Cellular Biology

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Cellular Biology
School of Life Sciences Shaanxi Normal University
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CHAPTER 12 TUMOR CELLS AND GENE THERAPY OF TUMORS
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Tumor (neoplasm) is the disease involved
gene mutation, but it can not be inherited. Tumor
is the abnormal proliferation and differentiation
of cells when the tumor inducer factors induced
genes mutated and lost the normal regulation to
cell growth.
Grow slowly
Benign tumors Obvious border with normal
tissue Tumors
No metastasis
Grow
fast Malignant tumors
(cancers) No border with normal tissue

Metastasis Cancer
(carcinoma) is the one of major killers to
people. It is second people killer in US (First
one is cardiovascular diseases) and first in
China. Almost every organ or tissue can be
developed as cancer, but most popular cancer easy
developed organs include lungs, stomach,
colon-rectal, liver, breasts, blood cells, and
others.
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Parenchymal part Tumor
cells. Tissue specificity. Tumor
Is composed of connective
tissues, vessels, Interstitial
Part and lymphatic vessels. Support tumor
with
nutrition. No tissue specificity.
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I. The major features of cancer cells
Generally, cancer cells keep three basic
characters as following 1. unlimited life 2.
metastasis 3. no contact inhibition. The
characters of morphology 1. Usually,
cancer cell is larger than the normal cells of
same tissue with size heterogeneity. The ratio of
nucleus/plasma is significantly raised to 11.
2. Morphology of nuclei are heterogeneity
with macronuclei, binuclei, and multinuclei. The
chromosomes are aneuploidy with some absence or
addition. If the described as above happened in
normal cell, the cell will turn to apoptosis. But
in cancer cells, no apoptosis happened because of
apoptotic signals inhibited. 3.
Mitochondria present polymorphosis, swelled,
regenerated. For example, macromitochondria in
liver cancer cells. 4. Cell skeleton is
changed and the tumor associated antigen is
appeared. The characters of physiology
1. Cell cycle gets out of control. 2.
Metastasis. Cell adhesion and linkage associated
molecules, such as ECM and CAM, are mutated or
absented, and relative signal pathways are
blocked, so, cancer cells are easy to move off
from tumor tissue. Most of cancer cells secret
some enzymes to enhance migration and metastasis.
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3. Loss of contact inhibition. 4.
Loss of anchorage dependence. Anchorage
dependence means that cells must attach to some
special ECM to grow and inhibit apoptosis. Tumor
cell can grow up on agar, methyl cellulose, and
others. 5. Dedifferentiation. More than 20
embryonic isozymic proteins are expressed in
cancer cells. For example, a- fetoprotein (AFP)
can be detected in the blood of liver cancer
patients. 6. The dependence on GF is
decreased. The selfcrine way and proliferation
signal way are not depended on GF. Cancer tissue
can secrets VEGF (Vascular endothelial growth
factor) to enhance tumor growth. 7.
Active metabolism. The activity of DNA and RNA
polymerases in cancer cells is higher than in
normal cells, and the nucleotide degeneration is
inhibited. 8. The synthesis of protein is
significantly enhanced and the degeneration of
protein is inhibited in cancer cells. This
feature results in cachexia for patients.
9. Disorders of mitochondrion functions. Tumor
energy supply is mainly depended on glycolysis.
10. Transplantability. Cancer cells can be
transplanted into other individuals or animals
without immunological rejection. So, cancer cells
can be transplanted into mice to form the
transplanted cancer models.
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Metastasis
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Loss of contact inhibition
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Migration in cultured Caco-2
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II. Oncogenesis Oncogenesis includes
mutation, latency, carcinogenesis, and
development. Initiation mutation will not form
tumor without a suitable environment, this stage
is called as latency. Carcinogenesis means that
the mutated cell will start proliferation with
carcinogenic factors, such as GF. Carcinogenesis
is reversible if the carcinogenic factors are
stopped. Development means that the tumor is
becoming powerful to invade and metastasis.
Development is irreversible. Oncogenesis is based
on the mutation of many genes during a long
time. The inner causes of oncogenesis
The oncogenesis of malignant tumor is involved
with the mutant accumulation of many genes
including proto-oncogenes and cancer suppressor
genes. Proto-oncogenes Proto-oncogenes
are the genes that are important to maintain the
cell proliferation. But, mutated proto-oncogenes
can cause oncogenesis.
