Neoplasia Flashcards
Types of tumors
Benign tumor – does not usually kill (name usually ends in “-oma”)
Malignant tumor – has the potential to kill (naming varies)
2 components of tumors
All tumors, benign and malignant, have two basic components
(1) Parenchyma, made up of transformed or neoplastic cells
Clonal = entire parenchyma of neoplasm arises from one genetically altered cell
(2) Stroma, host-derived, non-neoplastic supporting tissue
Scirrhous desmoplastic reaction – rock hard stroma
Cancer
a malignant neoplasm
Carcinoma
epithelial malignant neoplasm
Exception: Carcinoma in situ lacks the potential to cause metastasis
Melanoma
a melanocytic malignant neoplasm
Blastoma
tumor composed of very immature undifferentiated cells (usually malignant) resembling fetal blastemal tissue in anlage (e.g. nephroblastoma)
development of a cancer
normal cell. Initiating mutation (carcinogen induced)
Initiated precursor with stem cell-like properties
mutation affecting genomic integrity–>
Precursor with mutator phenotyp
additional driver mutations –>
Founding cancer cell
additional mutations, emergence of subclones –> genetically heterogeneous cancer
Benign vs Malignant (epithelial origin)
stratified squamous: Squamous cell papilloma vs. Squamous cell carcinoma
Basal cells- malignant is a basal cell carcinoma
Epithelial lining of glands or ducts: Adenoma / papillloma vs Adenocarcinoma
Liver cells: hepatic adenoma vs. hepatocellular carcinoma = hepatoma
Urinary tract epithelium: malignant is transitional cell carcinoma
Placental epithelium: hydatiform mole vs choriocarcinoma
testicular epithelium (germ cells) : malignant is seminoma
Tumors of melanocytes: melanocytic nevus vs. malignant melanoma
tumors, benign vs. malignant, of mesenchymal origin
Fibroma vs. Fibrosarcoma
Lipoma vs Liposarcoma
Chondroma vs. Chondrosarcoma
Osteoma vs. Osteogenic sarcoma
blood vessels: Hemangioma vs angiosarcoma
lymph vessels: lymphangioma vs. lymphangiosarcoma
mesothelium: benign fibrous tumr vs. mesothelioma
brain coverings: meningioma vs. invasive meningioma
Hematopoietic cells- malignant is leukemia
lymphoid tissue- malignant is leukemia & lymphoma
Muscle (smooth): Leiomyoma vs Leiomyosarcoma
muscle (striated): rhabdomyoma vs Rhabdomyosarcoma
gross appearance of polyps
tubular adenomy vs villous (finger-like) adenoma, e.g.
leiomyoma
is the same as the old term “uterine fibroid”
it is benign but has nothing to do with fibrous tissue
what is the key that tells you it is carcinoma/ malignant?
it’s invading
tissue loses organization
pleomophic adenoma
benign mixed tumor of salivary origin. From one germ cell layer.
Wilms tumor
nephroblastoma
derived from renal anlage
malignant
more than one neoplastic cell type
teratogenous = derived from more than one germ cell layer
Benign teratogenous tumor
mature cystic teratoma (dermoid cyst)
malignant teratogenous tumor
immature teratoma, teratocarcinoma
teratoma
A tumor arising from Totipotential Germ Cells which have the capacity to differentiate along the three germ layers:
Endoderm (ex.-gut and lung epithelium)
Ectoderm (ex.-skin, parathyroid glands epithelium)
Mesoderm (ex-fat, renal epithelial tubules)
Mature teratoma
(benign)
All tissues are mature
Dermoid cyst – mature cystic teratoma of ovary
Monodermal teratoma - contains a single tissue type (struma ovarii)
Immature teratoma
(malignant)
Elements of immature tissue (immature cartilage, immature neural tissue)
Regarded as malignant
Can be only one immature element
Malignant teratoma
Malignancy (carcinoma, sarcoma, etc.) arising within mature teratoma
Ectoderm deriatives
Epidermis & hair, skin, nails, etc.
