Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS291 > W3 Neoplasia and Cancer > Flashcards

W3 Neoplasia and Cancer Flashcards

1
Q

Define cellular proliferation and differentiation.

A

Cellular proliferation: Process of cell division.

Cellular differentiation: process of specialisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define neoplasia.

A

Neoplasia: abnormal rissue growth that occur by 2 ways: Problem with cell regulation

1) cells continue to divide and do not mature/differentiate normally
2) Cell do not undergoes apoptosis, ignoring signals to stop dividing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define carcinogenesis and outline environmental factors that damage DNA.

A

Carcinogenesis: Normal cells are transformed into cancer cells.The process initiating the formation of a neoplasm (abnormal growth).
1. Chemical carcinogens: diet, tobacco, alcohol, drugs. Occupational hazards, asbestos, diesel.
2. Radiation
- Carcinogenic effects of ionising radiation. Ultaviolet radiation (sun).
Oncogenic viruses” HPV, cervical cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain how carcinogenesis develops with cell cycle dysregulation

A

When cells divide they need to replicate the DNA and they make ‘copy mistake’. → apoptosis → additionally apoptosis may fail.

REGULATION: 1st regulator Proto-oncogenes 2nd regulator - tumor suppressor genes

Proto-oncogenes promote cell cycle progression; tumor suppressor gene inhibit cell cycl progression. If there is DNA damage, the tumour suppressor gene sense this and repair damage → apoptosis.
↓ Mutations will occur on gene that regulate the cell cycle. = dividing out of control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the roles of oncogenes and tumour supressor genes in carcinogenesis.

A

Proto-oncogenes are regulatory enzymes/ normal gens that code for normal proteins used in cell division

  • growth factors
  • growth factor rceptors
  • G proteins
  • Enzymes that produce second messengers
  • Genes that turn the production of these proteins oon/off

ONCOGENES: are mutated proto-oncogns → code for the proteins needed for cell division. Note: they may produc:

  • too much protein
  • abnormal protein
  • protein that turns on by itself
  • protein that is made when not needed
  • protein that cannot turn cell division off
  • protein that should b mad by a different cell

TUMOR SUPPRESSOR PROTEINS: Ar the chck points that usually stop the division of mutated cells and check for replication errors.
They keep most mutations from developing into cancre by
- inducing DNA repair (fixing mutation
- Inducing apoptosis,

Check points that control the checkpoints are call tumour suppressor proteins

  • Cyclins
  • cyclin-dependent kinases
  • cyclin inhibitors
  • When thye are mutated they allow many more mutations to accumulate in cell population
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Outline the main types of genetic mutation leading to neoplasia.

A
  1. Stimulat prolifereation
  2. Promot euncontrolled cll division; ↑ cell cycle erater and accumulation of abnormal cells
    a. Activation of proto-oncogne → oncogenes (reduc the timee clls spend in chck points
    b. Damage to tumour suppressor gene (DNA gene correctors)
  3. Disable gene that induc apoptosis: when the cell is old or defective

→ Multiple mutations are usually rquired for cancer cells to survive → proliferate → spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain the role of inherited mutation in cancer.

A

Inheritied mutations in tumour suppressor genes that may caus cancer
1. Altered BRCA1 gene (brast)
2. APC gene (colorectal cancer)
3. MLH1 &MLH2 genes (hereditary nonpolyposis.
If gene is inherited does not guarantee the person will have cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Discuss how inherited and somatic mutations may interact in carcinogenesis

A

PIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outline and discuss the main factors associated with carcinogenesis.

A
  1. Environmental factors (carcinogns)
  2. Heredity
  3. Hormonal factors
    Immunologic mechanisims

Two main protective factors against cancer:
1. T-killer cells: recognizes and eliminate neoplastic cells.
2. Immune surveillance against pathogns that induce DNA mutations
INFLAMMATION: chronic inflmmation creates probleems
OBESITY: adipose tissue release free fatty acids. ↑ fatty acids ↑ insulin resistance and causee chronic hyperinsulinemia
There are also virus associated with cancer development -
Hep B c
HPV
HSV
EBC
Bacterial implicated in cancer - helicobacter pylori
Note chronic stress ↓ immunity - constant release of glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the 3 phases of cancer development

A

Carcinogensis: th process of initiation the formation of a neoplasm.
1. INITIATION
a. exposur of cells to carcinogenic agent → irreversible changes in DNA.
b. Activation of fntic pre-disposition and transformation of cells
2 OromotionL inductinof unregulatd acceleratd growth in initiatd cells by chemical and growth factors (rvrsible).
ONCOGENESIS is the progression of noplasia aftere initiation to canceer
3. Progression: tumour cells acquir malignant phentypic changes that promot invasinss and metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Compare and contrast benign and malignant tumours.

