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BIOM3015 2024 > Cancer > Flashcards

Cancer Flashcards

1
Q

What are the primary hallmarks of cancer?

A

Sustaining proliferative signaling, evading growth suppressors, activating invasion and metastasis.

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2
Q

What are other key hallmarks of cancer?

A

Enabling replicative immortality, inducing angiogenesis, and resisting cell death

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3
Q

What does “oncogene addiction” refer to in cancer?

A

: It refers to tumors that become dependent on specific oncogenes, such as EGF, while others are not.

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4
Q

What are Receptor Tyrosine Kinases

A

Growth factor receptors and single transmembrane receptors involved in signaling pathways.

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5
Q

What is the EGF proliferation pathway?

A

EGF ➔ dimerization ➔ autophosphorylation ➔ Grb2 ➔ Sos ➔ Ras ➔ Raf ➔ MEK ➔ MAPK ➔ proliferation

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6
Q

How does the evasion of apoptosis occur in cancer?

A

: EGF ➔ dimerization ➔ autophosphorylation ➔ PI3K ➔ AKT ➔ evasion of apoptosis

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7
Q

What is AKT’s role in cancer

A

AKT is a central activation molecule common in most cancers

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8
Q

What are ErbB2 and ErbB4 associated with

A

ErbB2 is Her2 in breast cancer, while ErbB4 is associated with cardiac functions

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9
Q

How do anti-EGFR drugs work?

A

They bind to the EGF binding domain, preventing ligand binding, and downregulate all signaling pathways from that receptor.

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10
Q

What is the main Fab-dependent action of monoclonal antibodies in cancer treatment?

A

They inhibit proliferative/survival signaling

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11
Q

What is the Fc-dependent action of monoclonal antibodies

A

Antibody-dependent cellular cytotoxicity (ADCC), which recruits immune cells to kill tumor cells.

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12
Q

How does Trastuzumab target HER2 in breast cancer?

A

: It binds HER2, blocks dimerization, activates ADCC, causes tumor cell lysis, and degrades HER2.

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13
Q

How can Trastuzumab’s effectiveness be improved

A

By cross-linking it with toxins to inhibit microtubules, improving effectiveness and reducing recurrence.

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14
Q

What are the two main types of cancer resistance mechanisms

A

Intrinsic resistance and acquired drug resistance.

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15
Q

What is intrinsic resistance in cancer

A

Pre-existing resistance factors in tumors cause treatment to be ineffective

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16
Q

How does acquired drug resistance develop in cancer?

A

Through mutations, drug target changes, or alternate signaling pathways in response to treatment.

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17
Q

How can epigenetics lead to drug resistance in cancer?

A

Changes in DNA methylation can alter gene expression, making the cancer less responsive to treatment.

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18
Q

What is drug efflux in the context of cancer resistance

A

Cancer cells express pumps that actively pump out cancer drugs.

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19
Q

: How does DNA damage repair contribute to cancer resistance

A

Cancer cells repair DNA damage caused by treatments like chemotherapy and radiation.

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20
Q

How do cancer cells inhibit cell death to resist treatment?

A

They use anti-apoptosis mechanisms to survive despite treatments that aim to induce apoptosis.

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21
Q

What role does epithelial-mesenchymal transition play in cancer resistance

A

Cancer cells switch between states to avoid targeted therapies

22
Q

What is drug target alteration in cancer resistance?

A

Mutations (gatekeeper mutations) hinder drug binding, like with imatinib

23
Q

How do cancer cells use alternative pathways to resist treatment

A

They bypass targeted pathways using other signaling routes to maintain growth

24
Q

What is tumor heterogeneity, and how does it impact treatment?

A

Genetic and phenotypic variations in cells mean some cells survive treatment, leading to recurrence.

25
Q

How does the tumor microenvironment affect treatment success?

A

Stromal cells can secrete factors that protect cancer cells; in some cases, AB therapy resistance is addressed with fecal matter replacement

26
Q

What is the role of c-Kit mutations in cancer?

A

They contribute to proliferative tumors, especially in cancers like mast cell tumors and certain lymphomas.

27
Q

What are Gastrointestinal Stromal Tumors, and what are common treatments?

A

GISTs are soft-tissue sarcomas often treated with surgery and imatinib, targeting KIT and PDGFR mutations

28
Q

What is the role of C-Met/HGFR in cancer

A

It’s targeted to prevent metastasis

29
Q

How does immunotherapy help in cancer treatment

A

It increases immune activation and decreases immune suppression caused by tumors.

30
Q

What are the two types of immunotherapy responses

A

Adaptive (responds to new agents) and innate (first-line defense with proteins and cells).

31
Q

How does anti-PD1 mAb work in immunotherapy

A

: It blocks PD-1 interaction with PD-L1/PD-L2 on tumor cells, allowing T-cells to attack the tumor

32
Q

How do tumor cells use PD-L1 to evade the immune system?

A

PD-L1 on tumor cells binds PD-1 on T-cells, inhibiting immune response

33
Q

How do Antibody-Drug Conjugates (ADCs) kill cancer cells

A

They bind to antigens, undergo endocytosis, release cytotoxic drugs in lysosomes, and induce apoptosis

34
Q

What are different types of nanoparticle delivery systems in cancer treatment

A

Lipid-based, polymer-based, inorganic nanoparticles, viral nanoparticles, and drug conjugates.

35
Q

How does passive nanoparticle targeting work

A

Nanoparticles exploit fenestrated vasculature, common in rapidly growing tumors

36
Q

What is active nanoparticle targeting

A

It uses ligands on nanoparticles to target specific cell types, like those marked with luciferase siRNA.

37
Q

What is a hypoxic area in tumors?

A

A region with no blood supply, often resistant to therapy.

38
Q

: How do cancer stem cells differ from non-CSCs?

A

CSCs are chemo-resistant, while non-CSCs have higher mitochondria and reactive oxygen species.

39
Q

What are examples of next-generation cancer treatments?

A

ATRA (all-trans retinoic acid) and CPT (Camptothecin).

40
Q

: How do ATRA and CPT work in cancer stem cells

A

They induce differentiation and cytotoxicity through structural changes and reactive oxygen species elevation.

41
Q

How do CTLA-4 and PD-1 differ in immune regulation?

A

CTLA-4 inhibits early immune response in lymph nodes; PD-1 regulates response in peripheral tissue.

42
Q

What is the role of MHC in cancer immunotherapy?

A

MHC presents tumor-derived peptides to T-cells for immune recognition

43
Q

What are the steps of the cancer immunity cycle?

A
  1. Release antigens, 2. Antigen presentation, 3. T-cell priming, 4. T-cell trafficking, 5. Infiltration, 6. Recognition by T-cells, 7. Cancer cell killing.
44
Q

What pathway drives muscle wasting in cancer cachexia, and what protein can block this process?

A

The SMAD2/3 pathway drives muscle wasting through Myostatin and Activins; Follistatin can block this pathway.

45
Q

What proteins inhibit the BMP pathway, impacting muscle growth regulation in cancer cachexia?

A

Noggin, Chordin, and Gremlin.

46
Q

Define cancer cachexia.

A

Cancer cachexia is the unintentional loss of skeletal muscle, often with fat loss, associated with chronic disease, not reversible by nutritional support.

47
Q

What percentage of advanced cancer patients die due to cachexia?

A

30%.

48
Q

Describe the main features of cancer cachexia

A

Cancer cachexia is multifactorial, causing anorexia, cardiac atrophy, lipolysis, muscle atrophy, and weakness due to systemic inflammation

49
Q

What occurs in proteostasis imbalance in cancer cachexia?

A

There is an increase in catabolic processes and inhibition of anabolic muscle growth

50
Q

Outline the pro-inflammatory pathway in classic signaling in cancer cachexia

A

IL-6 binds to IL-6R → recruits gp130 → activates JAK kinase → STAT3 → drives inflammation and muscle atrophy.

51
Q

How does the trans-signaling pro-inflammatory pathway affect cancer cachexia?

A

IL-6R is cleaved, becomes soluble, binds IL-6, recruits gp130, activates JAK kinase, and drives inflammation.

52
Q

What role does the IGF-AKT pathway play in cancer cachexia?

A

It promotes protein synthesis and reduces degradation, helping to counter muscle atrophy.

BIOM3015 2024 (33 decks)

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