By:

Parth Mishra
XII-Science
STUDY OF
CANCER

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 BONAFIDE CERTIFICATE
ROLL
NO:

Certified that this is a Bonafide Record of work

done by Master Parth mishra of class 12"science"in DEDRAJ SEWALI DEVI
TODI KVB SCHOOL(DAV), biratnagar.

During the year: 2020-2021

Dated : ________________________

Teacher Incharge

Submitted for the practical examination held on

_____________________________________________________________

At ___________________________________________________________

Dated ___________________________________.

Internal Examiner External Examiner

Principal

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 ACKNOWLEDGEMENT

As a student of Class XII, I did this project as a part of my

studies entitled “Study of Cancer”. I owe a deep sense of
gratitude to my biology teacher Mrs.Jyoti mam, whose
valuable advice, guidance helped me in doing this project
from conception to completion.
At the same time, I cannot forget to express my gratitude to
our school Principal Mr. Ramesh Mishra for extending his
generous, patronage and constant encouragement.
Finally I am thankful to my parents for helping me
economically, and my friends for being a helping hand at
every step of this project.

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S.N CONTENTS PAGE
NO
O

1, WHAT IS CANCER ACTUALLY? 5

2, COMMON TYPES OF CANCER 6
3. STAGES OF CANCER 7
4. SIGN AND SYMPTOMS 8
5. HOW CANCER CELLS DIFFER FROM 9
NORMAL CELLS
6. CANCER AND IMMUNITY 10
7. CANCER AND GENES 11-16
8. CASE STUDY 17-18
9. DETECTION AND DIAGNOSIS OF 19
CANCER
10. HOW DOES CANCER CELLS ACTIVATE? 20
11. PREVENTION STEPS 21-22
12. DEVELOPMENT OF CANCER 23
13. MAIN CAUSES OF CANCER 24-25
14. TREATMENT OF CANCER 26-28

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 STUDY OF CANCER
1. What is Cancer actually?
Cancer is an abnormal and uncontrolled division of cells, known as cancer cells that
invade and destroy the surrounding tissues. Generally cancer is defined as uncontrolled
proliferation of cells in some aspects. They do not remain confined to the same part of
the body. They penetrate and infiltrate into the adjoining tissues and dislocate their
functions.

They form a subset of cancer cells expanding irregularly in unregulated manner forming
clones of cancer cells called neoplasm. A neoplasm or tumor often form a mass or lump,
but may be distributed diffusely.

Cancer cells stealing energy from normal

healthy cells.

Cancer develops when the cell’s genetic

material gets damaged or mutated.

2. Common types of Cancer

Cancer are classified on the basis of tissue from where they arose. Cancer are of three types :

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 1. Carcinomas: This type is mainly derived from epithelial cells. They are the malignant
growth of epithelial tissues ectodermal in origin.They include cervical (cervix is a part of
uterus) cancer, breast cancer, skin cancer, brain cancer, lung cancer, Stomach cancer,
etc. About 80% of all tumours are carcinomas.
 Cancerous growth of melanocytes ( a type of skin cells) is called Melanomas.
 Cancer of glands is called adenocarcinoma.
2. Sarcomas: These cancers are derived from primtive mesoderm. They are malignant
growth of tissues derived from primitive mesoderm.They include the cancers of bones,
cartilage ,tendons, adipose tissue and lymphoid tissue.
 Cancer of bones is called osteoma.
 Cancer of adipose tissue is called Lipomas.
 Cancer of lymphoid tissues is called Lymphoma. Hodgkin's disease is an
example of human lymphoma. In Hodgkin's disease there is chronic
enlargement of the production of lymphocytes by lymph nodes and spleen.
They are rare in humans; about 1% of tumours are sarcomas.
3. Leukemas : leukemias( = leukaemias) are characterized by abnormal increase of of
white blood corpuscles count due to their increased formation in the bone
marrow.Leukemias is also called Blood cancer.
 Cancer of muscle tissue are known as myoma.
 Cancer of glial cells of Central nervous system is called Glioma.
The most common cancers in india are mouth-throat cancer in men and
uterine-cervical cancer in women.