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The products of proto-oncogenes include ?
GF ? GF receptors, such as fms, erbB ? Protein
kinases and other signal transduction molecules,
such as Src, Ras, and Raf ? Cyclin, such as
bcl-1 ? Regulator of apoptosis, such as bcl-2 ?
Transcription factors, such as myc, fos, jun.
Oncoviruses contain many proto-oncogenes in
their genomes. Especially, reverse transcription
viruses can recombine their proto-oncogene
sequences into host genomes. Most of human
proto-oncogenes were from oncoviruses probably.
We call the proto-oncogenes that exist in
normal cells as c-onc, in viruses as v-onc. The
sequence of c-onc contains introns, and v-onc
contains no intron. The detail about
oncoviruses and proto-oncogenes will be presented
in your Virology later.
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The products of proto-oncogenes
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Functions of proto-oncogenes
Proto-oncogenes Function Tumors
sis GF Omental tumor
erb-B Receptor tyrosine kinase, EGF receptor Cancers of breasts, ovary, lungs, stomach
fms Receptor tyrosine kinase, CSF-1 receptor Leukemia
ras G-protein Cancers of lungs, colon, rectum
src Non receptor tyrosine kinase Rous sarcoma
Abl-1 Non receptor tyrosine kinase Leukemia
raf MAPKKK Carcinoma of parotid gland
vav Signaling linking protein Leukemia
myc Transcription factor Lymphoma, Lung cancer
myb Transcription factor Colo-rectal cancer
fos Transcription factor Bone sarcoma
jun Transcription factor  
erb-A Transcription factor Leukemia
bcl-1 Cyclin D1 B lymphoma
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Cancer suppressor genes Cancer suppressor
gene is also called anti-cancer gene. They are
contained in normal chromosomes probably. The
loss or mutation of cancer suppressor genes can
activate proto-oncogenes and cause oncogenesis.
The products of cancer suppressor genes can
inhibit tumor cell proliferation and metastasis,
and promote differentiation. The products
of cancer suppressor genes include ? Regulators
of transcription, such as Rb, p53 ? Down
regulator of transcription, such as WT ? Cyclin
depend kinase inhibitor (CDKI), such as p15, p16,
p21 ? Inhibitors of signal pathways, such as
NF-1, PTEN. ? DNA repairing factors, such as
BRCA1, and BRCA2 ? The molecules of signal
pathways associated with development and stem
cell proliferation, such as APC and Axin.
The ways of inactivation of cancer suppressor
genes ? If both anelle genes of cancer
suppressor gene are mutated or inactivated, the
cancer suppressor gene is inactivated ? The
dominant negative of cancer suppressor genes. The
mutated copy of cancer suppressor gene can
inactivate the wild type copy of cancer
suppressor gene. This inactivation is called as
dominant negative. ? Haplo-insufficiency theory.
The single copy of some cancer suppressor genes
can not be expressed enough to maintain normal
cell cycle. For example, the loss of one copy of
DCC gene can cause cell contact inhibition
inhibited to form a malignant cell clone.
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Retinoblastoma gene (Rb gene) is the
first cloned cancer suppressor gene. The mutation
of Rb gene causes retinoblastoma. Sporadic Rb is
happened in single eye usually. Genetic Rb is
developed in dual eyes at about three years old.
APC gene (adenomatous polyposis coli)
was named with the tissue name where it was
firstly identified. APC gene is located on
chromosome 5q21-22. APC protein can bind to
ß-catenin to enhance ß-catenin degeneration. The
accumulated ß-catenin can bind to T cell factor
(TCF) to promote relative gene expressions.
The peptide sequence of DCC gene (deleted in
colorectal carcinoma) is very similar to nerve
cell adhesion molecule (N-CAM). Inactivation of
DCC causes the changes of cell adhesion, contract
inhibition, and mobility, that pushes cell turn
to malignant growth and metastasis. The loss rate
of DCC in stomach cancer patients is about
4060.

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The mechanisms of sporadic and genetic function
loss of Rb
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The fuction of Rb gene Rb binds to E2F in
G1 phase to inhibit the activity of E2F. Rb is
phosphorated by CDK2 in G1/S phase and releases
E2F (transcription factor) out to promote protein
synthesis.
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Activation of proto-oncogenes The
oncogenesis of malignant tumors is based on the
activation of proto-oncogenes and the
inactivation of cancer suppressor genes.