Brain and nervous system, neuroendocrine cells, melanocytes
Mesoderm derivatives
notochord
somites–> muscle, outer covering of internal organs, excretory system, gonads
mesenchyme –> dermis, circulatory system, bones and cartilage
endoderm derivatives
embryonic gut –> inner lining of digestive tract, glands including liver and pancreas, inner lining of respiratory tract
Teratoma sites
Ovary and Testis
Midline of the body: pineal body, base of skull, mediastinum (anterior), retroperitoneal, sacroccocygeal
Immature Teratoma
Immature mesenchyme, neural and/or blastemal elements
Malignant Teratoma
Carcinoma, sarcoma and/or germ cell malignancy in teratoma
Hamartoma
A benign non-neoplastic tumor-like malformation resulting from faulty development in an organ and composed of abnormally arranged tissue elements normally present in that organ
e.g. pulmonary hamartoma
Choristoma
Congenital heterotopic (ectopic) rest of cells (tissue)
Not a neoplasm
Normal tissue in an abnormal location
Cowden Syndrome
Part of the PTEN hamartoma tumor syndrome (PTHS)
Autosomal dominant genetic disorder Multiple hamartomas (usually skin and thyroid)
Additional growths in many parts of the body
Hyperplasia
increase in number of cells/proliferation cells.
May result in the gross enlargement of an organ
+/- cytologic atypia
Metaplasia
the potentially reversible replacement of one differentiated cell type with another cell type
Dysplasia
Abnormal development or growth of tissues, organs, or cells
expansion of immature cells is often indicative of an early neoplastic process
What does eosinophilic esophagitis look like?
can show furrows (rings) in the mucosa
types of squamous epithelial dysplasia and where they occur
low grade/ mild
high grade/ moderate
high grade/ severe/ CIS
This can occur in any normal or metaplastic squamous epithelium at any body site
e.g. cervix, anus, oral cavity, skin, bronchus, etc.
characteristics of malignant neoplasia
Decreased differentiation and anaplasia
Higher rate of growth
Local invasion
Metastatic potential
Comparisons between Benign and Malignant Tumors: differentiation/ anaplasia
benign is well differentiated
malignant- some lack differentiation
Comparisons between Benign and Malignant Tumors: rate of growth
benign: usually progressive and slow;
mitotic figures rare and normal
malignant: slow to rapid; mitotic figures may be numerous and abnormal
Comparisons between Benign and Malignant Tumors: local invasion
benign: usually do not invate
malignant: locally invasive, infiltrating
Comparisons between Benign and Malignant Tumors: metastasis
benign: absent
malignant: frequent
an important exception to the comparison between benign and malignant tumors
Some malignant neoplasms are relatively bland looking resembling benign tissues
How do we determine when there is a malignancy (cancer)?
When the lesion has the potential to metastasize and cause death”
i.e. When the characteristics of the lesion are similar to those of other lesions previously noted to have metastasized and caused death!
Differentiation
Differentiation - how closely the tumor cells resemble the corresponding normal parenchymal cells
Well-differentiated – closely resembles normal
Moderately-differentiated – sort of resembles normal
Poorly-differentiated – does not resemble normal
Undifferentiated - The tissue of origin cannot be determined based on the histopathologic appearance of the neoplasm
Anaplasia
– lack of differentiation
Implies “dedifferentiation”, or loss of the structural and functional differentiation of normal cells
Cells appear more bizarre
Almost always indicative of malignancy
Anaplastic cells show
Pleomorphism - marked variation in size and shape of the cells and/or nuclei.
