By Dr Abiodun Mark A. “The only certain way of avoiding cancer is not to be born; to live is to...
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- Slide 1
- By Dr Abiodun Mark A
- Slide 2
- The only certain way of avoiding cancer is not to be born; to
live is to incur the risk -Robbins & Cotran PBD.
- Slide 3
- Introduction. A tumor is an abnormal mass of tissue,the growth
of which Is virtually autonomous and exceeds that of normal
tissues. Tumors are classified into 2 broad categories: -Benign
-Malignant. The type of neoplasm is based on the characteristics of
its parenchyma.
- Slide 4
- Tumor nomenclature. Tumors have 2 basic components: -The
transformed neoplastic cells aka the parenchyma -The supporting
component aka the stroma. Benign tumors: the names of this groups
of tumor typically(but not uniformly) ends with the suffix oma.
Malignant tumors are also referred to as cancers and are divided
into the following categories: -Carcinomas: from epithelial origin
-Sarcomas: from mesenchymal tissues.
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- Special tumors: Mixed tumors: are derived from one germ layer
that differentiates into more than one parenchyma cell type e.g.
pleomorphic adenoma. Teratomas: are made up of a variety of
parenchmal cells that are derivatives of more than one germ
layer(usually 3). Most teratomas are found in the gonads.
Choriostoma: Ectopic rests of normal tissues. Harmatomas: Masses of
disorganized tissues inherent to a particular site e.g. pulmonary
harmatoma.
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- Pulmonary Harmatoma.
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- Pulmonary hamartoma The pulmonary hamartoma is seen
microscopically to be composed mostly of benign cartilage on the
right that is jumbled with a fibrovascular stroma and scattered
bronchial glands on the left. A hamartoma is a neoplasm in an organ
that is composed of tissue elements normally found at that site,
but growing in a haphazard mass.
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- Misnomers Melanoma Seminoma Glioma Lymphoma Hepatoma Chordoma
They are all malignant tumors despite the fact that they all have
the suffix oma
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- Identify the slide
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- Teratoma. Encapsulated tumor with tissue or organ components
resembling normal derivatives of more than one germ layer.
Teratomas have been reported to contain hair, teeth, bone and, very
rarely, more complex organs or processes such as eyes, torso, and
hands, feet, or other limbs
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- IDENTIFY THE SLIDE?
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- Malignant melanoma. This excision of skin demonstrates a
malignant melanoma, which is much larger and more irregular than a
benign nevus. From the history provided by the patient, we know
that it grew quickly in size in 3 months. In contrast, a benign
nevus hardly seems to change at all over many years.
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- Identify the slide?
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- Tumors arising from Adipocytes. LIPOSARCOMA. LIPOMA
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- Identify the slide?
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- Squamous papilloma
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- Squamous papilloma. A Squamous cell papilloma is a generally
benign papilloma that arises from the stratified squamous
epithelium of the skin, lip, oral cavity,tongue,pharynx, larynx,
esophagus, cervix, vagi na or anal canal. Squamous cell papillomas
are a result of infection with human papillomavirus(HPV). A
papilloma is a benign neoplasm composed of epithelial cells forming
finger like projections.
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- What is the pathology here?
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- Carcinoma in situ
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- Biology of tumor growth. The major differences between a benign
and a malignant tumors can be analyzed using this 4 major criteria:
-Differentiation vs. Anaplasia -Rate of growth. -Local invasion
-Metastases.
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- Differentiation vs. Anaplasia. Differentiation is the extent to
which a tumor cell resembles the original cell thus tumors call be
well, moderately or poorly differentiated. Anaplasia refers to the
lack of differentiation and it is a hallmark of malignant cells.
The following are some qualities of anaplasia: -Nuclear and
cellular pleomorphism. -Hyperchromasia. -Nuclear cytoplasmic ratio.
-Abnormal mitosis -loss of polarity.
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- Nuclear Pleomorphism. Nuclear pleomorphism: Pleomorphism refers
to variation in the size and shape of the nuclei in comparison to
their neighbors. In this example of a sarcoma, the nuclei vary
greatly in size and shape.
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- Pleomorphism
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- Rate of growth. Most malignant tumors grow more rapidly than
benign tumors. Nevertheless some cancers grow slowly over the years
and then enter a rapid growth phase.
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- Local invasion. Benign tumors: most benign tumors grows as a
cohesive mass that develop a rim of expansile but condensed
connective tissue or capsule around its periphery. Malignant tumors
: are invasive and infiltrative and they destroy normal tissue
surrounding them. They also lack a well defined capsule. Surgical
treatment of a malignant tissue requires a wide excision.