Proto-oncogenes can be activated by variety of
mutations on proto-oncogene or the genes
regulator. 1. Site mutation The
mutation for ras family is site mutation. For
example, The c-Ha-ras gene cloned from carcinoma
of urinary bladder is different with the normal
c-Ha-ras by one base pair only. 2. DNA
rearrangement The gene DNA of the
normal proto-oncogenes can be rearranged by
shift, translocation, or location reverse. The
rearrangement can put proto-oncogene to the down
stream of some powerful promoter, and causes
excessive expression. The shift on the chromosome
of Burkitt lymphoma moves c-myc close to the
regulator of the heavy chain of immunoglobulin
(Ab) that is very actively expressed always, and
in addition, there is a powerful enhancer for
this promoter. So, the shifted c-myc will be
excessively expressed to cause oncogenesis.
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3. Inserted activation Some
reverse transcription viruses containing no v-onc
can insert their provirus DNA into host DNA to
cause inserted activation. MoSV (Mosaic virus)
can insert its LTR sequence that contains
powerful promoter and enhancer into a site closed
to the upper stream of c-mos in fibroblast of
mouse to cause a mouse sarcoma. The ALV (Avian
leukemia virus) contains no v-onc, but it can
insert to the upper stream of c-myc to cause
c-myc expressed excessively. 4.
Amplification of genes The
amplification of some proto-oncogenes is a
popular event in some blood tumors. c-myc can be
excessively amplified 8-32 folds in leukemia. The
parts of chromosome are amplified include ?
Double minute chromosomes (DMs) that are the
micro chromosomes without centromere and
distributed in pair. ? Homogenously stained
region (HSR). HSR is formed by the amplification
of chromosome region. ? Unequal sister chromatid
exchange (USCE). USCE happens in G2 phase causing
an allele chromosome in one generated cell is
short and another allele chromosome in another
generated cell is long. DMS and HSR are
the popular types of amplification. The c-myc
mRNA in the rectal carcinoma containing DMA or
HSR is 30 folds higher than normal. 5.
Low methylation of proto-oncogene The
cancer inducers can get the methylation of
proto-oncogene decreased to cause oncogenesis.
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The pathways of activation of proto-oncogene
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The DMs (yellow) of amplified c-myc (from
Molecular Biology of the Cell. 4th ed. 2002)
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The HSR (yellow) of amplified c-myc (from
Molecular Biology of the Cell. 4th ed. 2002)
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The external causes of oncogenesis 80
of human tumor are caused by external tumor
inducers. These external causes can be sorted as
three types with their quality chemical,
biological, and physical inducers. By their
functions, they can be sorted as initiator,
enhancer, and complete carcinogen.
Initiators means some molecules or conditions
that can change the DNA sequence by one time of
touch usually. Initiation is not reversible
usually. Enhancer can not cause
oncogenesis, but can push oncogenesis after
initiation. Dimethytenzanthracene (DMBA) is a
cancer initiator, and croton oil is an enhancer.
Smear DMBA on to the skin of mouse, then smear
croton oil onto same area of skin, the mouse skin
cancer will be caused. Some enhancers are
specific to enhance special cancers, for
examples, saccharin enhances the oncogenesis of
urinary bladder carcinoma, phenobarbital enhances
the oncogenesis of hepatocarcinoma.
Complete carcinogen means some molecules or
bio-molecules with the strong initiating and
enhancing function to cause oncogenesis. Complete
carcinogens include polycyclic aromatic
hydrocarbon, aromatic amine, amine nitrite,
carcinogenic viruses, and others.
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Initiator and enhancer (promoter) (from Molecular
Biology of the Cell. 4th ed. 2002)
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Chemical carcinogens ? Amine nitrites Strong
carcinogens. Amine nitrites are contained in many
quality changed vegetables and foods. Amine
nitrites can cause variety of tumors of digestion
system and kidneys. ? Polycyclic aromatic
hydrocarbons Polycyclic aromatic hydrocarbon can
cause skin carcinoma and sarcoma. Polycyclic
aromatic hydrocarbons are contained in the waste
gas from car, smoke, pitch, smoked foods, and
others. ? Aromatic amines Aromatic amine can
cause oncogenesis of urinary system. ? Alkylating
agents Alkylating agents can cause leukemia,
cancers of lungs and breasts. ?
