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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 1:1.
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, α- 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
7
Loss of contact inhibition
8
Migration in
cultured Caco-2
9
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 ① GF; ② GF receptors, such as
fms, erbB; ③ Protein kinases and other signal transduction molecules, such as
Src, Ras, and Raf; ④ Cyclin, such as bcl-1; ⑤ Regulator of apoptosis, such as
bcl-2; ⑥ 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
Protooncogenes
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 ① Regulators of
transcription, such as Rb, p53; ② Down regulator of transcription, such as WT; ③
Cyclin depend kinase inhibitor (CDKI), such as p15, p16, p21; ④ Inhibitors of
signal pathways, such as NF-1, PTEN. ⑥ DNA repairing factors, such as BRCA1,
and BRCA2; ⑥ 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: ① If both anelle genes
of cancer suppressor gene are mutated or inactivated, the cancer suppressor
gene is inactivated; ② 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. ③
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 β-catenin to enhance β-catenin degeneration. The
accumulated β-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 40%~60%.
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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 protooncogenes and the inactivation of cancer suppressor genes.
Proto-oncogenes can be activated by variety of mutations on protooncogene or the gene’s 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-Haras 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 ① Double minute chromosomes (DMs) that
are the micro chromosomes without centromere and distributed in pair. ②
Homogenously stained region (HSR). HSR is formed by the amplification of
chromosome region. ③ 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:
① 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.
② 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.
③ Aromatic amines: Aromatic amine can cause oncogenesis of urinary system.
④ Alkylating agents: Alkylating agents can cause leukemia, cancers of lungs
and breasts.
⑤ Aminoazo-compounds: Aminoazo-compounds cause hepatocarcinoma.
⑥ Base analogs: The DNA base pair can be replaced by base analogs, such as
5-FU and others, and interfere DNA replication.
⑦ 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.
⑧ 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:
① Reverse transcription viruses: HTLV (human T lymphocyte leukemia
virus), ATLV (adult T lymphocyte leukemia virus), and HIV.
② HBV.
③ HPV (human papilloma virus).
④ 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-κB.
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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 patient’s 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:
① Oncofetal proteins; ② Tumor-associated antigens; ③ Enzyme;
④ Special serum proteins; ⑤ Hormones; ⑥ 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 <5.8μg/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 <2.5μg/L in serum.
Pancreatic oncofetal antigen (POA) is a glycoprotein with normal
reference of <7U/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 (>30U/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 <37U/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 <35U/ml.
CA50: CA50 is the marker for pancreatic cancer and colorectal carcinoma
with normal reference of <20U/ml.
PSA (prostate specific antigen): PSA is the marker for prostate cancer
with normal reference of <2.5μg/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 (α-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.
γ-GT (γ-glutamyl transpeptidase): γ-GT is the glycoprotein on cell
membrane. 4%-30%gradient PAGE can sort serum γ-GT as 12-13
isoenzyme bands. γ-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 GSTα,
μ and π. GST-π 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.
β2m (β2-microglobulin): β2m is expressed on the surface of
most of nucleated cells, and the light chain of HLA (human lymphocyte
antigen). β2m 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 γ-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, bioproduct 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.
43
A bio-missile
44
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
45
Antisense DNA:
Antisense DNA is designed to inhibit or interfere some gene’s expression
using a oligonucleotide matched to the target sequence of the gene’s mRNA or
genome DNA (16bp).
RNAi (siRNA) or Antisense RNA:
Genomic DNA
mRNA
Antisense RNA
Synthesized
Expressed
RNAi or siRNA
46
Antisense DNA:
Genomic DNA
mRNA
Synthesized Antisense DNA
47
The presentation about Cellular Biology
is ended here.
We hope you, every one, will pass the test
of examination perfectly!
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