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- Metastasis. Metastasis unequivocally marks a tumor as malignant
because benign tumors do not metastasize. There are very few
exceptions to this rule, Basal cell carcinoma. Gliomas Are
malignant tumors that rarely metastasize. The major routes of
metastasis are: -Hematogeneous route -Lymphatic spread -Seeding via
the body cavities.
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- FEATURESBENIGNMALIGNANT Structure Resemblance to normal cells
(well differentiated) Growth rate Slow Mitoses Few Growth Usually
expansive Growth duration May stop growing Encapsulation Usually
Metastasis None Effect on host Slight harm, due to location or
complication Abnormal; less similarity to normal cells (anaplastic)
Rapid Relatively common Invasive Rarely stop growing Rarely
Frequent Significant harm, due to invasion & metastasis 28
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- Epidemiology A variety of factors predisposes an individual in
a population to cancer, they include: Geographic and environmental
factors. Age. Genetic predisposition. Precancerous lesions
etc.
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- Molecular basis of cancer. The literature of the molecular
basis of cancer continues to proliferate at such a rapid pace that
its easily to get lost in the growing forest of information Some
fundamental principles in the molecular basis of cancer are: Cancer
is a genetic disease: here non lethal damage acquired by somatic
cells are passed down/inherited. Tumor clonality: A tumor is formed
by clonal expansion of a single precursor cell that has incurred a
genetic damage.
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- Molecular basis of cancer. Regulatory genes: the 4 normal
regulatory genes are the target of genetic damage: -growth
promoting protooncogene. -growth inhibiting tumor suppressor genes.
-genes that regulate apoptosis. -genes that regulate DNA repair.
And finally carcinogenesis is a multistep process.
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- Tumor suppressor genes. A tumor suppressor gene, or
anti-oncogene, is a gene that protects a cell from one step on the
path to cancer. When this gene mutates to cause a loss or reduction
in its function, the cell can progress to cancer, usually in
combination with other genetic changes. Examples are: RB gene. P53.
APC/beta catenin pathway. NF1/NF2 WT1.
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- Essential Changes for Malignancy. Self sufficiency in growth
signals. Insensitivity to growth inhibitory signals. Evasion of
apoptosis. Defects in DNA repair. Continuous replicative
ability(telomerase) Sustained angiogenesis. Ability to invade and
metastasize. Ability to escape from immune recognition.
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- Carcinogens. Carcinogens are simply substances that causes
cancer. Carcinogens are either classifieds as: Biologic
carcinogens. Chemical carcinogens. Radiant energy.
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- Chemical carcinogens. Most chemical carcinogens are referred to
as procarcinogens because they require a mentabolic activation in
vivo to produce ultimate carcinogens. Only a few can act as a
direct carcinogen. DNA is the ultimate site of attack by all
procarcinogens and direct acting carcinogens. Chemical carcinogens
are mutagens that induce changes in the tumor suppressor genes,
protooncogenes and the genes that regulate apoptosis.
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- Scheme of chemical carcinogenesis.
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- Radiation carcinogenesis. Radiant energy is a form of UV rays
and ionizing radiation that causes cancer. UV rays especially from
the sun are associated with skin cancers via the following
mechanisms: 1)Damage to DNA by formation of pyridine dimers.
2)Immunosupression. Ionizing radiations ability to cause cancers is
due to the fact that it induces mutations. Miners or radioactive
ores are more susceptible to lung cancer.
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- Biologic carcinogens. A variety of DNA and RNA viruses are
known to cause cancer, they include: -Human papilloma virus.
-Epstein Barr virus. -Hepatitis B virus. -Kaposi sarcoma. -HTLV.
H.pylori is a bacteria associated with gastric cancer and
MALTomas.
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- HPV ROLE IN ONCOGENESIS. E6 binds to p53 and E7 binds to RB,
inducing the degradation of these proteins. The net effect of HPV
E6 and E7 proteins is to block apoptosis and remove the restrains
to cell proliferation
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- Clinical features of Cancers The utmost importance of neoplasm
lies on its effect on its host/patient. Indeed both malignant
tumors and benign tumors ma cause problems and they include: -Local
impingement on adjacent structures. -Hormonal synthesis and
paraneoplastic syndromes. -Bleeding and infection. -Symptoms from
rupture and infarction. -Cachexia or wasting.
- Slide 44
- Summary. Neoplasm are clonal, autonomous, while non neoplastic
tumor-like lesions e.g. hamartoma are polyclonal. Carcinogenesis is
a multistep process. Early diagnosis goes a long way in determining
the prognosis of any cancer. Therapeutic modalities of cancer
management are surgery radiotherapy and chemotherapy.
- Slide 45
- Gracias,Al final.