Aminoazo-compounds Aminoazo-compounds cause
hepatocarcinoma. ? Base analogs The DNA base
pair can be replaced by base analogs, such as
5-FU and others, and interfere DNA replication. ?
Chloroethylene Polychloroethylene is the most
popularly used plastic material composed of
chloroethylenes. Chloroethylene is the carcinogen
for the tumors of skin, lungs, and bones with a
long time of latency. ? Heavy mental Chromium
(Cr), Nickel (Ni), Arsenic (As), and others.
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Chemical carcinogens cause human tumors
with complicated mechanism of serial steps of
reactions. Some chemical carcinogens cause human
tumors directly, we call them as direct
carcinogen. Most of chemical carcinogens cause
human tumors indirectly by a serial of
transformation or modification to form the
terminal carcinogen. We call these carcinogens as
indirect carcinogen. P450 enzyme system is
important to the oncogenesis induce by indirect
carcinogen. Terminal carcinogens can
interact with DNA, RNA, and proteins to cause
base pair shift, absence, DNA conjugated, DNA
broken, and abnormal chromosome.
Chemical carcinogens can inhibit methylase to
cause a low methylation, and activate
proto-oncogenes. Direct or indirect
carcinogens cause DNA mutated, and we call them
as genotoxic carcinogen. The chemical carcinogens
mentioned above are those. The
carcinogens for the cancers of breasts, prostate,
and uterus are the hormonic sterol compounds that
do not cause DNA damaged, but enhance cell
proliferation. We call them as non-genotoxic
carcinogen.
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Bio-carcinogens Bio-carcinogens include
viruses, bacteria, and fungi. Virus is most
important bio-carcinogen. 1. Oncoviruses
? Reverse transcription viruses
HTLV (human T lymphocyte leukemia virus), ATLV
(adult T lymphocyte leukemia virus), and HIV.
? HBV. ? HPV (human papilloma
virus). ? Epstein-Bars virus (EBV).
Virus infection is very important to cause
oncogenesis. There are many complicated contents
will be presented in your Virology. 2.
Fungi Tens of fungi have been
identified as bio-carcinogens so far. Aflatoxins
are important carcinogen from the foods,
especially peanuts and corns contaminated by
fungi. Aflatoxin B1 is the one of the strongest
hepatocarcinogen we know so far.
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Some oncoviruses
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Physical carcinogenic conditions 1.
Ionizing radiation Ionizing radiation
can cause the tumors of variety of organs or
tissues. There are distinguished instances fro
that The death of Mrs. Curie, and the high
incidence of leukemia in Japan after the nuclear
bomb attack in Second World War.
Ionizing radiation cause chromosome and DNA
mutated, or activate proto-oncogenes. Ionizing
radiation can cause the malignant tumors for
breasts, lungs, skin, bone, leukemia and
lymphoma. 2. Ultraviolet ray
Ultraviolet ray cause DNA broken and conjugated,
chromosome mutated. Ultraviolet ray inhibit
immunity to tumor immunity escaped. All above
benefit oncogenesis.
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The initiation and development of tumors
There are two theories to understand tumor
initiation that are from the dedifferentiated
somatic cells, or from stem cells. Somatic cell
is not of the ability of self renewal. Stem cells
always keep self renewal ability, so, mutation is
easy to be accumulated in stem cells. Many
scientists believe that the tumor initiation is
from stem cells. Some tissues, such as
liver and kidneys, are not of ability of self
renewal, but their cells can turn to division
under some special condition, so, these cells are
also the target cells for carcinogens.
Stem cells have some similarities with tumor
cells 1. Self renewal and unlimited
proliferation 2. High telomerase activity 3.
Same signal ways to regulate self renewal, such
as Wnt, Hedgehog, Notch, NF-?B.
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Signal pathways to cause oncogenesis (From
Molecular Biology of the Cell. 4th ed. 2002)
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Most of tumors are initiated from
monoclonal cell. Different isozymes are expressed
in different cells. The isozymes are isolated
from a tumor are same one. This result indicates
that all cells of a tumor are proliferated from a
monoclonal cell. Some tumor cells are of
strong proliferation ability, we call them as
tumor stem cell. The aim of tumor
therapy is to kill tumor cells as much as
possible. Many scientists believe that when a
tumor became small means the therapy is
effective. But, most of cases will relapse again.
This recurrence means that tumor stem cells were
not killed completely. Many scientists think that
the tumor therapy should kill tumor stem cells as
much as possible in spite of the tumor is not
becoming small.