Abnormal nuclear morphology -hyperchromatic, large nuclei, bizarre nuclear shapes, prominent nucleoli
Increased mitotic activity, and atypical mitoses
Loss of polarity - cellular orientation is markedly disturbed from normal
Benign vs. Malignant tumors: cell size, mitotic rate, symmetry, margins, necrosis
Benign: sized 2-5x normal, normal or up to 2-3x increase mitotic rate, symmetric, circumscribed margins, necrosis is uncommon
Malignant: 2-100x normal cell size, 2-20x increase in mitotic rate with atypical mitoses, asymmetric, indistinct margins, necrosis is common
Features of Malignancy
Hyperchromaticity
Marked increase in DNA content per nucleus (more intense staining by Hematoxylin (H of H&E)
Desmoplasia
Increased fibrous tissue surrounding invading parenchymal cells
Angiogenesis
Increased blood vessels
Ischemic tumor necrosis occurs with insufficient angiogenesis
Neo-angiogenesis
Vessels sprout from existing capillaries
Vasculogenesis
Endothelial cells are recruited from the bone marrow
carcinomas and capusles/ invasion
Carcinomas have no capsules or invasion of parenchyma through the tumor capsule
Grading Neoplasms
Histologic grade - essentially differentiation (anaplasia)
Nuclear grade – essentially pleomorphism (bizarreness)
Alterations in Malignant Transformation
Self-sufficiency in growth signals
Oncogene activation with oncoprotein production (gain of function)
Insensitivity to growth-inhibitory signals
Evasion of apoptosis
- p53 and other tumor suppressor gene inactivation (loss of function)
Activation of anti-apoptotic genes (gain of function)
Inactivation of apoptotic genes (loss of function)
Limitless replicative potential
Sustained angiogenesis
Ability to invade and metastasize
Defects in DNA repair
- May fail to repair DNA damage (loss of function)
Alterations in cell metabolism (e.g. Warburg effect)
Ability to evade host immune response
EGF-receptor family
ERBB1 (EGFR) and ERRB2(HER)
Adenocarcinoma of lung
Breast carcinoma
receptor for neurotrophic factors: RET
Multiple endocrine neoplasia 2A and B
KIT
GI stromal tumors
ALK
Adenocarcinoma of the lung
KRAS
Colon, lung, and pancreatic tumors
NRAS
Melanomas, hematologic malignancies
GNAS
Pituitary adenoma, other endocrine tumors
ABL
Chronic myeloid leukemia
Acute lymphoblastic leukemia
BRAF
Melanomas
JAK2`
Myeloproliferative disorders
C-MYC
Burkitt lymphoma
N-MYC
Neuroblastoma
L-MYC
Small-cell carcinoma of the lung
CCND1 (Cyclin D)
Mantle cell lymphoma
PAX Genes acting as proto-oncogenes
PAX 3 and PAX 7- embryonal rhabdomyosarcoma
PAX 5- b-cell leukemias/ lymphomas
PAX 8 - renal, thyroid and ovarian carcinomas
Chronic myelogenous leukemia genes
(9;22)(q34;q11)/BCR-ABL
Affected genes:
ABL 9q34
BCR 22q11
Burkitt lymphoma genes
translocation: (8;14)(q24;q32)
Affected gnese: c-MYC 8q24
IGH 14q32
Ewing arcoma genes
translocation: (11;22)(q24;q12)
affectd genes: FL1 11q24
EWSR1 22q12
Mutations: CDK4; D cyclins
Form a complex that phosphorylates RB, allowing the cell to progress through the G1 restriction point
Mutations: INK4/ARF family (CDKN2A-C)
(cell cycle inhibitor)
p16/INK4a binds to cyclin D-CDK4 and promotes the inhibitory effects of RB
p14/ARF increases p53 levels by inhibiting MDM2 activity
Mutations: RB
Tumor suppressive “pocket” protein that binds E2F transcription factors in its hypophosphorylated state, preventing G1/S transition; also interacts with several transcription factors that regulate differentiation
Mutations: p53
Tumor suppressor altered in the majority of cancers; causes cell cycle arrest and apoptosis. p53 is required for the G1/S checkpoint and is a main component of the G2/M checkpoint.
NF1 gene
Neurofibromatosis type 1
NF2
Neurofibromatosis type 2
PTCH
Gorlin syndrome (familial)
basal cell carcinoma (sporadic cancer)
PTEN
Cowden syndrome
RB
Retinoblastoma; osteosarcoma
VHL
Von Hippel Lindau syndrome
sporadic cancer: renal cell carcinoma
E-cadherin
protein
Gastric carcinoma, lobular breast carcinoma
TP53 gene
protein: p53
Li-Fraumeni syndrome (diverse cancers)
BRCA1, BRCA2
Familial breast and ovarian carcinoma
WT1
Wilms tumor
MEN1
Multiple endocrin neoplasia-1
sporadic cancers: pituitary, parathyroid, and pancreatic endocrine tumors
Rate of growth
Rate of tumor growth - determined by three main factors
Doubling time of tumor cells
Fraction of tumor cells in the replicative pool
Rate at which cells are shed/die
doubling of neoplastic cells and clinical detection
30 doublings –> 1 gm. 10 to the 9th cells, which is the smallest clinically detectable mass.