Some of the other types of cancer.

Bladder Cancer
Colorectal Cancer
Kidney Cancer
Lymphoma- Non Hodge skin
Oral and Oropharyngeal Cancer
Pancreatic Cancer
NOTE: World cancer day is February 4. Prostate Cancer
Thyroid cancer

3.Cancer stages

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Once cancer is diagnosed, your doctor will work to determine the extent (stage)
of your cancer. Your doctor uses your cancer's stage to determine your treatment
options and your chances for a cure.

Staging tests and procedures may include imaging tests, such as bone scans or
X-rays, to see if cancer has spread to other parts of the body.

Cancer stages are generally indicated by Roman numerals — I through IV, with
higher numerals indicating more advanced cancer. In some cases, cancer stage
is indicated using letters or words. When you're diagnosed with cancer, your
doctor will tell you what stage it is. That will describe the size of
the cancer and how far it's spread. Cancer is typically labeled in stages from I
to IV, with IV being the most serious. Those broad groups are based on a
much more detailed system that includes specific information about the
tumor and how it affects the rest of your body.
Staging Groups

Your doctor will use information from test results (clinical stage) or possibly
the tumor itself (pathologic stage) to decide your overall stage.
Most cancers that involve a tumor are staged in five broad groups. These are
usually referred to with Roman numerals. Other kinds, like blood
cancers, lymphoma, and brain cancer, have their own staging systems. But
they all tell you how advanced the cancer is.

 Stage 0 means there's no cancer, only abnormal cells with the potential
to become cancer. This is also called carcinoma in situ.
 Stage I means the cancer is small and only in one area. This is also called
early-stage cancer.
 Stage II and III mean the cancer is larger and has grown into nearby
tissues or lymph nodes.
 Stage IV means the cancer has spread to other parts of your body. It's
also called advanced or metastatic cancer.

4. Signs and Symptoms

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It produces no symptoms at the beginning of cancer, the actual symptoms starts when
there is a mass growth or Ulcerates. People may become anxious or depressed post-
diagnosis. The risk of suicide in people with cancer is approximately double.

Mass effects from lung cancer can block the bronchus resulting in cough or Pneumonia;
Esophageal Cancer can cause narrowing of the Esophagus, making it difficult or painful
to swallow; and Colorectal Cancer may lead to narrowing or blockages in the Bowel,
affecting bowel habits. Masses in breasts or testicles may produce observable lumps.
Ulceration can cause bleeding that, if it occurs in the lung, will lead to coughing up
blood, in the bowels to anemia or rectal bleeding, in the bladder to blood in the urine
and in the uterus to vaginal bleeding.

These are some local symptoms which can show up the growth of cancer cells. Signs and
symptoms caused by cancer will vary depending on what part of the body is affected.
Some general signs and symptoms associated with, but not specific to, cancer, include:

I. A persistant cough and hoarsness in as smoker.

II. A persistant change in digestive and bowel or bladder habits.
III. A change in a wart or a mole
IV. A lump or hard area in the breast.
V. Unexpected loss of weight.
VI. An uncurable ulcer
VII. An unexpected loss of apetite and unexpected low-grade fever.
VIII. Bleeding in vagina at times other than menstruation.
IX. Non-injury bleeding from the surface of the skin, mouth or other opening of the body.

Ulcerates: Sore on the skin or a mucous

membrane accompanied by disintegration of
tissue. Results in complete loss of epidermis.