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Female Barr body (Sex chromatin) indicates that
tumor is initiated from monoclonal cell (From
Molecular Biology of the Cell. 4th ed. 2002)
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III. The diagnosis and therapy of tumor
Like the diagnosis of other diseases, the medical
history and sign checking are the basic methods
to the diagnose tumors. The methods to diagnose
tumor include X-ray photo, ultrasonic image,
endoscopic image, histochemical section, biopsy,
cellular biological items, CT, and serial special
laboratory items including tumor specific marker.
The diagnosis of tumor, especially malignant
tumor, is very important to save patients life
or delay his/her death from tumor. The diagnosis
of tumor should be figured out as early as
possible. As a non-medical student of
life sciences, you should know how important is
the tumor marker to the early diagnosis of tumor,
and what the tumor markers are.
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Tumor marker Tumor markers are the
special proteins or polypeptides from tumor
tissue. Good tumor marker should be isolated or
detected out from specific tumor only!
Tumor marker can be used to tumor diagnosis,
therapy, therapy efficiency evaluation, and
prognosis evaluation. So far, the
following types of tumor marker have been
researched ? Oncofetal proteins ?
Tumor-associated antigens ? Enzyme ? Special
serum proteins ? Hormones ? Proto-oncogenes,
tumor suppressor genes, and their products.
Tumor markers are used to diagnose tumor for
many years. But, no any tumor marker is very
specific, sensitive, or convenient to be used so
far. So, several markers are used together to
co-diagnose a tumor usually. To find
more specific, sensitive and convenient tumor
marker is still a very important and valuable
research project now.
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Oncofetal proteins During the
individual development, some proteins are
expressed in fetal stage. But, some tumor cells
can be dedifferentiated to express these
proteins. We call these tumor expressed fetal
proteins as oncofetal proteins.
Alpha-fetoprotein (AFP) Normal reference is
lt5.8µg/L in serum after one year post birth. High
AFP expression is the specific sign to primary
hepatocarcinoma. Carcinoembryonic
antigen (CEA) is the glycoprotein located on the
colon carcinoma and embryonic colon epithelial
cells. Normal reference is lt2.5µg/L in serum.
Pancreatic oncofetal antigen (POA) is a
glycoprotein with normal reference of lt7U/ml in
serum. POA is specific marker to pancreatic
cancer.
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Carcinomic antigen or cancer antigen (CA)
Carcinomic antigen is the carbohydrate antigen
(CA) that is content of cell membrane. CA was
identified by monoclonal antibody.
CA15-3 CA15-3 is secreted by the secreting
epithelial cells of breasts, lungs, uterus,
stomach and intestine. This antigen appears at
high level (gt30U/ml) with cancers of breasts,
lungs, prostate, ovary, stomach and intestine.
CA15-3 can be used as a good parameter to
evaluate the prognosis of surgery on breasts
cancer. CA19-9 CA19-9 is glycolipid
with normal reference of lt37U/ml. 85-95 of
pancreatic cancers present high level of CA19-9.
A high level of CA19-9 after the surgery
operation on pancreatic cancer indicates the
recurrence. CA125 CA125 is the marker
for the cancer of ovary and uterus with normal
reference of lt35U/ml. CA50 CA50 is the
marker for pancreatic cancer and colorectal
carcinoma with normal reference of lt20U/ml.
PSA (prostate specific antigen) PSA is the
marker for prostate cancer with normal reference
of lt2.5µg/L.
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Enzymes as markers The activity of some
enzymes or the spectrum of some isoenzymes can be
changed in tumors. PAP (prostatic acid
phosphatase) Eosin phosphatase is the marker of
lysosome. PAP is 100-1000 folds higher in
prostate than in other tissues. PAP level in
original prostate cancer can be normal, but tens
folds higher in metastasis of prostate cancer
than normal. LDH (lactate dehydrogenase)
LDH activity can be increased in cancers. But it
is high also in some other diseases, such as
cardiovascular diseases. The activity of LDH4 and
LDH5 can be higher than normal in malignant
tumors with lower activity of LDH1 and LDH2. The
activity of LDH5 is higher than LDH4 in primary
hepatocarcinoma, but the activity of LDH4 is
higher than LDH5 in secondary hepatocarcinoma.