Mechanisms by which tumors evade the immune system
T cell recognition of tumor antigen leading to T cell activation
Lack of T cell recognition of tumor
Lack of T cell recognition of tumor
Inhibition of T cell activation
Warburg Effect
metabolic alterations
Also known as aerobic glycolysis
Tumor cells shift their glucose metabolism away from the oxygen hungry mitochondria to aerobic glycolysis leading to lactose (fermentation)
Mode of glycolysis allows visualization of tumors via positron emission tomography (PET)
Differences Between Oxidative Phosphorylation, Anaerobic Glycolysis, and Aerobic Glycolysis
Oxidative phosphorylation-
Produce CO2 and 36 mol ATP/1 mol glucose
Anaerobic glycolysis-
Produce lactate and 2 mol ATP/1 mol glucose
Aerobic glycolysis -
Warburg observed that cancer cells tend to convert most glucose to lactate regardless of whether oxygen is present (aerobic glycolysis/fermentation via the glycolytic pathway)
95% of glucose used to produce metabolic intermediates used in synthesis of cellular components & 4 mol ATP/1 mol glucose
what unequivocally marks a tumor as malignant?
Metastasis unequivocally marks a tumor as malignant because “benign tumors do not metastasize”
However benign conditions can “spread”
Local invasion is a less reliable indicator of malignancy
local invasion by malignant tumors
Infiltrate, invade, destroy adjacent tissue
Metastasize to other parts of body
Not (or incompletely) encapsulated
Metastasis
Tumor implants discontinuous with the primary tumor
Patterns of metastasis:
- Direct seeding of body cavities or surfaces
Lymphatic spread
- Transport through the lymphatics to lymph nodes
Sentinel Lymph Nodes
Hematogenous spread
- Portal blood supply drains to the liver
- Caval blood travels to the lung
- Hepatic, renal, and adrenocortical cancer propagate in veins
Mechanisms of metastasis development within a primary tumor.
A, Metastasis is caused by rare variant clones that develop in the primary tumor.
B, Metastasis is caused by the gene expression pattern of most cells of the primary tumor, referred to as a metastatic signature.
C, A combination of A and B, in which metastatic variants appear in a tumor with a metastatic gene signature.
D, Metastasis development is greatly influenced by the tumor stroma
The metastatic cascade
Changes (“loosening up”) of tumor cell-cell interactions
Degradation of ECM
Attachment to ECM components
Migration (locomotion ) of tumor cells
Clumping in vessels
Adhesion to the endothelium
Egress through the vascular basement membrane
Batson (Paravertebral) Veins /Plexus
Venous connections that extend from pelvis to the skull along the vertebral column
Important in dissemination of some metastatic cancers throughout the spine
Classic for prostatic cancer, but similar for renal, breast, rectal and bladder cancers
Sentinal lymph nodes
Inject vital dye and/or radioactive tracer into tumor or biopsy cavity and follow flow to lymphatics to the sentinel node(s)
Originally developed for skin melanomas
Now used for lots of cancers, especially breast cancer
Cancer Cachexia
Marasmus-like protein-energy malnutrition
Paraneoplastic Syndromes
Symptom complexes that cannot readily be explained by
Local or distant spread of the tumor or
By the elaboration of hormones indigenous to the tissue from which the tumor arose
Symptoms from
Products produced by the tumor cells (e.g. hormones) or
Immune reaction of the body to the tumor cells (e.g. myasthenia gravis with neoplasms of the thymus)
Occurs in ~10% of persons with malignant disease
cancer related to cushing syndrome
small cell carcinoma of the lung
ACTH is the causal mechanism
cancer related to syndrome of inappropriate antidiuretic hormone secretion (SIADH)
small cell carcinoma of lung
causal mechanism: Antidiuretic hormone
cancer related to hypercalcemia
squamous cell carcinoma of lung
causal mechanism: parathyroid hormone-related protein (PTHRP), TGF-alpha, TNF, IL-1
cancer related to polycythemia
gastric carcinoma
renal carcinoma
causal mechanism: erythropoietin
causal mechanism of carcinoid syndrome
causal mechanism: serotonin, bradykinin
Carcinoid syndrome
Heart:
- pulmonic and tricuspid valve thickening and stenosis
- endocardial fibrosis
Liver: hepatomegaly
GI: diarrhea, cramps, nausea, vomiting
Skin: cutaneous flushes, apparent cyanosis
Respiratory: cough, wheezing, dyspnea
Retroperitoneal and pelvic fibrosis
Paraneoplastic syndrome: myasthenia
from tymic neoplasms