5. How cancer cells differ from normal cells?

Normal cells have a limited lifespan. They are usually replaced by new cells through cell division
and cell differentiation . Their production is regulated in such a manner that the number of cell

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type remains nearly constant. Normal cells show a property called contact inhibition . Cancer
cells seems to have lost the property of contact inhibiton. Due to this property they contact
with other cells, inhibit uncontrolled growth. In contact inhibition normal cells keeps in touch
with the other cells so uncontrolled growth gets avoided but as cancer cells are haphazardly
arranged so they don’t come in contact with other cells so they lose contact inhibition and their
uncontrolled and unregulated growth of cancer cells happens by forming clones of cells and
tumors are formed. Cancer cells do not respond to normal growth control mechanism

Types of Tumours : There are two types of tumours

1. Benign Tumour( = Nonmalignant tumour) : It remains confined to the site of its origin
and does not spread to other parts of the body. It causes limited damage to the body. It
is non-cancerous
2. Malignant Tumour( = Cancerous tumour) : It first grows slowly. No symptoms are
noticed . This stage is latent stage. The tumour later grows quickly. The cancerous cells
go beyond adjacent tissue and enter the blood and lymph. Once this happens, they
migrate to many other sites in the body where the cancer cells continue to divide. A
phenomenon in which cancer cells spread to distant sites through body fluids to develop
secondary tumour is called Metastasis. Only malignant tumours are properly designated
as cancer.

6. Cancer and immunity

When adaptive immunity is inactivated, the frequency of certain

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cancers increases dramatically. For example, the risk of developing Kaposi’s sarcoma is
20,000 times greater for untreated AIDS patients than for healthy people. This
observation was unanticipated. If the immune system recognizes only nonself, it should
fail to recognize the uncontrolled growth of self cells that is the hallmark of cancer. It
turns out, however, that viruses are involved in about 15–20% of all human cancers.
Because the immune system can recognize viral proteins as foreign, it can act as a
defense against viruses that can cause cancer and against cancer cells that harbor
viruses. Scientists have identified six viruses that can cause cancer in humans. The
Kaposi’s sarcoma herpesvirus is one such virus. Hepatitis B virus, which can trigger liver
cancer, is another. A vaccine directed against hepatitis B virus that was introduced in
1986 was demonstrated to be the first vaccine to help prevent a specific human cancer.
Rapid progress on virus-induced cancers continues. In 2006, the release of a vaccine
against cervical cancer, specifically human papillomavirus (HPV), marked a major victory
against a disease that afflicts more than half a million women worldwide every year.

Vaccinating Against Cervical Cancer

I n the 1970s, Harald zur Hausen, working in Heidelberg, Germany,

proposed that human papillomavirus (HPV) causes cervical cancer.
Many scientists were skeptical that cancer could result from infection
by HPV, the most common sexually transmitted pathogen.

However, after more than a decade of work, zur Hausen isolated two
particular types of HPV from patients with cervical cancer. He
quickly made samples available to other scientists, leading to development
of highly effective vaccines against cervical cancer. In 2008,
zur Hausen shared the Nobel Prize in Physiology or Medicine for his
discovery. This computer graphic image of an HPV particle illustrates
the abundant copies of the capsid protein (yellow) that is used
as the antigen in vaccination.

WHY IT MATTERS Cervical cancer kills more than 4,000 women

annually in the United States and is the fifth-most common cause
of cancer deaths among women worldwide. Administering an HPV
vaccine, either Gardasil or Cervarix, to preteen girls and young
women greatly reduces their chance of being infected with the HPV
viruses that cause most cervical cancers.

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7. Cancer and genes

Cancer results from genetic changes that affect cell cycle control

We considered cancer as a set of diseases in

which cells escape from the control mechanisms that normally
limit their growth. We are ready to look at cancer more closely. The gene regulation
systems that go wrong during cancer turn out to be the very same systems that play
important roles in embryonic development, the immune response, and many other
biological processes. Thus, research into the molecular basis of cancer has both benefited
from and informed many other fields of biology.

Types of Genes Associated with Cancer

The genes that normally regulate cell growth and division during the cell cycle include
genes for growth factors, their receptors, and the intracellular molecules of signaling
pathways.Mutations that alter any of these genes in somatic cells can lead to cancer. The
agent of such change can be random spontaneous mutation. However, it is likely that
many cancer-causing mutations result from environmental influences, such as chemical
carcinogens, X-rays and other high-energy radiation, and some viruses.

