Cancer Biology and Tumor Classification

Swallowing, Dental, Oral, and Speech Complications Related to Cancer Treatment

Overview

• Important aspects of oral hygiene and complications associated with cancer treatments such as therapy and radiation.

• Involvement of cancer-related conditions and their impact on areas including the tongue, speech, and overall oral health.

Complications

• Tumor cells may spread within lymphatic areas, creating additional challenges.

• The risks associated with oral and dental complications in cancer patients.

Reference

• Adapted from slides modified by C. Constantin PhD, RNC, Elsevier.

Cancer Unit Specific Learning Outcomes

• Understand the key distinctions and classifications related to cancer, including:

  • Differences between benign and malignant tumors.

  • Biology of cancer cells, focusing on:

  • Transformation and differentiation of cells.

  • Definitions of proto-oncogene, oncogene, and tumor suppressor gene.

  • Importance of tumor markers in cancer detection.

  • Grading and Staging of Cancer to predict outcomes and treatment paths.

Understanding Cancer

Definition

• Cancer is defined as a disease characterized by disordered growth and differentiation of cells, resulting in uncontrolled cell division.

Mechanism

1. Normal Cell Functioning

   • Cells undergo normal processes of growth, division, and programmed cell death (apoptosis).

2. Genetic Alterations

   • Cancer occurs when normal genetic regulation is disrupted, leading to uncontrolled proliferation of abnormal cells.

   • Cancerous cells evade their programmed self-destruction, leading to excessive growth.

Biology of Cancer

Key Features of Cancer Cells

• Altered Expression of Genes

  • Cancer is related to a shift in the expression of genes responsible for regulating cell proliferation and differentiation.

  • Links between environmental exposures and genetic predispositions to cancer.

  • Susceptibility may also be inherited through mutations that predispose individuals to cancer.

Environmental and Lifestyle Factors

• Important Risk Factors

  1. Increasing Age

  2. Tobacco Use

  • The primary cause of cancer fatalities with a mere 15% survival rate for lung cancer. Also linked to cancer of the pancreas, bladder, kidneys, mouth, and esophagus.

  1. Nutrition

  • High-fat diets related to cancers such as breast and colon; low-fiber intake linked to colorectal cancer.

  • Mixed evidence on the impact of alcohol consumption on cancers including breast and liver.

  1. UV Radiation

  • Connection to skin cancers.

  1. Viral Infections

  2. Environmental Toxins

Tumors

Classification

• Benign Tumors

  • Typically composed of well-differentiated cells; encapsulated, and generally do not spread aggressively.

• Malignant Tumors

  • Characterized by rapid growth rates, poor differentiation, and a loss of normal cellular organization (anaplasia). They possess potential for metastasis.

Neoplasm Definition

• A term describing new growth (tumor), emphasizing that not all neoplasms are cancerous, showcasing the contrast between malignant and benign tumors.

Benign vs. Malignant Tumors Summary

Progression of Cancer

Stages of Development

• Transition from normal cells through stages of dysplasia and anaplasia leading to cancer progression, with the precursor stages being generally reversible:

  • Dysplasia: Abnormal tissue development but not cancerous.

  • Anaplastic Cells: Indicative of cancer with significant loss of normal architecture.

  • Carcinoma in situ: Pre-invasive cancer potentially treatable before full progression.

Historical Context and Definitions

Carcinoma in Situ (CIS)

• Refers to early-stage cancerous tumors, originating from epithelial cells but have not invaded surrounding tissues, making them more manageable.

Comparison of Features

Benign and Malignant Tumors

Benign example features:

• Grows slowly, is encapsulated, and has a low mitotic index.

Malignant example features:

• Grows rapidly, has a high mitotic index indicating rapid cell division, and can metastasize.

Biology of Cancer Cells

Aging and Mutations

• Cancer predominantly affects older adults due to the accumulation of multiple mutations over time that collectively enable the emergence of cancerous characteristics.

Characteristics of Cancer Cells

1. Clonal Proliferation: Cells diverging from a parent cell gain advantageous mutations enabling selective growth.

2. Decreased Growth Factor Dependency: Cancer cells often proliferate without the normal need for external growth signals.