Paraneoplastic syndrome: acanthosis nigricans
from Gastric carcinoma
Lung carcinoma
Uterine carcinoma
causal mechanism: immunological; secretion of epidermal growth factor
paraneoplastic syndrome: dermatomyositis
bronchogenic or from breast carcinoma
causal mechanism: immunological
paraneoplastic syndrome: venous thrombosis (Trousseau phenomenon)
from pancreatic carcinoma
causal mechanism: tumor products (mucins that activate clotting)
paraneoplastic syndrome: disseminated intravascular coagulation
from acute promyelocytic leukemia and prostatic carcinoma
causal mechanism: tumor products that activate clotting
paraneoplastic syndrome: nonbacterial thrombotic endocarditis
from advanced cancers
causal mechanism: hypercoagulability
Incidence
probability of being diagnosed with a disease during a given period of time
Number of new cases of a disease divided by the number of persons at risk
Usually expressed as new cases/year per 100,000 population
Morbidity
= illness
Indicated by prevalence
Prevalence
the total number of cases of disease existing in a population
Total number of cases of a disease existing divided by the total population
Usually expressed as total cases per 100,000 persons
mortality
= death
mortality rate
number of deaths divided by the total population
Indicated by deaths per year per 100,000 people
cancer and age
Carcinomas tend to occur in the later years of life (>55 years)
Main cause of death ♀40 to 79 and ♂ 60 to 79
~10% of all deaths in children ˂ 15
Common childhood cancers are significantly different from adults
Acute leukemia and primitive neoplasms of the central nervous system are responsible for approximately 60% of childhood cancer deaths
The common neoplasms of infancy and childhood are “small round blue cell tumors”
Neuroblastoma
Wilms tumor (nephroblastoma)
Retinoblastoma
Acute leukemias/lymphomas
cancer and chimney sweeps
In 1775 London surgeon Sir Percival Pott attributed scrotal skin cancer in chimney sweeps to chronic exposure to soot
note: NOT testicular cancer
The change in incidence of various cancers with migration from Japan to the United States
provides evidence that the occurrence of cancers is related to components of the environment that differ in the two countries.
alkylating carcinogens include
anticancer drugs. Cause many cancers, especially leukemias
Procarcinogens that require metabolic activation
polycyclic and heterocyclic aromatic hydrocarbons
aromatic amines, amides, azo dyes
natural plant and microbial products:
** Aflotoxin B1 (Liver cancer via p53 inactivation)
** Betel nuts (oral cancer)
Occupational cancers from arsenic and arsenic compounds
skin carcinoma, (lung)
occupational cancers from asbestos
Lung, esophageal, gastric, and colon carcinoma; mesothelioma
from construction, brake linings, floor tiles
occupational cancers from benzene
acute myeloid leukemia
occupational cancers can also come from…
beryllium and beryllium compounds
cadmium and cadmium compounds
chromium compounds
nickel compounds
cancer related to radon and its decay products
lung carcinoma
from decay of minerals containing uranium, hazard in quarries and underground mines
cancer from vinyl chloride
hepatic angiosarcoma
from monomer for vinyl polymers (PVC industry)
note– it’s not from PVC itself
Radiation carcinogenesis
Ultraviolet Rays–>
Nonmelanoma (squamous cell/ basal cell) skin cancers (total cumulative exposure)
Melanomas (sunbathing)
Ionizing radiation (Electromagnetic or particulate)
Oncogenic RNA viruses
HTLV-1–> adult T-cell leukemia/ llymphoma
HCV–> hepatocellular carcinoma
Oncgenic DNA viruses
HBV–> hepatocellular carcinoma
HPV –> carcinomas of cervix, anus, penis & oropharynx (types 16 & 18); papillomas
HHV-8–> Kaposi sarcoma & primary effusion lymphoma
EBV–> Burkitt lymphoma, Hodgkin lymphoma& nasophryngeal carcinoma
oncogenic fungi
aspergillus- aflotoxin B1–> hepatocellular carcinoma (p53 mutation)
oncogenic parasites
schistosoma haematobium–> bladder cancer
oncogenic bacteria
H. pylori–> extranodal marginal zone (MALT) lymphoma and gastric adenocarcinoma
Genetic Predisposition To Cancer
Large # of cancer types have combined environmental influences and hereditary predispositions
2 hit theory
Hit 1 in first mutated gene (abnormal) is inherited
Hit 2 in second mutated gene (originally normal) is acquired
Genes associated with hereditary cancers are generally also involved in the much more common sporadic forms of the same tumor