A

Tumour: the growth of a mass of new cells exceeding those required. If these cells resemble closely the cells that should be there, =benign tumour.
BENING
1. Composed of well-differntiatd clls that rsembl eth cells of tissu origin
2. Thy ar charactrisede by a slow, progrssiv growth rate that may stop or regress.
3. Thy grow by xpansion and rmain localisede to thir primary tumor site.
4. Thy lack capacity to infiltrat, invad or metastasize (spread)

MALIGNANT NEOPLASM: If a neoplasm continues to grow in volume → distrupts surround tissue cause damage / pentrating into different tissue via invasion + blood vessls from where cancer can spread to other parts of the body (metastasis)

  • Grow rapidly
  • Invade and infiltrate nearby tissues
  • sprad → scndary tumors
  • note* som malignancis:
  • Secrete horomes and/or cytokins that stimulat thir own grothr and growth of nw blood and lymphatic vessels. (angiogensis
  • librate enzymes adn toxins to induce an inflammatory rspons that injures normal tissu

CANCR IS A DISEASE CAUSED BY MALIGNANT NeOPLASIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain the role of angiogenesis and metastasis in oncogenesis.

A

Angiognsis: new blood vessels allows furthre tumour growth.
→ blood supply oxygen to cancer cells = growth
→ allows cancer cell to reach the blood systemic circulation = spread
Local → regional → → metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain how nomenclature is used to indicate benign and malignant tumors.

A

Benign tumors: tissue name + “-oma”
MALIGNANT TUMOUR
Epithelial tissue → tissu ename + “carcinoma”
Meesenchymal tissues (fat, bone, muscle → tissue name + “sarcoma”
Blood: Leukemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline the main hallmarks of cancer

A

Cancer have specific properties which allow them to avoid the bodies normal removal mechanisms, hence survival and proliferation,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline cancer risk factors and preventive behaviour.

A 
1. Physical activity
↓ insulin levels
↓obesity
↓ inflammatory mediators
↑ gut motility
↓ decrases exposure to sex hormones
2. Gut health microbiome ↑ immunity
↓ inflammation
3. Nutrient intake
↑ fibre + low bad fats and meat
↑ gut health
↓ inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline the most common types of cancer in males and females.

A

pic

17
Q

Outline the main local effects of tumour growth.

A
  • Disruptd tissus integrity
  • bleeding
  • comprssion of blood vessels
  • superior vena cava syndrom
  • hypertnsion
  • compression of lymph vessels
  • oedema, ascites, effusion
  • compression of hollow organs
  • compression of nerves
  • pain
  • paralysis
18
Q

Describe the main generalised clinical manifestations of cancer.

A

Fatigueee: sleep disturbance, biochemical changes, psychosocial factors, nutritional status, anaemila.
FEVER: ↑ cytokines
ANOREXIA & INVOLUNTARY WEIGHT LOSS: eaerly satiety, taste alterations, altreed metabolisim,
Anemia (low haemoglobin)
Thrombocytopaenia (low platelets
Infection (due to ↓ WBC)) chronic bleeding, malnutrition, auto immune responses.

  • Many of these are compounded by tx side affects.

Paraneoplastic Syndromes: cancer mutations lead to cell synthesis different proteins.

19
Q

Outline 3 conventional methods utilised in cancer diagnosiss.

A
  1. Blood and urine tests for tumour markers
  2. Imaging techniques
  3. Biopsy → histology → cell grading
20
Q

Discuss how molecular technologies can improve diagnosiss and treatment.

A

Investigating jth molecular characteristics of each cancer to find th bst availabl, individualised tx for the patient. → more effective; less adverse reactions.
Genomics, proteomics, epigeenomics, metabolmics, tumour microenvironmnt

21
Q

Define “grading” and “staging” diagnosis methods.

A

Low grade = cancer cells closely resemble normal counterparts
High grade = cancer cell poorly differentiated; can be difficult to determine tissue of organ
Nuclear grade: refers to the size and shape of the nucleus im tumour cells.

TNM clafficiation =
T = size of primary tumour
N= nearby lymph nodes involved
M= distant metastasis (the spread of cancer from one body part to the other).

Staging:

22
Q

Outline the main current strategies of cancer treatment.

