Transcript NEOPLASIA

NEOPLASIA
DR.ROOPA
Pathophysiology
Premed 3
Neoplasia
Means new growth.
 Is the uncontrolled, disorderly proliferation
of cells, resulting in a benign or malignant
tumor or neoplasm.
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A neoplasm , as defined by Willis , is
 “an abnormal mass of tissue the growth of
which exceeds and is uncordinated with
that of the normal tissues and persists in
the same manner after the cessation of
the stimuli which evoked the change”.
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Dysplasia- is a reversible change.
 Often precedes malignancy.
 Morphologically manifests by disorderly
maturation and spatial arrangement of
cells, marked variability in nuclear size and
shape and increased, often abnormal ,
mitosis .
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nomenclature
A neoplasm is often referred to as a tumor,
and the study of tumors is called oncology.
 Oncos – tumor, logos –study of
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Types
 Benign tumor
 Malignant tumor( cancer)
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Benign tumors: In
general , benign
tumors are
designated by
attaching the suffix –
oma to the cell type
from which the tumor
arises.
Eg.fibrous tissue
tumor is a fibroma.
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Malignant tumors:
Mesenchymal tissue
or its derivatives are
called sarcomas.
Eg fibrosarcoma
Epithelial tissue
origuin are called
carcinoma.
Eg:adenocarcinoma
Malignant
(+) invasion: spread
to nearby structures
 (+)metastasis: spread
to distant structures
 (+)anaplasia :
cells are very different
from the normal cells
(poorly differentiated)
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vs
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Benign
(-) invasion
(+) capsule
(-)metastasis
Resemble the tissue
of origin (well
differentiated)
Tumor characteristics
Differentiation and anaplasia
 Rate of growth
 Local invasion
 metastasis
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Anaplasia
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A state of complete un differentiation
Anaplastic cells show:
Pleomorphism
Hyperchromatism (dark nuclei)
Increased nuclear-cytoplasm ratio
Abnormal mitosis
Prominent nucleoli
Basic underlying cause of
cancer
4 kinds of genes are damaged:
 Genes that promote growth
 Genes that inhibit growth
 Genes that regulate apoptosis
 Genes involved in DNA repair
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Cancers develop in multiple steps.
“cancer genes “cause bad
things in cells
Autonomous growth
 Insensitivity to growth – inhibitory signals
 Evasion of apoptosis
 Limitless replication
 Sustained angiogenesis
 Invasion and metastasis
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Forms of Malignant tumors
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Carcinoma: malignant tumor of epithelial origin
1. squamous cell carcinoma
cancer of the skin
cancer of the esophagus
2. adenocarcinoma: glands
cancer of the breast
cancer of the pancreas
3. transitional cell carcinoma
cancer of the bladder
Forms of Malignant tumors
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Sarcoma: of mesenchymal origin
osteosarcoma
rhabdomyosarcoma
leiomyosarcoma
liposarcoma
Teratoma: from all 3 germ layers
skin, bone, cartilage, teeth,
ovaries and testis: most common
may also be benign
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teratomas consist of bits of
bone,INTESTINAL epithelium, muscle, fat,
nerve, tooth, etc.
Osteosarcoma
Liposarcoma
Teratoma
Forms of Benign tumors
Papilloma: Adenoma: glandular epithelium
-ovary, breast
 Mesenchymal origin
-leiomyoma, lipoma, fibroma, chondroma
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Papilloma
epithelium of skin, larynx and tongue; fingerlike
projections
Properties of Neoplasms
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Monoclonality
the neoplasm comes from a single
precursor cell
Invasion
enters the blood vessels and
lymphatics
Metastases
blood vessels: sarcomas
lymphatic: carcinoma
Properties of Neoplasms
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Common sites of metastases
liver, lung, brain,
adrenal glands, lymph nodes
bone marrow
Clinical signs of malignancy
Cachexia
wasting, weakness, weight loss, anemia, infection
.- Endocrine abnormalities
prolactinoma
ovarian tumors
 Paraneoplastic syndrome is a disease or symptom that
is the consequence of the presence of cancer in the
body, but is not due to the local presence of cancer
cells.they commomnly presented with cancers of the
lung, breast, ovaries or lymphatic system.
eg:ectopic production of hormones
lung cancer : ACTH
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summary :Risk factors
Chemical agents
 Physical agents
 Viruses
 Activation of cancer-promoting genes
 Inhibition of cancer-suppressing genes
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Carcinogenesis and carcinogens
Cigarette smoking : lung CA, laryngeal CA
 Excessive sun: Skin CA
 Asbestos: Mesothelioma
 Nitrosamines: Gastric CA
 Alcohol: Esophageal CA
 Low-fiber diet: Colon CA
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Carcinogenesis and carcinogens
High-fat diet: Breast CA
 Aniline dyes: bladder Ca
 Aflatoxin: liver CA
 PVC: Angiosarcoma of the liver
 DES: Clear cell adenocarcinoma of the
vagina
 Nickle, chromium, uranium: lung CA
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Carcinogenesis and carcinogens
HTLV – 1: Adult T cell leukemia
 HPV: cervical CA
 EBV: Nasopharyngeal CA, Burkitts
lymphoma
 HBV: Hepatocellular CA
 HHV-8: Kaposi sarcoma
 Helicobacter pylori: Gastric CA
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Cancer suppresor genes
(anti oncogene)
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p53: “ guardian of the genome” ,gatekeeper gene
mutated in 50% of all malignant tumors
causes cell cycle arrest in G1, time for DNA repair
unsuccessful repair: apoptosis
LI-FRAUMENI SYNDROME
familial cancers of the breast, soft tissue sarcomas,
brain tumors, leukemias
Cancer suppresor genes
(anti oncogene)
WT-1 and WT-2: Wilms tumor( Wilms
tumour of the kidney)
 BRCA -1: breast and ovarian CA
 *BRCA – 2: breast CA
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RB codes for pRB protein, master brake on cell cycle
(retinoblastoma, bone, bladder, lung, and breast cancer)
Grading: degree of differentiation of the
cells
 Staging: spread of the tumor or degree of
localisation
-uses the TNM system
Tumor size
Lymphonode involvement
Metastasis
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CANCER TREATMENT
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CHEMOTHERAPY
CYTOTOXIC DRUGS+BODY DEFENSES
SINGLE AGENT
COMBINATION CHEMOTHERAPY
_AVOIDS SINGLE AGENT RESISTANCE
CAN USE LOWER DOSE
BETTER REMISSION AND CURE RATE
RADIATION
TARGETS DNA
KILL TUMOR WITHOUT DAMAGE TO SURROUNDING
TISSUES
TUMOR MUST BE ACCESSIBLE
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SURGERY
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METHOD OF CHOICE,CAN REMOVE ENTIRE
TUMOR,DEBULKING
ADJUVANT CHEMOTHERAPY OR RADIATION
IMMUNOTHERAPY
.ELIMINATES CANCER CELLS ONLY
.PROVIDES PROTECTION AGAINST RECURRENCE
.T_CELL BASED OR ANTIBODY RESPONSES
.CONJUGATED ANTIBODIES
.NONSPECIFIC ENHANCEMENT OF THE IMMUNE
SYSTEM
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