Defective DNA Repair- autosomal recessive
xeroderma pigmentosa
ataxia telangiectasia
bloom syndrome
fanconi anemia
Xeroderma pigmentosa
Nucleotide excision repair abnormality associated with extreme sensitivity to ultraviolet (UV) rays affects the eyes and skin (cancers), may also have CNS problems (increased pyrimidine dimers)
Ataxia telangiectasia
ATM gene defect (involved in DNA repair) associated with progressive difficulty with coordinating movements, weakened immune system, leukemias and lymphomas
Bloom syndrome
Helicase abnormality associated with short stature, sun-sensitive skin changes, an increased risk of cancer, and other health problems
Fanconi anemia
FA process defects associated with aplastic anemia, hypopigmentation, café-au-lait spots, skeletal problems, defects of the genitourinary tract; gastrointestinal tract; heart; eye and ears with hearing loss and acute myeloid leukemia
Hereditary nonpolyposis colorectal cancer (HNPCC) = Lynch syndrome
autosomal DOMINANT
DNA mismatch repair abnormality leading to microsatellite instability associated with colorectal, endometrial, gastric, ovarian, ureteral, CNS, small bowel, hepatobiliary tract and skin cancers
inherited cancer syndromes
Usually a point mutation in a single allele of a tumor supressor gene
The second event incite tumorigenesis involve a second mutation in the other remaining previously normal allele
nonhereditary predisposing conditions
chronic inflammation
Precancerous conditions: repair leads to cellular dysplasia
- leukoplakia (oral cavity, vulva, penis)
- adenomatous polyps
- solar keratosis
asbestosis –>
meothelioma, lung carcinoma
inflammatory bowel disease –>
colorectal carcinoma
lichen sclerosus et atrophicus –>
vulvar squamous cell carcinoma
chronic pancreatitis –>
pancreatic carcinoma
can be related to alcoholism
chronic or recurrent bronchitis –>
lung carcinoma,
agents: asbestos, smoking
reflux eophagitis, barrett esophagus –>
esophageal carcinoma
agent: gastric acids
Sjogren syndrome, hashimoto thyroiditis, H. pylori gastritis –>
MALT lymphoma
agent associated with cholangiocarcinoma
liver flukes (Opisthorchis viverrini)
gastritis/ ulcers –>
gastric adenocarcinoma, MALT
agent: h. pylori
hepatitis –>
hepatocellular carcinoma
agent: hep B and/ or C virus
osteomyelitis –>
carcinoma in drainingn sinuses
agent involved in cervical carcinoma
HPV
agent involved in bladder carcinoma
schistosoma haematobium
grading and staging of tumors
Grading of a cancer is based on the degree of differentiation of the tumor cells and, in some cancers, the number of mitoses or architectural features
Staging of cancers is based on the size of the primary lesion, its extent of spread to regional lymph nodes, and the presence or absence of blood-borne metastases
The major staging system currently in use is the American Joint Committee on Cancer Staging.
T for primary tumor
N for regional lymph node involvement
M for metastases
most important prognostic indicator
stage
skin lethality
melanoma more likely to be lethal
basal cell carcinoma less likely to be lethal
thyroid lethality
undifferentiated carcinoma of the thyroid more likely to be lethal
papillary carcinoma of the thyroid less likely to be lethal
breast lethality
infiltrating ductal carcinoma of the bresat more likely to be lethal
tubular carcinoma of the breast less likely to be lethal
leukemia lethality
acute leukemia more likely to be lethal
chronic lymphocytic leukemia less likely to be lethal
bladder cancer lethality
grade III papillary transitional cell carcinoma of the bladder more likely to be lethal
grade 1 less likely
lung lethality
small cell carcinoma of the lung more likely to be lethal
carcinoid tumor of the lung less likely to be lethal
fibrosarcoma lethality
retroperitoneal fibrosarcoma more likely to be lethal
subcutaneous fibrosarcoma less likely to be lethal
clinical endometrial cancer staging
stage 2- the cancer has grown into the cervix stage 3a- spread to ovary 3b- has spread into the vagina 3c- spread into the lymph nodes stage 4a- in bladder or bowel 4b- in other organs
cytology sampling
Exfoliative-the microscopic examination of desquamated cells for diagnostic purposes. The cells are obtained from lesions, sputum, secretions, urine, and other material by aspiration, scraping, a smear, or washings of the tissue
Aspiration biopsy cytology (ABC)-the microscopic study of cells obtained from superficial or internal lesions by suction through a fine needle.