Cancer research led to the discovery of cancer-causing genes called oncogenes (from the
Greek onco, tumor) in certain types of viruses. Subsequently, close counterparts of viral
oncogenes were found in the genomes of humans and other animals. The normal versions
of the cellular genes, called proto-oncogenes, code for proteins that stimulate normal cell
growth and division.

How might a proto-oncogene—a gene that has an essential function in normal cells—
become an oncogene, a cancer causing gene? In general, an oncogene arises from a
genetic change that leads to an increase either in the amount of the proto-oncogene’s
protein product or in the intrinsic activity of each protein molecule. The genetic changes
that convert proto-oncogenes to oncogenes fall into three main categories: movement of
DNA within the genome, amplification of a proto-oncogene, and point mutations in a
control element or in the proto-oncogene itself.

Cancer cells are frequently found to contain chromosomes that have broken and rejoined
incorrectly, translocating fragments from one chromosome to another (see Figure
15.14).Now that you have learned how gene expression is regulated, you can understand
the possible consequences of such translocations. If a translocated proto-oncogene ends

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up near an especially active promoter (or other control element), its transcription may
increase, making it an oncogene. The second main type of genetic change, amplification,
increases the number of copies of the proto-oncogene in the cell through repeated gene
duplication. The third possibility is a point mutation either (1) in the promoter or an
enhancer that controls a proto-oncogene, causing an increase in its expression, or (2) in
the coding sequence, changing the gene’s product to a protein that is more active or more
resistant to degradation than the normal protein. All these mechanisms can lead to
abnormal stimulation of the cell cycle and put the cell on the path to malignancy.

Tumor-Suppressor Genes

In addition to genes whose products normally promote cell division, cells contain genes
whose normal products inhibit cell division. Such genes are called tumor-suppressor
genes because the proteins they encode help prevent uncontrolled cell growth. Any
mutation that decreases the normal activity of a tumor-suppressor protein may contribute
to the onset of cancer, in effect stimulating growth through the absence of suppression.

The protein products of tumor-suppressor genes have various functions. Some tumor-
suppressor proteins repair damaged DNA, a function that prevents the cell from
accumulating cancer-causing mutations. Other tumor-suppressor proteins control the
adhesion of cells to each other or to the extracellular matrix; proper cell anchorage is
crucial in normal tissues— and is often absent in cancers. Still other tumor-suppressor
proteins are components of cell-signaling pathways that inhibit the cell cycle.

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Interference with Normal
Cell-Signaling Pathways

The proteins encoded by many proto-oncogenes and tumor suppressor genes are
components of cell-signaling pathways. Let’s take a closer look at how such proteins
function in normal cells and what goes wrong with their function in cancer cells. We will
focus on the products of two key genes, the ras protooncogene and the p53 tumor-
suppressor gene. Mutations in ras occur in about 30% of human cancers, and mutations
in p53 in more than 50%.

The Ras protein, encoded by the ras gene (named for rat sarcoma, a connective tissue
cancer), is a G protein that relays a signal from a growth factor receptor on the plasma
membrane to a cascade of protein kinases (see Figure 11.7). The cellular response at the
end of the pathway is the synthesis of a protein that stimulates the cell cycle. Normally,
such a pathway will not operate unless triggered by the appropriate growth factor. But
certain mutations in the ras gene can lead to production of a hyperactive Ras protein that
triggers the kinase cascade even in the absence of growth factor, resulting in increased
cell division. In fact, hyperactive versions or excess amounts of any of the pathway’s
components can have the same outcome: excessive cell division.