3. Immortalization: Presence of telomerase contributes to unlimited cell division.

4. Anchorage Independence: Ability to grow without attachment to a surface, traditionally required for normal cell growth.

Hallmarks of Cancer Cells

Six Key Characteristics

1. Self-sufficiency in growth signals: Tumors can produce their own growth signals (autocrine stimulation).

2. Resistance to anti-growth signals: Cancer cells ignore signals that typically halt cell proliferation.

3. Evading apoptosis: Cancer cells develop mechanisms to circumvent programmed cell death.

4. Limitless replicative potential: Cancer cells can divide indefinitely.

5. Sustained angiogenesis: Formation of new blood vessels to support tumor growth.

6. Tissue invasion and metastasis: Cancer cells invade surrounding tissues and may spread to distant parts of the body.

Tumor Markers

Definition and Importance

• Tumor markers are biological substances produced by cancer cells or in response to cancerous conditions. They include hormones, proteins, enzymes, and genetic material.

Examples of Tumor Markers

Cancer's Seven Warning Signs

General Warning Signs

1. Change in bowel or bladder habits.

2. A sore that does not heal.

3. Unusual bleeding or discharge.

4. Thickening or lump in breast or elsewhere.

5. Indigestion or difficulty swallowing.

6. Obvious changes in warts or moles.

7. Nagging cough or hoarseness.

Warning Signs Specific to Children

1. Continued, unexplained weight loss.

2. Headaches with vomiting in the morning.

3. Increased swelling or persistent pain in bones or joints.

4. Lump or mass in abdomen, neck, or elsewhere.

5. Development of a whitish appearance in the pupil of the eye.

6. Recurrent fevers not caused by infections.

7. Excessive bleeding or bruising.

8. Noticeable paleness or prolonged tiredness.

Diagnosis of Cancer

Diagnostic Features

• Varied signs and symptoms related to the tumor’s characteristics.

• Tumor markers may provide preliminary indications.

• Physical examinations may reveal pressure symptoms, obstruction, and persistent sores.

Biopsy Importance

• A biopsy is critical for obtaining tissue samples for histological examinations, facilitating the analysis of genetic alterations.

Grading and Staging of Cancer

Purpose

• Grading and staging are essential for predicting tumor behavior and determining suitable treatment options.

Grading

• Refers to the histological characterization of tumors based on the extent of anaplasia.

  • Grade 1: Well-differentiated with minimal deviation from normal.

  • Grade 2: Moderately well-differentiated with observable structural changes.

  • Grade 3: Poorly differentiated with significant structural changes.

  • Grade 4: Very anaplastic with minimal resemblance to normal cells.

Staging

• Staging describes the tumor location, spread, and involvement of lymph nodes and other organs. It incorporates factors such as tumor size and metastasis presence.

Staging Classification Using TNM System

• T: Primary tumor characteristics.

• N: Node involvement (lymph nodes).

• M: Distant metastasis presence.

Clinical Staging Breakdown

• Stage 0: Cancer in situ (no invasion).

• Stage I: Localized tumor growth.

• Stage II: Limited local spread.

• Stage III: Extensive regional spread.

• Stage IV: Present distant metastasis.

Staging Criteria and Their Importance

Detailed Staging Factors

1. Tumor Size and Local Extent: Size marked as T (e.g., T1 for <2 cm).

2. Local Lymph Node Involvement: Assessed as N (e.g., N0 indicating no involvement).

3. Distant Metastasis: Evaluated as M (e.g., M0 indicating no metastasis).

Cancer worksheet

Cancer Worksheet

1.     Describe the differences between benign and malignant tumors.

Benign Tumors

• Growth rate: Slow growing.

• Capsule: Surrounded by a capsule → contained, easier to remove.

• Invasion: Do not invade nearby tissues.

• Differentiation: Cells look similar to normal cells (well‑differentiated).

• Mitosis: Low mitotic index (few cells dividing).

• Metastasis: Do not spread to other parts of the body.

• Clinical impact: Can still cause problems if large or pressing on vital organs (e.g., brain tumor pressing on tissue).

Malignant Tumors

• Growth rate: Rapid, uncontrolled growth.

• Capsule: Not encapsulated → harder to remove surgically.

• Invasion: Invade and destroy surrounding tissues.