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AFU (a-L-fucosidase) AFU is the marker
for primary hepatocarcinoma. ALP
(Alkaline phosphatase) ALP is the marker for
primary bone cancer and the metastasis of liver
and bone from the cancers of other tissues.
?-GT (?-glutamyl transpeptidase) ?-GT is the
glycoprotein on cell membrane. 4-30gradient
PAGE can sort serum ?-GT as 12-13 isoenzyme
bands. ?-GT I', II and II' is the primary
hepatocarcinoma. NSE (neuron-specific
enolase) NSE is the marker for neuroblastoma and
microcytic pulmonary carcinoma. GST
(glutathione S-transferase) Isozymes of GST
include GSTa, µ and p. GST-p can be used as the
marker of malignant tumors of digestion system.
Telomerase Telomerase is a reverse
transcriptase to repair telomere sequence.
Telomerase is almost inactivated in normal
tissues, but activated in tumors.
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Hormones The harmonic factors in the
cancers of non-endocrine tissues are called as
ectopic hormones. The increased hormones in
endocrine cancers are called as abnormal hormones
in situ. Both of them can be used as the markers
for cancers. CT (calcitonin) The serum
CT is obviously increased in medullary carcinoma
of thyroid gland, lung adenocarcinoma, and
microcytic pulmonary carcinoma. Serum CT can be
high also in other tumors and diseases.
hCG (human chorionic gonadotropin) hCG can be
increased in pregnancy, chorionic epithelioma,
and other cancers of genital system.
Other hormones human placental lactogen (HPL),
adrenocorticotropic hormone (ACTH), growth
hormone (GH), parathyroid hormone (PTH), and
others.
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Plasma proteins Protein markers were
used as tumor marker earlier than others. The
specificity of protein markers is not so good,
but they are easy to detect. ß2m
(ß2-microglobulin) ß2m is expressed on the
surface of most of nucleated cells, and the light
chain of HLA (human lymphocyte antigen). ß2m is
used to co-diagnose the malignant tumors from
lymphocytic system. Fer (ferritin) Fer
is used to co-diagnose the hepatocarcinoma,
breasts cancer and other cancers. BJP
(Bence-Jones protein) BJP is the specific marker
for multiple myeloma.
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Therapy of tumors Therapy of tumors is
aimed to clean all tumor cells or decrease the
tumor cells as much as possible to maintain the
life of patients in his/her whole life, or change
the quality of tumor cells to save the life of
patients. The routine treatments for
tumor therapy include surgery, radiation therapy,
and chemical therapy. The successful
tumor surgery therapy is depended on early
diagnosis, individual features and the features
of tumors. Radiation therapy (X-ray or
?-ray) takes severe side effects.
Chemical therapy means that some chemical
medicines (5-FU, Oxaliplatin, and others) are
used to inhibit or clean the tumor cells. But,
usually, chemical therapy takes so severe side
effects that cause patients died from the
chemical therapy, not from cancer.
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Generally speaking, by our current
medical technology level, no any good, effective
or perfect method to save the life of malignant
tumor patients! Tumor has been, and will be a
great research target to us for a long time!
Now, some new therapy methods are researched
and developed. For examples, inhibition of
vascular genesis, enhancement of tumor
differentiation, immunological treatment, and
gene therapy. Every new therapy method
is the current hot research project, especially
gene therapy. I introduce the gene
therapy research to you briefly as the
follows Target therapy Target therapy
means that delivery the effective medicine,
bio-product or other unspecific agents to a tumor
target directorially by some special methods. For
example, by the gene engineering (gene
modification, recombination, or mimicry), the one
of arms (Fv, ScFv) of IgG can be changed to bind
target cell, another one can be changed to bind a
agent molecule. This complex can shoot the target
like a missile.
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A bio-missile
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Gene knockout Gene knockout means that
some harmful or benefitial gene is artificially
damaged or blocked completely and persistantly.
It can be used to construct cell or animal models
for reasearches.
Inserts
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Antisense DNA Antisense DNA is designed
to inhibit or interfere some genes expression
using a oligonucleotide matched to the target
sequence of the genes mRNA or genome DNA (16bp).
RNAi (siRNA) or Antisense RNA
Genomic DNA
mRNA
Synthesized
Expressed
Antisense RNA
RNAi or siRNA
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Antisense DNA
Genomic DNA
mRNA
Synthesized Antisense DNA
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The presentation about Cellular Biology is ended
here. We hope you, every one, will pass the test
of examination perfectly!