Figure below shows a pathway in which a signal leads to the synthesis of a protein that
suppresses the cell cycle. In this case, the signal is damage to the cell’s DNA, perhaps as
the result of exposure to ultraviolet light. Operation of this signaling pathway blocks the
cell cycle until the damage has been repaired. Otherwise, the damage might contribute to
tumor formation by causing mutations or chromosomal abnormalities. Thus, the genes for
the components of the pathway act as tumor-suppressor genes. The p53 gene, named for
the 53,000- dalton molecular weight of its protein product, is a tumorsuppressor gene.
The protein it encodes is a specific transcription factor that promotes the synthesis of cell
cycle–inhibiting proteins. That is why a mutation that knocks out the p53 gene, like a
mutation that leads to a hyperactive Ras protein, can lead to excessive cell growth and
cancer

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14 | S T U D Y O F C A N C E R
The p53 gene has been called the “guardian angel of the genome.” Once the gene is
activated—for example, by DNA damage—the p53 protein functions as an activator for
several other genes. Often it activates a gene called p21, whose product halts the cell
cycle by binding to cyclin-dependent kinases, allowing time for the cell to repair the
DNA. Researchers recently showed that p53 also activates expression of a group of
miRNAs, which in turn inhibit the cell cycle. In addition, the p53 protein can turn on
genes directly involved in DNA repair. Finally, when DNA damage is irreparable, p53
activates “suicide” genes, whose protein products bring about programmed cell death
(apoptosis; see Figure 11.21). Thus, p53 acts in several ways to prevent a cell from
passing on mutations due to DNA damage. If mutations do accumulate and the cell
survives through many divisions—as is more likely if the p53 tumor-suppressor gene is
defective or missing—cancer may ensue.

The many functions of p53 suggest a complex picture of regulation

in normal cells, one that we do not yet fully understand. For the present,
the diagram in Figure 18.24 is an accurate view of how mutations can
contribute to cancer, but we still don’t know exactly how a particular cell
becomes a cancer cell. As we discover previously unknown aspects of gene
regulation, it is informative to study their role in the onset of cancer. Such
studies have shown, for instance, that DNA methylation and histone
modification patterns differ in normal and cancer cells and that miRNAs
probably participate in cancer development. While we’ve learned a lot
about cancer by studying cell-signaling pathways, there is still a lot left to
learn.

The Multistep Model of Cancer Development

More than one somatic mutation is generally needed to produce all the changes
characteristic of a full-fledged cancer cell. This may help explain why the incidence of
cancer increases greatly with age. If cancer results from an accumulation of mutations
and if mutations occur throughout life, then the longer we live, the more likely we are to
develop cancer.

The model of a multistep path to cancer is well supported by studies of one of the best-
understood types of human cancer, colorectal cancer. About 135,000 new cases of
colorectal cancer are diagnosed each year in the United States, and the disease causes
60,000 deaths each year. Like most cancers, colorectal cancer develops gradually . The
first sign is often a polyp, a small, benign growth in the colon lining. The cells of the
polyp look normal, although they divide unusually frequently. The tumor grows and may
eventually become malignant, invading other tissues. The development of a malignant
tumor is paralleled by a gradual accumulation of mutations that convert proto-oncogenes
to oncogenes and knock out tumor-suppressor genes. A ras oncogene and a mutated p53
tumor-suppressor gene are often involved.

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About half a dozen changes must occur at the DNA level for a cell to become fully
cancerous. These changes usually include the appearance of at least one active oncogene
and the mutation or loss of several tumor-suppressor genes. Furthermore, since mutant
tumor-suppressor alleles are usually recessive, in most cases mutations must knock out
both alleles in a cell’s genome to block tumor suppression. (Most oncogenes, on the other
hand, behave as dominant alleles.) The order in which these changes must occur is still
under investigation, as is the relative importance of different mutations.

Recently, technical advances in the sequencing of DNA and mRNA have allowed
medical researchers to compare the genes expressed by different types of tumors and by
the same type in different individuals. These comparisons have led to personalized cancer
treatments based on the molecular characteristics of an individual’s tumor.

