6: Marker types and associations] Which marker is associated with hepatocellular carcinoma and nonseminomatous germ-cell tumors?

Alpha-fetoprotein (AFP).

[LO4/6: Marker types and associations] Where is AFP synthesised early in fetal life, and which protein does it resemble?

The yolk sac; AFP has similarities to albumin.

[LO4/6: Marker types and associations] Does an elevated AFP necessarily indicate cancer?

No. It can also occur in nonmalignant liver disease and in pregnancy with certain fetal abnormalities.

[LO4/6: Marker types and associations] How is AFP used in the lecture?

To support liver-cancer diagnosis and treatment monitoring, and to assess prognosis and treatment response in germ-cell tumors.

[LO4/6: Marker types and associations] Which glycoprotein marker is most closely associated with ovarian cancer?

CA-125.

[LO4/6: Marker types and associations] What is the stated normal CA-125 concentration?

Less than 35 U/mL.

[LO4/6: Marker types and associations] What are the principal clinical uses of CA-125?

Supporting diagnosis, assessing treatment response, and evaluating recurrence; levels can correlate with tumor mass.

[LO4/6: Marker types and associations] Is CA-125 elevated in every ovarian cancer?

No. The lecture reports elevation in about 75% overall and about 50% of stage-I cases; a normal value does not exclude disease.

[LO4/6: Marker types and associations] Is CA-125 specific to ovarian cancer?

No. Elevations can occur with other cancers, including pancreatic and digestive-tract cancers.

[LO4/6: Marker types and associations] Which oncofetal marker is prominently associated with colorectal cancer?

Carcinoembryonic antigen (CEA).

[LO4/6: Marker types and associations] What is CEA's biochemical nature and embryonic source?

A complex glycoprotein produced by embryonic tissues, including liver and intestine.

[LO4/6: Marker types and associations] Why is CEA unsuitable as a reliable stand-alone colorectal-cancer screening test?

It lacks sufficient sensitivity and specificity and may rise in nonmalignant conditions and heavy smokers.

[LO4/6: Marker types and associations] Which nonmalignant examples can increase CEA?

Liver disease, pancreatitis, inflammatory bowel disease, and heavy smoking; some healthy people also have elevated levels.

[LO4/6: Marker types and associations] What is the stated CEA reference range and its main clinical role?

0–5 µg/L; monitoring treatment and detecting recurrence or spread.

[LO4/6: Marker types and associations] Which marker is associated with pancreatic and colorectal carcinomas?

CA 19-9.

[LO4/6: Marker types and associations] Which tissues produce CA 19-9 according to the slides?

Pancreatic and biliary duct cells and epithelial cells in several other organs, including stomach and colon.

[LO4/6: Marker types and associations] What is the stated normal CA 19-9 level?

Less than 37 U/mL.

[LO4/6: Marker types and associations] How is CA 19-9 used in pancreatic and colorectal cancer?

Monitoring treatment and recurrence; pancreatic-cancer levels can correlate with stage, and rises may precede clinical or imaging evidence of recurrence.

[LO4/6: Marker types and associations] Can CA 19-9 rise in benign disease?

Yes, including pancreatitis and other gastrointestinal or hepatobiliary conditions.

[LO4/6: Marker types and associations] Which breast-cancer marker is mainly useful for therapy monitoring rather than diagnosis?

CA 15-3.

[LO4/6: Marker types and associations] What is the stated normal CA 15-3 level?

Less than 30 U/mL.

[LO4/6: Marker types and associations] Is CA 15-3 exclusive to breast carcinoma?

No. It can increase in other cancers and in benign breast or liver disease.

[LO4/6: Marker types and associations] Which additional marker in the final table is associated with breast-cancer recurrence and metastasis?

CA 27.29.

[LO4/6: Marker types and associations] Which cells normally synthesise hCG?

Placental syncytiotrophoblasts.

[LO4/6: Marker types and associations] Which hCG subunit is specific, and which is shared with other hormones?

The beta subunit is specific; the alpha subunit is shared with FSH, TSH, and LH.

[LO4/6: Marker types and associations] Which conditions are associated with increased hCG in the lecture?

Hydatidiform mole, choriocarcinoma, and germ-cell tumors, including some testicular cancers.

[LO4/6: Marker types and associations] How is hCG used as a tumor marker?

To assess stage, prognosis, and response to treatment.

[LO4/6: Marker types and associations] Which marker is produced by prostate secretory epithelium?

Prostate-specific antigen (PSA).

[LO4/6: Marker types and associations] What is PSA's normal physiological function?

It is a protease that liquefies the seminal coagulum.

[LO4/6: Marker types and associations] With a borderline total PSA, what free-PSA pattern is associated with greater malignancy likelihood in the slides?

A lower free-PSA fraction is associated with a higher likelihood of malignant prostate disease.

[LO4/6: Marker types and associations] What are PSA's clinical uses in the lecture?

Supporting diagnosis, assessing response to treatment, and detecting recurrence.

[LO4/6: Marker types and associations] Which breast-cancer tissue markers help select endocrine therapy?

Estrogen receptor (ER) and progesterone receptor (PR).

[LO4/6: Marker types and associations] Where are ER and PR located in the tissues described?

In the nuclei of breast and uterine tissue cells.

[LO4/6: Marker types and associations] Which receptor helps predict response to tamoxifen?

Estrogen receptor (ER).

[LO4/6: Marker types and associations] How does combined ER/PR status relate to endocrine-treatment response in the lecture?

ER/PR double-negative tumors respond poorly; double-positive tumors are more likely to respond.

[LO4/6: Marker types and associations] What ER/PR tissue thresholds are given in the lecture?

Less than 6 fmol/mg protein is negative; greater than 10 fmol/mg protein is positive.

[LO4/6: Marker types and associations] Which breast-cancer receptor is also called HER2/neu or erbB-2?

HER2, a growth-signalling receptor.

[LO4/6: Marker types and associations] What is the effect of increased HER2 expression?

Increased activation and signalling can drive more aggressive growth and spread.

[LO4/6: Marker types and associations] How is HER2 usually assessed, and which treatments are named for HER2-positive disease?

Usually in tumor tissue; the slides name trastuzumab and lapatinib.

[LO4/6: Marker types and associations] What is beta-2-microglobulin (B2M)?

A component of MHC class I on nucleated cells, especially abundant in lymphocytes and monocytes.

[LO4/6: Marker types and associations] Which cancers are associated with elevated B2M?

Multiple myeloma, chronic lymphocytic leukemia, and some lymphomas.

[LO4/6: Marker types and associations] What does a higher B2M level generally indicate, and what can confound it?

A poorer prognosis in the cancers discussed; non-cancerous kidney disease can also increase B2M.

[LO4/6: Marker types and associations] What is the stated normal B2M level and its monitoring application?

Usually below 2.5 mg/L; it can help monitor treatment response in multiple myeloma.