A
  1. Surgery
  2. Radiotherapy
  3. Chemotherapy
  4. Hormone therpy
  5. Stem cell transplants
  6. Immunotherapy
23
Q

Outline the roles of surgery in cancer treatment.

A

Curative - to remove malignant tissue, which is meant to cure disease.
Debulking remove as much tumour as possible
Palliative relieving pain without dealing with the cause of the condition

24
Q

Outline the roles of radiotherapy in cancer treatment.

A

Damagees the DNA of cancer cells with high-dos radiation localised to the area, may affct surrounding healthy cells,
Internal beam/external beam.

25
Q

Outline the roles of chemotherapy in cancer treatment.

A

Th use of antinoplastic drugs (cancer killing) to stop or slow jthe growth ofquickly dividing cancer cells.

The route depends on the type and location of the cancer.
- Orally, intravenously, intrapritoneal, intrathecal, intra-arterial or topically onto skin. It can be used before surgery to reduce tumour size, or prior to stem cell transplant.

Most effective against small tumours

26
Q

Explain the mechanisms of action of antineoplastic drugs used in chemotherapy.

A

Cytotoxic agnts (stop cell cycle)

  1. Anti metabolitees → interference in normal production of DNA.
  2. Alkylating agents and platinum compounds →cross link strands of DNA preventing replication - cell cycle blocked at S phase.
  3. Anti-tumour antibiotics → blocks transcription from DNA to RNA
  4. Mitotic inhibitors → block formation of mitotic spindles in metaphase
  5. Topoisomerasee inhibitors - Topoisomerase eenzymes involved in untwisting, nicking and resealing DNA strands during DNA duplication.
  6. Tyrosine Kinase TK inhibitors: inhibit growth factors recptors, ↓ division of tumour cells by those growth factors. SE: bone marrow supprssion, GI disorders, fluid retention
  • Cytotoxic drugs stop rapidly dividing cells - any proliferating clls are vunerable to cytotoxix agents. most affected are bone marrow, hair follicle, GIT.
    Limitation lack of specificity,
27
Q

Describe adverse reactions of chemotherapy and how this form of treatment is managed.

A

Tumour lysis syndrome: massive reelease of cellular breakdown products from tumour clls killed by chemotherapeutic agnts. Most common in leukaemias and lymphomas.
Tx: allopurinol, reduc synthesis of uric acid, hydration and urinary alkalisers.

28
Q

Explain what hormone therapy is and exemplify.

A

Primarily used for brast and prostate cancer (sex hormones). Agnts ar used to prvnt th hormones from being produced or blocking the hormons attaching to its rcptor.
Surgery to rmov the hormon producing glands.
- Glucocorticoids
-Antioestrogns
-Androgen anatagonists
-Progestins

29
Q

Describe how stem cell transplants is used in cancer treatment

A

Primarily used with leukaemia and lymphoma - may also b used for multipl myloma and neuroblastoma.
↑ Doss of radiation ar given to destroy the persons cancerous stem cells. Intravnous.

You can transplant:

  1. Allogneic (someone else)
  2. Syngeneic (idenitcal twin)
  3. Autologous (from persons own body)
30
Q

Explain what immunotherapy is and exemplify

A

Eliminates cancer cells without damaging normal tissues. It recognises antigens this anti tumour immune injection responses can selctively eliminate cancer cells while sparing normal cells.

  1. Monoclonal antibodis: are cultured antibodis that recognise spcific protein on the surface of cancerous cells and destroy them. → Used in combination with chemotherapy. S: will not cause severe BM suppression , nausea and hair loss.
    - Hypersnsitivity reactins and cardiotoxicity can occur
  2. Check point nhibitors: Pd-1 masks a t-cell acting as a cancer cell, receptor is activated and it is not attacked by the cancer cell. Able to recognise the tumour as abnormal and to attach it;s cells
31
Q

Outline the main adjuvant medicaments potentially used in cancer treatment.

A

Tx that is givn in addition to the primary initial tx. Designde to help reach the ultimate goal.

32
Q

Explain the implications of age in cancer treatment.

A
  • Cancer in children: leukaemias and lymphomas most common; tend to respond btter to chmo, tolerat advrse sid affct thn adults.
    Cancr in thos of rproductiv age: consider fertility in m/f; cytoxic agnt should not be takn during prgnancy
    Cancer in older: ↓ ability to withstand the effcts of cancer & its tx
33
Q

Define cancer cure, remission and relapse.

A

Cure: several years without evidence of tumour and high probability of return
Remission: signs and symptoms of the tumour are no longer detectable
Relapse: signs and symptoms detectable again

BMS291 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions