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Immuno-Sero LEC > Tumor Immunology > Flashcards

Tumor Immunology Flashcards

1
Q

the study of the relationship between the immune system and cancer cells

A

Tumor immunology

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2
Q

• understood with a background on the origin of cancer cells and their differences from normal cells

A

Tumor immunology

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3
Q

• Cell growth and division are carefully regulated processes designed to produce new cells

• inhibit division when enough cells are present, and limit cell lifespan through apoptosis.

A

NORMAL CELL GROWTH

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4
Q

• Unchecked cell growth and division can lead to the development of an abnormal cell mass¥¥¥ called a **tumor or neoplasm.*

• Tumors can be classified as benign or malignant, with distinct characteristics and implications for health.

A

TUMOR FORMATION

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5
Q

CLASSIFICATION OF TUMOR

A

Benign

Malignant

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6
Q

slowly growing, well-differentiated cells, similar to their tissue of origin.

A

Benign tumor

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7
Q

surrounded by a capsule, preventing circulation to other body parts.

A

Benign tumor

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8
Q

• disorganized masses, rarely encapsulated, allowing invasion of nearby organs.

A

Malignant

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9
Q

exhibit metastasis, spreading through blood to distant sites.

A

Malignant

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10
Q

Vary in differentiation, with
undifferentiated tumors
growing more aggressively.

A

Malignant

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11
Q

CLASSIFICATION OF MALIGNANT
TUMORS

A

Carcinomas
Leukemia
Sarcomas

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12
Q

• skin or epithelial linings of internal organs or glands

A

CARCINOMAS

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13
Q

• Types of carcinomas

A

• Adenocarnoma
• Squamous Cell Carcinoma
• Basal Cell Carcinoma

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14
Q
  • Global Impact: Cancer causes over______ deaths annually.
  • U.S. Impact: It is the______ leading cause of death, accounting for nearly 1 in 4 deaths
A

8 million

second

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15
Q
  • Grow rapidly and are disorganized.
    • Rarely encapsulated, allowing invasion into surrounding tissues.
    • Can spread (metastasize) to other body parts.
A
  • Malignant Tumors (cancers):
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16
Q
  • Slow-growing.
    • Well-organized and resemble normal tissues.
    • Encapsulated by a fibrous cover, preventing them from spreading.
A
  • Benign Tumors:
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17
Q

The term “cancer” comes from the____\ word ______, due to the invasive nature of malignant tumors.

Malignant tumors can vary in their resemblance to normal tissues, with those that are less differentiated (less like normal tissue) tending to be more aggressive.

A

Latin word for crab

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18
Q

Types of Cancers by Origin
Arise from the skin or linings of organs and glands.

Involve blood cells or lymphatic system.

Originate from bone or soft tissues (e.g., fat, muscles, nerves).

A
  • Carcinomas (80% of cancers):
  • Leukemias/Lymphomas (9%):
  • Sarcomas (1%):
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19
Q

Physicians use staging systems to classify cancers and guide treatment. The most common system is the TNM System, developed by the American Joint Committee on Cancer (AJCC):
• T:
• N:
• M:

A

Size of the primary tumor (T0 to T4).

Degree of spread to nearby lymph nodes (N0 to N3)

Presence of metastasis (M0 if absent, M1 if present).

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20
Q

Environmental factors cause mutations in DNA:

Chemical Carcinogens: Asbestos, cigarette smoke.

Radiation: UV rays from the sun, x-rays.

Viruses: Some viruses are linked to specific cancers.

A

Initiation

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21
Q

These mutations affect the control of cell growth

______ : Normal genes promoting cell growth can mutate into oncogenes, causing uncontrolled cell division.

______: Normally prevent damaged cells from dividing. When mutated, they lose this control, leading to unchecked cell growth.

A

Genetic Changes

Proto-oncogenes

Tumor Suppressor Genes

22
Q

Multiple mutations accumulate over time, leading to the transformation of a normal cell into a malignant tumor.

A

ACCUMULATION OF MUTATIONS

23
Q

HALLMARKS OF CANCER
(Hanahan and Weinberg)

A
  1. Invasion and merastasis
  2. Inflamation
  3. Enabling replicative Immorality
  4. Angiogenesis Induction
  5. Sustaining proliferative signalling
  6. Evading immune
    destruction
  7. Metabolism reprogramming
  8. Cell death resistance
  9. Evading growth
    suppressors
  10. Genome Instability
24
Q

TUMOR HETEROGENEITY AND IMPLICATIONS

Different cancer cells within the same tumor can exhibit varying characteristics and behaviors.

The extent of heterogeneity can influence how aggressively the cancer progresses.

Tumor heterogeneity can affect the overall outlook and survival rates for patients.

Understanding tumor heterogeneity is crucial for selecting appropriate therapies and predicting treatment responses.

A

INTRATUMOR HETEROGENEITY

DISEASE AGGRESSIVENESS

PATIENT PROGNOSIS

TREATMENT DECISIONS

25
Q

Definition

▪ unique to tumor cells of an individual
patient or shared by a limited
number of patients with the same
type of tumor.

A

Tumor specific antigens

26
Q

Origin
• coded for by viral oncogenes, host proto-oncogenes, suppressor genes
or that tumor have undergone genetic mutations.

A

Timor specific antigens

27
Q

Tumor specific antigens

  • p53
  • BRAF V600E
  • BCR-ABL in CML
A
  • Mutated Proteins
  • Fusion Proteins

• Viral Antigens
- Carcinogen-Induced

28
Q

Definition
- expressed in both normal cells and tumor cells, but abnormally in terms of concentration, location, or stage of differentiation in tumor cells.

A

TUMOR-ASSOCIATED ANTIGENS (TAAS)

29
Q

Categories
• Shared TSAs
• Differentiation antigens
• Overexpressed antigens.

A

TUMOR-ASSOCIATED ANTIGENS (TAAS)

30
Q

Clinical Significance
• serve as tumor markers that can be detected in clinical laboratories and used for diagnosis or monitoring of cancer progression.

A

TUMOR-ASSOCIATED ANTIGENS (TAAS)

31
Q

Changes in genes like proto-oncogenes or tumor suppressor genes can create_____.

A

TSAs

32
Q

TSAs can serve as specific targets for_____, where treatments are designed to target these unique tumor markers.

A

immunotherapy

33
Q

They can be overproduced, located in unusual areas of the cell, or appear at different stages of cell development.

A

TAAS

34
Q

• Melanoma antigen gene
(MAGE) proteins expressed by melanoma tumors.

A

Shared TSAs

35
Q

expressed in many tumors but not in most normal tissues

• found in testicular germ cells, placental trophoblasts, and ovaries.

epithelial or mesenchymal origin

A

Shared TSAs

36
Q

• CD10 antigen on pre-B cells
• Oncofetal or embryonic antigens: CEA, AFP, PSA

A

Differentiation Antigens

37
Q

• lineage-specific

• silenced during development of the embryo, but the process of malignant transformation allows them to be re-expressed

A

Differentiation Antigens

38
Q

• Human Epithelial Growth
Factor Receptor 2 (HER2): breast cancer

• Cancer antigen: CA 125, CA 19-9

A

Overexpressed Antigens

39
Q

• higher levels on malignant cells than on normal cells

• mutations occur during transformation

A

Overexpressed Antigens

40
Q

• biological substances that are found in increased amounts in the blood, body fluids, or tissues of patients with a specific type of cancer

• produced by the tumor itself or by the patient’s body in response to the tumor or related benign conditions.

A

Tumor markers

41
Q

Tumor Markers

Concentration Factors

A

• Tumor proliferation
• Tumor size
• Proteolytic activities of the tumor
• Release of markers from dying tumor cells

42
Q

TUMOR MARKERS

•CHARACTERISTICS OF IDEAL TUMOR
MARKERS

A
  1. Produced by the tumor or the body in response to the tumor.
  2. Secreted into biological fluids for easy and inexpensive quantification.
  3. Long half-life to allow concentration rise with tumor load.
  4. Clinically significant levels when the disease is still treatable.
  5. High sensitivity to detect most individuals with the cancer.
  6. High specificity to avoid false positives in individuals without the disease.
43
Q

TUMOR MARKERS
CLINICAL APPLICATION (4)

A

Screening
Diagnosis
Prognosis
Monitoring

44
Q

Used to screen asymptomatic individuals in a population for the presence of cancer, particularly in high-risk groups

A

SCREENING

45
Q

Aids in differential diagnosis, helping physicians distinguish between diseases with similar symptoms

A

DIAGNOSIS

46
Q

Assesses the likely course of cancer progression and helps determine appropriate treatment strategies

A

PROGNOSIS

47
Q

Tracks known cancer patients to evaluate treatment effectiveness and check for tumor recurrence

A

MONITORING

48
Q
  • Objective: Detect cancer in its early stages, when it’s more treatable.

Pros:
* Early detection can lead to less aggressive treatment.
* Provides reassurance for those who test negative.

Cons:
* False positives can cause anxiety and unnecessary procedures.
* False negatives can lead to a false sense of security.

A

Screening for Cancer

49
Q
  • Helps distinguish cancer from other diseases with similar symptoms.
  • Often involves combining multiple tumor markers or using markers alongside other tests (like imaging and biopsies).
  • Example:
    • Using biopsy markers to determine the origin of a suspicious lung nodule.
A

Diagnosis of Cancer

50
Q
  • High initial levels or increasing tumor markers indicate a worse prognosis.
  • Used to guide treatment choices.
  • Examples:
    • In breast cancer, HER2 overexpression suggests anti-HER2 therapy like trastuzumab.
    • Estrogen receptor status in breast cancer guides the use of hormonal treatments like tamoxifen
A

Prognosis of Cancer

51
Q
  • Objective: Track the effectiveness of treatment and detect recurrence early.
  • A baseline tumor marker level is established before treatment, and subsequent changes are monitored:
    • Decrease in marker levels suggests effective treatment.
    • Increase after treatment suggests recurrence.
  • Clinical Example:
    • Monitoring PSA levels in prostate cancer to track remission or relapse.
A

Monitoring Treatment Response and Recurrence:

52
Q

TUMOR MARKERS
SERUM TUMOR MARKERS

A

ALPHA-FETOPROTEIN (AFP)

Hepatocellular Carcinoma (HCC)

Nonseminomatous Germ Cell Cancers of the Testes (NSGCT)

CANCER ANTIGEN 125 (CA 125)

CARCINOEMBRYONIC ANTIGEN (CEA)

HUMAN CHORIONIC GONADOTROPIN (hCG)

PROSTATE-SPECIFIC ANTIGEN (PSA)

Immuno-Sero LEC (30 decks)

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