• Differentiation: Cells are abnormal, poorly differentiated (don’t resemble normal tissue).

• Mitosis: High mitotic index (many cells dividing).

• Metastasis: Can spread (metastasize) through blood or lymph to distant organs (lungs, liver, bone).

• Clinical impact: Life‑threatening, disrupts organ function, systemic effects (weight loss, fatigue, cachexia).

Quick NCLEX Memory Aid

• Benign = “contained and calm” → slow, encapsulated, no spread.

• Malignant = “mean and moving” → fast, invasive, spreads.

Comparison Table

👉 Think NCLEX question style: If asked “Which tumor type is more likely to metastasize and invade surrounding tissues?” → Malignant tumor. If asked “Which tumor type grows slowly and is encapsulated?” → Benign tumor.

2.     Describe what causes cancer and list characteristics of cancerous cells.

What Causes Cancer

Cancer develops when normal cell growth and death controls are lost.

• Genetic mutations: Damage to DNA changes how cells grow and divide.

• Proto‑oncogenes → oncogenes: Normal “growth genes” mutate and become stuck in the “ON” position → uncontrolled growth.

• Tumor suppressor genes: Normally act like brakes to stop growth. If mutated, the brakes fail → cells keep dividing.

• Environmental exposures: Tobacco, radiation, chemicals, viruses.

• Lifestyle factors: Poor diet, alcohol, UV exposure.

• Age: Risk increases with age because mutations accumulate over time.

• Inherited mutations: Some families carry cancer‑causing genes (e.g., BRCA1/2).

👉 Think of it like a car:

• Oncogenes = gas pedal stuck down.

• Tumor suppressor genes = broken brakes.

• Together → uncontrolled cell growth = cancer.

Characteristics of Cancer Cells

Cancer cells look and behave very differently from normal cells.

• Uncontrolled growth: Divide rapidly, ignore normal “stop” signals.

• Loss of differentiation (anaplasia): Cells don’t resemble normal tissue.

• Abnormal cell cycle: Skip checkpoints, keep dividing.

• Immortality: Use telomerase to keep dividing forever.

• No contact inhibition: Normal cells stop growing when crowded; cancer cells pile up.

• Anchorage independence: Can grow without being attached to a surface.

• Evade apoptosis: Don’t die when damaged.

• Angiogenesis: Stimulate new blood vessels to feed the tumor.

• Metastasis: Invade nearby tissue and spread to distant sites.

Quick NCLEX Memory Aid — Six Hallmarks of Cancer on slide (all cancers mut acquire mutations in these areas, but the order of acquiring these capabilities varies in different cancers)

1. Self‑sufficiency in growth signals (make their own “grow” signals).

2. Insensitive to anti‑growth signals (ignore “stop” signals).

3. Evade apoptosis (don’t die when damaged).

4. Limitless replication (immortal).

5. Sustained angiogenesis (grow their own blood supply).

6. Tissue invasion & metastasis (spread).

Comparison Table

👉 NCLEX‑style takeaway: If asked “Which characteristic best describes malignant cells?” → Rapid growth, poor differentiation, ability to metastasize.

3.     Define the following:

a. Proto‑oncogenes

• Definition: Normal genes that control cell growth and division.

• Function: Act like the “gas pedal” of the cell cycle — they tell cells when to grow and divide.

• Normal role: Help with normal tissue growth, repair, and development.

• Problem: If mutated, they can become oncogenes (stuck in the “ON” position).

👉 Memory aid: Proto‑oncogene = “potential to cause cancer if mutated.”

b. Oncogenes

• Definition: Mutated or overactive proto‑oncogenes.

• Function: Cause uncontrolled cell growth.

• Problem: The “gas pedal” is stuck down → cells keep dividing even when they shouldn’t.

• Result: Leads to tumor formation and cancer progression.

👉 Memory aid: Oncogene = “ON” gene → always telling the cell to grow.

c. Tumor Suppressor Genes

• Definition: Normal genes that act like the “brakes” of the cell cycle.

• Function: Stop cell division when growth is not needed, repair DNA damage, or trigger apoptosis (cell death) if the cell is abnormal.

• Problem: If these genes are mutated or lost, the brakes fail → cells divide uncontrollably.

• Examples: p53 (guardian of the genome), RB gene.

👉 Memory aid: Tumor suppressor = “STOP signal.” When broken, cancer cells speed out of control.

Quick NCLEX Comparison Table

👉 NCLEX‑style takeaway:

• Proto‑oncogenes = normal growth genes.

• Oncogenes = mutated, stuck “ON” growth genes.

• Tumor suppressor genes = brakes; when broken, cancer develops.

4.     Describe how cancer is classified in terms of grading and staging.

Cancer Classification: Grading vs. Staging

Grading (Microscope View)

• Definition: Grading describes how abnormal the cancer cells look compared to normal cells.

• Focus: Cell appearance and differentiation (histology).

• Scale:

  • Grade 1: Well‑differentiated → cells look almost normal, grow slowly.

  • Grade 2: Moderately differentiated → some abnormal changes.

  • Grade 3: Poorly differentiated → very abnormal, aggressive.

  • Grade 4: Undifferentiated/anaplastic → cells look nothing like normal tissue, very aggressive.

• Key NCLEX point: Higher grade = more malignant potential.

👉 Think of grading as “how ugly the cells look under the microscope.”

Staging (Patient View)

• Definition: Staging describes how far the cancer has spread in the body.

• Focus: Tumor size, lymph node involvement, metastasis.

• System: TNM classification

  • T = Tumor size/extent

  • N = Node involvement

  • M = Metastasis (spread to distant organs)

• Clinical stages:

  • Stage 0: Cancer in situ (localized, not invasive).

  • Stage I: Localized tumor.

  • Stage II: Limited local spread.

  • Stage III: Extensive local and regional spread.

  • Stage IV: Distant metastasis.

• Key NCLEX point: Higher stage = more advanced disease.

👉 Think of staging as “how far the cancer has traveled in the body.”

Quick Comparison Table

NCLEX‑Style Takeaway

• Grading = microscope (cell appearance).

• Staging = body (spread pattern).

• Both are used together to guide treatment and predict prognosis.

a.     What is meant by anaplasia?

b.     What is evaluated when describing the stage of a cancer?  

Cancer Classification: Grading vs. Staging

Grading (Microscope View)

• Definition: Grading describes how abnormal the cancer cells look compared to normal cells.

• Focus: Cell differentiation and appearance.

• Scale:

  • Grade 1: Well‑differentiated (cells look almost normal).

  • Grade 2: Moderately differentiated (some abnormal changes).

  • Grade 3: Poorly differentiated (very abnormal).

  • Grade 4: Anaplastic (no resemblance to normal tissue).

• Key NCLEX point: Higher grade = more aggressive tumor.

👉 Think of grading as “how ugly the cells look under the microscope.”

Staging (Patient View)

• Definition: Staging describes how far the cancer has spread in the body.

• Focus: Tumor size, lymph node involvement, and metastasis.

• System: TNM classification

  • T = Tumor size/extent

  • N = Node involvement

  • M = Metastasis (spread to distant organs)

• Clinical stages:

  • Stage 0: Cancer in situ (localized, not invasive).

  • Stage I: Localized tumor.

  • Stage II: Limited local spread.

  • Stage III: Extensive local and regional spread.

  • Stage IV: Distant metastasis.

👉 Think of staging as “how far the cancer has traveled in the body.”

a. What is Meant by Anaplasia?

• Definition: Anaplasia = loss of differentiation, poorly differentiated

• On slide (Greater anaplasia= greater malignant potential in general)

• Cells no longer look or act like the tissue they came from.

• Features:

  • Abnormal size/shape (pleomorphism).

  • Large, irregular nuclei.

  • High mitotic activity.

  • Disorganized tissue structure.

• Key NCLEX point: Anaplasia = hallmark of malignancy. The more anaplastic, the more aggressive the cancer.

b. What is Evaluated When Describing the Stage of a Cancer?

When staging, clinicians evaluate:

• Tumor size and extent (T).

• Lymph node involvement (N).

• Presence or absence of distant metastasis (M).

• Together, these determine the stage (0–IV), which guides treatment and prognosis.

Quick NCLEX Comparison Table

👉 NCLEX‑style takeaway:

• Grading = microscope (cell appearance, anaplasia).

• Staging = body (tumor size, lymph nodes, metastasis).

5.     Describe the pathology and clinical manifestations of leukemia.

Pathology of Leukemia

• Definition: Leukemia is a cancer of the bone marrow and blood.

• Cause: A single stem cell undergoes malignant transformation → becomes a clonal disorder.

• Process:

  • Bone marrow produces large numbers of immature WBCs (blast cells).

  • These abnormal cells crowd out normal RBCs, WBCs, and platelets.

  • Normal blood cell production stops → pancytopenia (↓ RBCs, ↓ platelets, ↓ functional WBCs).

• Spread: Leukemic cells spill into the bloodstream and infiltrate organs (liver, spleen, lymph nodes).

• Result: Systemic disease with widespread effects.

👉 Think of it like this: The bone marrow factory is broken — instead of making a balanced mix of workers (RBCs, WBCs, platelets), it only churns out defective trainees (blast cells) that don’t do their jobs.

Clinical Manifestations of Leukemia

Because normal blood cells are crowded out, symptoms fall into three main categories:

1. From ↓ RBCs (Anemia)

• Fatigue, weakness

• Pallor

• Shortness of breath

2. From ↓ Platelets (Thrombocytopenia)

• Easy bruising

• Petechiae (tiny red spots)

• Purpura, ecchymosis (larger bruises)

• Nosebleeds, gum bleeding

• Hemorrhage risk

3. From ↓ Functional WBCs (Leukopenia)

• Frequent infections

• Fever

• Poor wound healing

Other Systemic Signs

• Weight loss (cancer metabolism)

• Bone pain (marrow overcrowding)

• Liver, spleen, lymph node enlargement (infiltration)

• Elevated uric acid (from rapid cell breakdown → risk of gout or kidney stones)

Quick NCLEX Table

NCLEX‑Style Takeaway

• Pathology: Malignant blast cells overcrowd bone marrow → pancytopenia + organ infiltration.

• Clinical manifestations: Anemia, bleeding, infection, bone pain, organ enlargement, weight loss.

a.     What are the 4 types of leukemia?

The 4 Types of Leukemia

1. Acute Lymphocytic Leukemia (ALL)

• Cell type: Immature lymphocytes (T or B cells).

• Onset: Sudden, rapid progression.

• Age group: Most common in children (ages 3–7).

• Key features: High blast count, bone pain, fever, enlarged lymph nodes, hepatosplenomegaly.

• NCLEX clue: ALL = “All Little ones” → most common childhood leukemia.

2. Acute Myelogenous Leukemia (AML)

• Cell type: Immature myeloid cells (precursors to neutrophils, monocytes, etc.).

• Onset: Sudden, aggressive.

• Age group: More common in older adults (>60 years).

• Risk factors: Strongest link to toxins (radiation, benzene, chemotherapy drugs).

• Key features: Anemia, bleeding, infection, fatigue.

• NCLEX clue: AML = “Adults Mostly” → common in older adults.

3. Chronic Lymphocytic Leukemia (CLL)

• Cell type: Mature but abnormal lymphocytes.

• Onset: Slow progression.

• Age group: Most common in older adults (>45 years).

• Key features: Often asymptomatic at first, later → enlarged lymph nodes, fatigue, infections.

• NCLEX clue: CLL = “Chronic in Later Life.”

4. Chronic Myelogenous Leukemia (CML)

• Cell type: Mature but abnormal myeloid cells.

• Onset: Slow progression, but can transform into acute phase (“blast crisis”).

• Age group: Adults (middle age).

• Key feature: Philadelphia chromosome (t[9;22]) present in ~90% of cases.

• NCLEX clue: CML = “Chromosome Mutation Leukemia” → Philadelphia chromosome hallmark.

Quick Comparison Table

👉 NCLEX‑style takeaway:

• Acute = immature blast cells, rapid onset.

• Chronic = more mature cells, slower onset.

• ALL = kids, AML = older adults, CLL = later life, CML = Philadelphia chromosome.

b.     What is the Philadelphia chromosome and which type of leukemia is associated with this?

Philadelphia Chromosome [mentioned on EXAM!]

• Definition: The Philadelphia chromosome is a genetic abnormality caused by a translocation (swap of DNA)between chromosome 9 and 22.

• On slide [mentioned on EXAM!]: Chronic Myelocytic Leukemia (CML) – Philadelphia chromosome is marker in 90% of cases (translocation between chromosome 9 & 22)

• Result: This translocation creates the BCR‑ABL fusion gene.

• Effect: The fusion gene produces an abnormal tyrosine kinase enzyme that signals cells to keep dividing uncontrollably → cancer.

👉 Think of it like this: Two chromosomes accidentally “swap parts,” creating a super‑charged growth signal that never turns off.

Leukemia Associated

• Most strongly linked to: Chronic Myelogenous Leukemia (CML) — present in ~90% of cases.

• Can also be seen in: Some cases of Acute Lymphoblastic Leukemia (ALL) and rarely Acute Myeloid Leukemia (AML).

• NCLEX clue: If you see “Philadelphia chromosome” on a test → think CML first.

Quick NCLEX Table

👉 NCLEX‑style takeaway:

• Philadelphia chromosome = hallmark of CML.

• BCR‑ABL fusion gene drives uncontrolled growth.

c.     Which type of leukemia is more common in children?

Leukemia Most Common in Children

·       The type of leukemia most common in children is Acute Lymphocytic Leukemia (ALL).

·       Age group: Peak incidence between ages 3–7 years.

·       Pathology: Involves malignant transformation of immature lymphocytes (blast cells).

·       Onset: Sudden, rapid progression.

·       Clinical features:

o   Bone pain, fever, fatigue

o   Enlarged lymph nodes, liver, spleen

o   Anemia, bleeding, frequent infections

Quick NCLEX Memory Aid

·       ALL = “All Little ones” → most common childhood leukemia.

·       AML = Adults Mostly → more common in older adults.

👉 NCLEX‑style takeaway: If asked “Which leukemia is most common in children?” → Acute Lymphocytic Leukemia (ALL).

6.     Describe the pathophysiology and clinical manifestations of lymphoma.

Pathophysiology of Lymphoma

• Definition: Lymphoma is a malignant cancer of the lymphatic system (lymph nodes, spleen, bone marrow).

• Origin: Begins with a mutation in a lymphocyte (usually a B cell, sometimes T or NK cell).

• Process:

  • Mutated lymphocytes undergo clonal expansion → uncontrolled growth.

  • They accumulate in lymph nodes and other lymphatic tissues.

  • Normal immune function is disrupted.

• Types:

  • Hodgkin Lymphoma (HL): Characterized by Reed–Sternberg cells (giant abnormal B cells). Spreads in an orderly, predictable pattern from one lymph node group to the next.

  • Non‑Hodgkin Lymphoma (NHL): No Reed–Sternberg cells. Spread is random, non‑contiguous, often involves extranodal sites (GI tract, skin, CNS).

👉 Think of it like this: Normal lymphocytes = soldiers of the immune system. In lymphoma, one soldier mutates and clones itself endlessly, forming an army of defective cells that crowd out normal defenses.

Clinical Manifestations of Lymphoma

General Symptoms (Both HL and NHL)

• Painless lymph node enlargement (most common first sign)

• “B symptoms”:

  • Fever

  • Night sweats

  • Unexplained weight loss

• Fatigue, malaise

• Pruritus (itching)

• Hepatosplenomegaly (enlarged liver/spleen)

Describe the differences between Hodgkin’s and Non-Hodgkin’s lymphoma.

Hodgkin Lymphoma Specific

• Reed–Sternberg cells present.

• Predictable spread (often starts in cervical nodes above the diaphragm).

• High cure rate, especially in early stages.

• On slide: Hodgkin’s lymphoma (or disease) (15% of all lymphomas)

  • Malignant disorder of lymph nodes characterized by presence of Reed-Sternberg cells (though to be malignant B lymphocyte)

  • High rates of cure (83% 5 year survival rate)

Non‑Hodgkin Lymphoma Specific

• No Reed–Sternberg cells.

• Harder to treat

• Unpredictable spread, often widespread at diagnosis.

• Cure rate varies depending on subtype (low‑grade vs high‑grade).

Quick NCLEX Table

NCLEX‑Style Takeaway

• Pathophysiology: Malignant lymphocytes proliferate uncontrollably, disrupting immune function.

• Clinical manifestations: Painless lymphadenopathy + B symptoms (fever, night sweats, weight loss).

• Key distinction: Reed–Sternberg cells = Hodgkin lymphoma; absence = Non‑Hodgkin lymphoma.

Hodgkin’s Lymphoma (HL)

·       Key diagnostic feature: Presence of Reed–Sternberg cells (“owl’s eye” appearance).

·       Spread pattern: Predictable, orderly spread from one lymph node group to the next (contiguous).

·       On slide: Grow in predictable manner – originates in one lymph node metastasizes typically along contiguous lymphatic pathways.

·       Age group: Bimodal distribution → peaks in young adults (20s) and again in older adults (>50).

·       Symptoms:

o   Painless lymph node enlargement (often cervical/above diaphragm)

o   “B symptoms”: fever, night sweats, weight loss

o   Pruritus (itching), fatigue

·       Prognosis: High cure rate (especially in early stages).

·       On slide: High cure rate 90 – 95% in early stages

·       She mentions: start in one lymph node then go in neck, usually first sign is painless swollen lymph node in neck.

Non‑Hodgkin’s Lymphoma (NHL)

·       Key diagnostic feature: No Reed–Sternberg cells.

·       Spread pattern: Unpredictable, non‑contiguous spread; often involves extranodal sites (GI tract, skin, CNS).

·       Age group: More common in older adults (>50).

·       Symptoms:

o   Painless lymphadenopathy (any node group)

o   B symptoms (fever, night sweats, weight loss)

o   Organ‑specific symptoms depending on site (abdominal pain, CNS changes).

·       Prognosis: Variable — depends on subtype (low‑grade vs high‑grade). Cure rates generally lower than Hodgkin’s.

·       On slide (she mentioned emphasized): Overall 5 year survival rate is about 50%

7.     What causes multiple myeloma?

Pathophysiology: What Causes Multiple Myeloma

·       Definition: Multiple myeloma is a cancer of plasma cells (a type of B lymphocyte that normally makes antibodies).

·       On slide: A B cell cancer characterized by the proliferation of malignant plasma cells that infiltrate the bone marrow and aggregated into tumor masses throughout the skeletal system.

·       Cause:

o   Starts when one clone of plasma cells mutates and begins producing large amounts of abnormal immunoglobulin (usually IgG, sometimes IgA).

o   These abnormal antibodies are defective and don’t fight infection.

o   The malignant plasma cells accumulate in the bone marrow, crowding out normal blood cell production.

·       Genetic changes:

o   Mutations in proto‑oncogenes (like RAS).

o   Chromosome translocations and abnormalities.

·       Result:

o   Overproduction of M protein (monoclonal antibody).

o   Excess light chains (Bence Jones proteins) that can damage kidneys.

o   Stimulation of osteoclasts → bone breakdown and high calcium levels.

👉 Think of it like this: The plasma cell factory goes rogue — instead of making helpful antibodies, it mass‑produces defective ones and clogs up the bone marrow.

Clinical Manifestations (Classic Features)

·       Bone lesions & pain: Malignant plasma cells stimulate bone breakdown → fractures, spinal compression.

·       Hypercalcemia: Bone destruction releases calcium → weakness, confusion, constipation.

·       Renal failure: Bence Jones proteins damage kidneys.

·       Anemia: Crowding out of RBC production → fatigue, pallor.

·       Infections: Abnormal antibodies don’t protect → increased risk of infection.

·       Other signs: Amyloidosis (protein deposits in tissues), neuropathy, edema.

Quick NCLEX Memory Aid — CRAB

The hallmark features of multiple myeloma can be remembered with CRAB:

·       C = Calcium ↑ (hypercalcemia) [on EXAM to know increase calcium level and renal failure]

·       R = Renal failure (proteinuria, Bence Jones proteins)

·       A = Anemia (↓ RBCs)

·       B = Bone lesions/pain (fractures, lytic lesions)

NCLEX‑Style Takeaway

·       Cause: Malignant plasma cells producing abnormal antibodies (M protein, Bence Jones protein).

·       Result: Bone destruction, hypercalcemia, renal failure, anemia, infections.

·       Classic mnemonic: CRAB.