College of Dentistry - General Pathology: Course Material: Neoplasia

College of Dentistry – General Pathology
COURSE MATERIAL:
NEOPLASIA
REFERENCE:
College of Dentistry– General Pathology

GOALS & OBJECTIVE
At the end of this course material for Neoplasia; You should be able to:
1. Understand the Basic Mechanism and the definition of Cancer Biology and Development.
2. Significance between Benign and Malignant Tumor and its Prognosis.
3. Nomenclature and Overview Different Common Tumors.
4. Spread, Metastasis and Different Pathways.
5. General Clinical Effects with Cancer Patient.
6. Occupational Hazards and 2019 Common Tumors by Epidemiology.
7. Staging
8. Investigations How to Deal with Cancer.

INTRODUCTION
Neoplasia – “New Growth”
Neoplasms – Collection of cells and stroma
comprising of new growths.
- Genetic disorder of cell growth that are
triggered by acquired and (less common)
inherited mutations by affecting cells.
2 General Types Neoplasms
1. Benign
2. Malignant
Tumor – swelling associated inflammation but
now equated with neoplasm.
Oncology – Study of tumors or neoplasms.

NORMAL MAMMARY DUCT IDCA
LOSS OF ARCHITECTURE OF TISSUE & LOSS RECOGNIZE THE HIGHLY ORDERED
PHENOTYPE

BASICS OF NEOPLASIA
Two Basic Components of TUMOR CELLS:
1. Tumor parenchyma (Distinguishing cell of the tumor) – mostly
composed of neoplastic cells.
Liver – Liver Parenchyma/Liver Cells
Epithelial Type – Derived from its name
Squamous Epithelium - SCCA
- This is the basis of classification of tumors and its biologic
behavior.
2. Reactive Stroma (Connective Tissue, Blood Vessels, and
Innate/Adaptive Immune System)
- Supporting System of the Tumor
- Basis of the Growth and Spread of the tumor.
- Scant connective tissue – neoplastic tissue is soft and fleshy by
gross.

BASICS OF NEOPLASIA
Desmoplasia/Desmoplastic
Reaction
– Abundant Collagenous stroma
formations that is formed by
parenchymal tumor cell.
- If abundant collagen is
present it becomes stony and
hard (SCIRRHOUS)
- If scanty amounts (SOFT TO
FLESHY)

NEOPLASTIC MASSES CONFUSED WITH NEOPLASM
1.Keloid – Excessive repair by thick
colloid tissue.
2.Hyperplasia – Adaptive Changes
producing increased number of
normal cells.
3.Hypertrophy – Adaptive Changes
producing a increase in size and
weight of the cells.
4.Metaplasia – Replacement of one
adult type of cells with another
adult cell type of cells.

colloid tissue.
normal cells.

colloid tissue.
normal cells.

NOMENCLATURE: BENIGN TUMORS
Mesenchymal Origin – Follows this rule: - Characterized by tumors that remains
CELL OF ORIGIN - add suffix “(–oma)” localized at their site of origin and generally
amenable for surgical removal.
Chondrocytes/Cartilaginous – Benign Chrondroma
- Prognosis is much better than malignant.
Fibrous Tissue/Cells – Benign Fibroma
- EXCEPTION: When vital organs are affected
Epithelial Origin – Different Rule: (Complex by the this tumor. (Brain).
Nomenclature)
1.Cells of Origin ( Adenoma – Glandular Origin) –
weather it forms or not glandular structures.
2.Microscopic Pattern (Papilloma – Finger Like
Projections )
3.Microscopic Architecture (Cystadenoma – Cystic
Masses)
Polyp / Adenomatous Polyp – when there grossly
visible projections with stalk. (If with glandular latter)


Capsule – Flattened/compressed
fibrous tissue (FIBROBLAST) separates
tumor parenchyma to the surrounding
normal tissue. (Activated by stromal
cells due to compression effects leading
to tissue hypoxia)

NON-ENCAPSULATED BENIGN CAVERNOUS HEMANGIOMA

`
INVASIVENESS is the most reliable feature

that differentiates BENIGN to MALIGNANCY
NOMENCLATURE: MALIGNANT TUMORS
MALIGNANT TUMORS and Where it Arises: - Characterized by tumors that INVADE the
1. Solid Mesenchymal Tumors (Sarcomas) adjacent structures and SPREAD to
DISTANT SITES (Metastasis).
2. Blood Forming Cells (Leukemias/Lymphomas)
3. (3) Germ Layers of Epithelial Origin “(Carcinomas)”
- Collectively TERMED as Cancers “CRAB”
in Lantin Word.
Squamous Cell Carcinoma – Resemble as stratifies squamous
epithelium. - Some can be discovered early but others
too late.
Adenocarcinoma – Neoplastic Epithelial Cells that usually grow
on glandular pattern. (Sometime solid if this becomes poorly - Management is by Surgical Removal with
differentiated) Chemotherapy, Therapeutic Antibodies, and
We Add Tissue/Organ + SCA Radiotherapy.
We Add Tissue/Organ + Adenocarcinoma
LUNG + Adenocarcinoma = Lung Adenocarcinoma
Undifferentiated Carcinoma – When cannot identify Cell of
Origin.

INVASIVENESS is the most reliable feature

that differentiates BENIGN to MALIGNANCY

NOMENCLATURE: BENIGN & MALIGNANT TUMORS

NOMENCLATURE: BENIGN & MALIGNANT TUMORS

TUMORS with BENIGN SOUNDING “OMA”

BUT MALIGNANT
1. Melanoma – Arises from neoplastic
melanocytes.
2. Lymphoma – Arises from Blood WBC
3. Mesothelioma – Arises from the Pleura
4. Seminoma – Arises from Germ Cell Testes

NOMENCLATURE: HAMARTOMA VS. CHORISTOMA TUMORS – BENIGN CELLS
PULMONARY HAMARTOMA – Excess of Tissue innate

to that site of involvement
Hamartoma – Disorganized Masses Composed of

cells indigenous to the involved tissue.
- Associated with CLONAL CHROMOSOMAL
ABERRATIONS by SOMATIC MUTATION.
Choristoma – heterotopic (misplaced) rest cells

NOMENCLATURE: MIXED TUMORS
MIXED TUMORS
-Can be BENIGN/MALIGNANT tumor usually seen in
Salivary Gland
-Pleomorphic Adenoma – Combination of Epithelial

components with myxoid stroma that may contain
Mesenchymal components: bone/cartilage.
-Teratoma (Ovary & Testis, Anterior Mediastinal Mass)

– 2 or 3 more germ layers. – Arises from Totipotential
Germ Cells (NB: This can be Benign or Malignant)
Ovary – Most Common Teratoma (Dermoid Cyst) – More

on Ectodermal Lines of Squamous Epithelium (Hair,
Sebum)

NOMENCLATURE: MIXED TUMORS

DIFFERENTIATION & ANAPLASIA TUMORS
DIFFERENTIATION – means resemblance of the ANAPLASIA – cells that are poorly differentiated or
parenchymal neoplastic cell to normal LACK OF DIFFERENTIATION
parenchymal cell of origin. (morphological and
functional) - Can be Benign or Malignant
Benign or Malignant and Well Differentiated
Tumors (Endocrine Neoplasm) – Can secrete
variable amounts of hormones.
a.Well Differentiated (resemblance is similar) –
Usually Seen in Benign Cases but also in
Malignancy.
b.Poorly Differentiated (more solid/or loss of
differentiation)
c.Moderately Differentiated (between the A & B)

DIFFERENTIATION
MALIGNANT WELL DIFFERENTIATED BENIGN WELL DIFFERENTIATED

SAMPLE WITH WELL DIFFERENTIATED VS. POORLY DIFFERENTIATED TUMORS
NO
KERATIN KERATIN
PEARLS PEARLS
SQUAMOUS CELL CARCINOMA, POORLY

SQUAMOUS CELL CARCINOMA, WELL DIFFERENTIATED
DIFFERENTIATED

MODERATELY DIFFERENTIATED & ANAPLASIA
NO
BILE
HEPATOCELLULAR CARCINOMA, POORLY

HEPATOCELLULAR CARCINOMA, WELL DIFFERENTIATED
DIFFERENTIATED

MODERATELY DIFFERENTIATED & ANAPLASIA

Well Differentiated
Poorly Differentiated
Moderately Differentiated

MORPHOLOGIC FEATURE CHARACTERISTICS: MALIGNANT TUMORS
Pleomorphism (Variation in Size and Shape)
MAY AFFECT THE NUCLEAR GRADING SYSTEM

Abnormal Nuclear Morphology (Nuclear/Cytoplasmic Ratio) or N/C Ratio.
Normal is (1:4 or 1:6) Malignant: If Reversal N:C ratio or specially 1:1!

Nuclear Shape and Nuclear Molding:

Irregularly or angulated – Malignant.

Prominent chromatins or nucleoli

Mitosis – REFLECTS THE HIGH PROLIFERATIVE

ACTIVITY of the parenchymal neoplastic cell. The
presence mitosis may not indicate that the neoplastic cell
is malignant, however prognostication and degree of
aggressiveness may somehow affects it.
High Suspicion of Malignancy (AMF) – Abnormal

Mitotic Figures (Atypical or Bizarre)
Ki67/MIB-1 – proliferative index marker (Its not a marker

for mitosis)

Loss of Polarity – orientation of the neoplastic cells against the
surface of the basement membrane.

Hyperchromatic – More darkly stained

nuclei.

Ischemic Necrotic Changes – when the vascular supply

doesn’t reach to the parenchymal cells the tumor becomes
necrotic in a disorganized fashion.
METAPLASIA, DYSPLASIA & CARCINOMA IN- SITU
METAPLASIA – replacement of one type of cell to another type.
- Associated with tissue damage, repair, and regeneration.
- This is prone for MALIGNANT TRANSFORMATION.
INTESTINAL METAPLASIA ESOPHAGUS


DYSPLASIA – Disordered growth.

- Individual cells exhibits pleomorphism,
hyperchromatism, and increase N/C Ratio.
- Mild-Severe Dysplasia can be Reversible.
- Mild Dysplasia – May already have already
mutation and associated carcinoma.
- Severe Dysplasia – High Risk Transformation
and always adjacent with carcinoma.
- Dysplastic epithelium is usually accompanied
with Metaplastic epithelium.
- If REMOVED it will NOT PROGRESS TO
CANCER.
- SHOWCASE ARCHITECTURAL DISARRAY
and ODERLY OF DIFFERENTIATION.
- THERE IS NO INVASIVENESS.

CARCINOMA IN-SITU –
severe Dysplasia occurs but
still doesn’t penetrate the
BASEMENT MEMBRANE.
- Commonly Seen : Skin,
Breast, Bladder, and Cervix.

INVASIVE CARCINOMA/ LOCAL
INVASION – if it penetrates the beyond the
basement membrane.
- Cancers usually associated with
accumulation of mutations.
- This will become progressive.
- Will cause damage of surrounding
tissues.
- Systemic spread is imminent.

METASTASIS & INVASION
– Spread of tumor to other Sites that are Physically
Discontinuous with the Primary Tumor that undergo
“Metastatic Cascade”
- Due to the INVASIVENESS OF THE BEHAVIOR of
Tumor Cells that permits them to penetrate the blood
vessels and the lymphatic system, thus allowing it to
spread.

METASTASIS
- Invasion is one of the requirements for this mechanism to occur. Direct Extension nearby sites.
- Invasion is not Metastasis.
Likelihood of Metastasis of Solid Tumors:
- Influenced by lack of differentiation of the parenchymal tumor cell, tumor behavior/aggressiveness, larger tumor
size, and rapid growth.
- (Not true all the time, there are smaller tumors, slow growing, well differentiated may also metastasize widely and
early) – Small Cell carcinomas.
- Reduces the chance of survival of patients.
Tumors that Rarely/Infrequently Metastasize: But they can Cause Invasion.
1. Gliomas – Tumor Glial Cells
2. Basal Cell Carcinoma – Tumor of Skin
Tumors Disseminated Spread/Liquid Tumors: Leukemias and Lymphomas

PATHWAYS OF SPREAD
3 PATHWAYS OF SPREAD:
1. Direct Seeding of Body Cavity and Surfaces.
2. Lymphatic Spread
3. Hematogenous Spread
4. Iatrogenic Spread – Instrument Inoculation
Direct Seeding of Body Cavity and Surfaces:

- Malignant cells penetrates into open field that lacks
physical barriers “Peritoneal Cavity” – Common
- Others: Pleural, Pericardial, Subarachnoid, and
Joint Spaces.
- Example from Ovarian/Appendiceal Tumor.

PATHWAYS OF SPREAD
LYMPHATIC SPREAD
- Transport to lymphatic system/vessels is
THE MOST COMMON & INITIAL
DISSEMINATION PATHWAYS.
- SARCOMAS – is usually uses this route.
NB: Tumors do not have functional lymphatic
system. The surrounding lymphatic vessels
located at the margin is the site.
SENTINEL LYMPH NODE:

- This is the FIRST LYMPH NODE That
receives the lymph flow from the PRIMARY
TUMOR. (Breast, Colon, Melanoma)

PATHWAYS OF SPREAD
HEMATOGENOUS SPREAD
- Typical for Sarcomas and also with
CARCINOMAS.
- Penetration of small vessels (Small Veins and
Arteries Invasion) at the site of the Primary
Tumor.
- Liver and Lungs – Most commonly involved in
metastatic dissemination (Portal and Caval Blood
Flow).

GENERAL CLINICAL EFFECTS OF CANCER
Local and Hormonal Effects

Cancer Cachexia – Hypermetabolic state of loss
muscle mass and with or without fat.
Paraneoplastic Syndromes – occur 10% of
patients with Cancers. This can be earliest sign
manifestation show cancer is present.
- Most common form is HYPERCALCEMIA.



CANCERS CAN BE PREVENTED

CANCERS CAN BE PREVENTED
IONIZING RADIATION
Radiation- energy that travels in waves

and or high speed particles
• Non ionizing radiation – UV,
microwave etc
• Ionizing Radiation- has sufficient
energy to remove tightly bound
atoms; indispensible for medical
practice; mutagenic, carcinogenic
and teratogenic
• X-rays and γ rays-
electromagnetic waves of high
frequencies
• Alpha and beta particles

RESISTANT
AFFECTED
DNA damage and Carcinogenesis
EARLY EFFECTS
The most serious damage to DNA is caused
by Double Stranded Breaks (DSB) LATE EFFECTS
Two repair systems: LATE EFFECTS
1.Homologous recombination LATE EFFECTS

2.Non-homologous end joining (NHEJ)
NHEJ- most common, repair often produces EARLY EFFECTS
mutations , if the replication of cells LATE EFFECTS
containing DSB’s is not stopped by cell cycle

checkpoint→ initiate carcinogenesis EARLY EFFECTS
Fibrosis
- Occur weeks and months after irradiation
LATE EFFECTS
- Vascular damage, killing of tissue stem EARLY EFFECTS
cells→release of cytokines and
chemokines→ fibroblast activation
GRADING AND STAGING OF NEOPLASMS
Based on Histologic Findings:

Low Grade – More Differentiated
High Grade – Undifferentiated/ Highly
Anaplastic
Based on Tumor Size (Affects The
Staging)
Based on Nodal Spread (Affects The
Staging)
Metastasis (Affects The Staging)
TNM Staging – Will depends on the

consensus to which what organ / primary
of cancer originated.
Staging I – IV: Affects the life

expectancy 5 years
DIAGNOSTIC PROCEDURES & EARLY DECTECTION IS KEY SURVIVAL
Tissue Biopsy – Obtain a sample for
histomorphologic evaluation diagnosis.
Section
Excision
Punch
Needle (FNAB) - #21-23 G
Needle (Core Needle Biopsy/ Silverman
Needle) – Histomorphologic Evaluation
Aspiration
Curettage/ Scrapings
Frozen Biopsy – Do not place sample in
water and formalin
Cytologic Examination (PAP Smear)
Tumor Markers

College of Medicine – Department of Pathology
ASPECTS OF LOSS OF CONTROL LEADING TO CANCER DEVELOPMENT (HALLMARKS OF CANCER)

THANK YOU
College of Medicine – Department of Pathology

College of Dentistry - General Pathology: Course Material: Neoplasia

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College of Dentistry – General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

NON-ENCAPSULATED BENIGN CAVERNOUS HEMANGIOMA

College of Dentistry– General Pathology

INVASIVENESS is the most reliable feature

College of Dentistry– General Pathology

INVASIVENESS is the most reliable feature

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

TUMORS with BENIGN SOUNDING “OMA”

College of Dentistry– General Pathology

PULMONARY HAMARTOMA – Excess of Tissue innate

Hamartoma – Disorganized Masses Composed of

College of Dentistry– General Pathology

-Pleomorphic Adenoma – Combination of Epithelial

-Teratoma (Ovary & Testis, Anterior Mediastinal Mass)

Ovary – Most Common Teratoma (Dermoid Cyst) – More

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

MALIGNANT WELL DIFFERENTIATED BENIGN WELL DIFFERENTIATED

College of Dentistry– General Pathology

SQUAMOUS CELL CARCINOMA, POORLY

College of Dentistry– General Pathology

HEPATOCELLULAR CARCINOMA, POORLY

College of Dentistry– General Pathology

College of Dentistry– General Pathology

College of Dentistry– General Pathology

Pleomorphism (Variation in Size and Shape)

MAY AFFECT THE NUCLEAR GRADING SYSTEM

College of Dentistry– General Pathology

Abnormal Nuclear Morphology (Nuclear/Cytoplasmic Ratio) or N/C Ratio.

Normal is (1:4 or 1:6) Malignant: If Reversal N:C ratio or specially 1:1!

College of Dentistry– General Pathology

Nuclear Shape and Nuclear Molding:

College of Dentistry– General Pathology

Prominent chromatins or nucleoli

College of Dentistry– General Pathology

Mitosis – REFLECTS THE HIGH PROLIFERATIVE

High Suspicion of Malignancy (AMF) – Abnormal

Ki67/MIB-1 – proliferative index marker (Its not a marker

College of Dentistry– General Pathology

College of Dentistry– General Pathology

Hyperchromatic – More darkly stained

College of Dentistry– General Pathology

Ischemic Necrotic Changes – when the vascular supply

INTESTINAL METAPLASIA ESOPHAGUS

College of Dentistry– General Pathology

College of Dentistry– General Pathology

DYSPLASIA – Disordered growth.

College of Dentistry– General Pathology