Bisc 3150 General Pathology: Neoplasia Wednesday, January 31, 2018 Friday, February 2, 2018 Judy Maloney, PHD
Bisc 3150 General Pathology: Neoplasia Wednesday, January 31, 2018 Friday, February 2, 2018 Judy Maloney, PHD
Bisc 3150 General Pathology: Neoplasia Wednesday, January 31, 2018 Friday, February 2, 2018 Judy Maloney, PHD
General Pathology
Neoplasia
Wednesday, January 31, 2018
Friday, February 2, 2018
Cause Reversible?
Hypertrophy
or hyperplasia
Neoplasia
There are a couple of approaches to ‘curing
cancer’. One is to target the support tissue
of a tumor. This might involve:
Develops specialized
structures (differentiate)
Malignant tumors
Well
Anaplastic
differentiated
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL069.html
With malignant neoplasms, the cells also
show atypical cytology
Cytology Name
Cell size and Varies Pleomorphism
shape
Nuclear size Varies, many Nuclear
and shape large pleomorphism
Nuclear to Increased
cytoplasmic
ratio
Color or Intensely Hyperchromatic
intensity of staining or dark nuclei (high
nucleus DNA content)
Identify some features of malignant cells
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL044.html
Dot in the nucleus = nucleolus
A normal
tissue
Metaphase Anaphase
Mitosis at a Glance; J Oral Maxillofac Pathol. 2014 Sep; 18(Suppl 1): S2–S5.
Common features of malignant cells
Cytology Name
Number of Increased
mitotic (rapidly
figures dividing)
Shape of Can be irregular Atypical mitosis
mitotic and bizarre
figures
Nucleolus Very prominent
Examples of abnormal mitotic figures
Tripolar Tetrapolar or
formation Quadripolar
formation
Mitosis at a Glance; J Oral Maxillofac Pathol. 2014 Sep; 18(Suppl 1): S2–S5.
Anaplastic neoplasm
Can you identify the abnormal mitosis?
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL044.html
Anaplastic neoplasm
Can you identify the very prominent nucleoli?
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL041.html
Is this A) benign or B) malignant?
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL043.html
Colon
Epithelial layer
Connective
tissue Cut
mucus
Lumen
Columnar cells
Benign neoplasm of the colon. Is it well-
differentiated or poorly differentiated?
Normal Benign neoplasm Not as
‘clear
looking’
by the
lumen
Cells are
columnar with
orderly
arrangement
Malignant neoplasms of the colon. Which is well-
differentiated, poorly differentiated, anaplastic?
Identify the types of tumors
Normal adipose
tissue
Adipocyte
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL013.html
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL053.html
Identify the types of tumors
Normal smooth
muscle
Capsule
Homogeneous
cut surface
https://library.med.utah.edu/WebPath/ENDOHTML/ENDO024.html
What is characteristic about this tumor?
Malignant tumor
(thyroid carcinoma)
No capsule
There is progressive
infiltration, invasion
and destruction of
surrounding tissue
Primary
tumor
Metastases
Tumor cell breaks off and spreads to a
different part of the body that is not directly
connected with it
Identify the benign and malignant liver tumors?
http://library.med.utah.edu/WebPath
Are these lung tumors benign or malignant?
Lymph Tan area
node
Tan
area
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL028.html
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL029.html
Ways cancer can spread
Lymphatics
Blood
Spread of cancer – seeding into a body cavity
Mesentery
Many small,
tan tumor
nodules
A. Breast
B. Colon
C. Esophagus
D. Kidneys
E. Lungs
http://library.med.utah.edu/WebPath/LIVEHTML/LIVER059.html
Carcinogenesis: the
molecular basis of cancer
or
Cancer Genes
Principal targets of genetic damage in
most neoplasms
1. Proto-oncogenes (mutated oncogenes)
2. Tumor suppressor genes
3. Genes that regulate apoptosis
4. Genes that regulate interactions between
tumor cells and host cells
Alteration in more
than one gene
Unregulated cell growth and
differentiation
Transcription factor
(e.g. MYC)
Uncontrolled growth or
progression through the cell cycle
Tumor suppressor genes that sense genomic damage
e.g. Tumor promoter p53 or TP53
Normal cell
Carcinogenic agent
DNA damage
(e.g. toxic chemicals,
p53
radiation, or UV light)
Decides if the
cell will either:
Progression
Tumor Progession
Henrietta Lacks
died in 1951 of
cervical cancer
HeLa cells
How can cancer cells get the nutrients and
oxygen (i.e. blood supply) they need for survival?
Growth of
Angiogenic new blood
factor vessels
(e.g. VEGF) into the
Tumor tumor
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL069.html
Staging of Malignant Neoplasms
Stage Definition
Tis In situ, non-invasive (confined to epithelium)
T1 Small, minimally invasive within primary organ site
T2 Larger, more invasive within the primary organ site
Larger and/or invasive beyond margins of primary organ
T3
site
Very large and/or very invasive, spread to adjacent
T4
organs
N0 No lymph node involvement
N1 Nearby lymph node involvement
N2 Regional lymph node involvement
N3 More distant lymph node involvement
M0 No distant metastases
M1 Distant metastases present
http://library.med.utah.edu/WebPath/NEOHTML/NEOPL069.html
What is the advantage of having a
staging and grading schema for
malignant neoplasms?