8. Case study

BREAST CANCER STUDY CASE

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 Scenario A
Carol Edwards, a 39 year-old premenopausal woman, had a screening mammogram
which revealed an abnormality in the right breast. She had no palpable masses on
breast exam. A mammographically localized surgical biopsy was done and revealed a
small (0.9 cm) grade III infiltrating ductal carcinoma with some associated ductal
carcinoma-in-situ (DCIS). The surgical margins were not clear (cancer cells were found at
the posterior margin). Estrogen and progesterone receptors are negative. The patient
has been given the diagnosis in a telephone conversation with the surgeon a few days
after the biopsy, and they are now meeting to discuss definitive treatment. Surgical
treatment must address two issues: local control and staging. LOCAL CONTROL
can be achieved by mastectomy or by wide re-excision (known as “lumpectomy” or
partial mastectomy) followed by radiation to the breast. The latter is known as breast
conservation therapy (BCT) and it is imperative that margins be clear and cosmetic
results acceptable to the patient to qualify for this option. In addition to this, there must
be unifocal disease only, not multicentric cancers. If there are multiple foci of
carcinoma, the patient should have a mastectomy. Following healing, radiation to the
remaining breast tissue is generally administered over a 6 week period (5 days/week).
Side effects are minimal, consisting of fatigue and some local swelling and minor
soreness of the breast with associated erythema (and occasionally sloughing of the
epidermis which will heal). If chemotherapy is required, the radiation is scheduled to
follow the completion of the chemotherapy; radiation and chemotherapy are not, as a
rule, administered concomitantly. Radiation following total mastectomy is only
recommended in select cases – in patients with inflammatory breast cancer and in
patients with locally advanced disease (as manifested by tumor size >5 cm and/ or with
4 or more positive nodes).
SURGICAL STAGING
(To determine if there are regional metastases) is done by axillary lymph node
dissection (ALND). There are no radiologic methods to reliably detect nodal metastases;
microscopic confirmation must be achieved by removing some of the axillary nodes.
Axillary node status is the single most important prognostic factor in determining breast
cancer survival. Regardless of which local control option is desired, mastectomy or
lumpectomy with radiation, ALND should be done. In this particular patient the
information is especially important as it will determine whether or not adjuvant
chemotherapy will be recommended. Because her hormone was hormone receptor-
negative, the use of tamoxifen is not an option. For patients with tumors that have a
favorable prognosis (as defined by size smaller than 1 cm and negative nodes) the
potential benefits of adjuvant chemotherapy are probably outweighed by the risks.
However, if nodes are positive, chemotherapy should improve survival. The information
in bold type below is from UpToDate: 2
INTRODUCTION
— The lymphatic drainage pathways of the breast (axillary, internal mammary [IM], and
supraclavicular nodal groups) are the regional areas most likely to be involved with
metastatic breast cancer.
RISK FACTORS FOR AXILLARY NODE INVOLVEMENT

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— The axillary lymph nodes (ALNs) receive 85 percent of the lymphatic drainage from all
quadrants of the breast; the remainder drains to the IM chain. The likelihood of ALN
involvement is related to tumor size and location, histologic grade, and the presence of
lymphatic invasion. Tumor size and margins — The likelihood of ALN involvement
increases as the size of the primary tumor increases. In one series of 2282 women with
invasive breast cancer or ductal carcinoma in situ (DCIS), the incidence of ALN
involvement was as follows: • Tis — 0.8 percent • T1a — 5 percent • T1b — 16 percent
• T1c — 28 percent • T2 — 47 percent • T3 — 68 percent • T4 — 86 percent ALN
metastases are relatively common even with invasive breast cancers 1 cm in size. In a
second report of 919 such women who underwent ALN dissection (ALND); ALN
metastases were detected in 16 and 19 percent of those with T1a (tumor size between
0.1 and 0.5 cm in greatest dimension) and T1b tumors (tumors between 0.5 and 1.0 cm),
respectively. Many database series report a higher rate of ALN metastases for T1a than
T1b disease. The higher rate in this group may be related to multifocal disease in DCIS,
undersampling of the primary tumor, or high grade microinvasive carcinoma. Nodal
positivity rates are also higher in women who are found to have residual tumor after
reexcision for positive margins following lumpectomy for breast conservation therapy
(BCT). In one series, women with T1b tumors who had residual disease were
significantly more likely to harbor ALN metastases than those whose tumors were either
excised to a negative margin initially or who had negative reexcisions for an initially
positive margin (36 versus 5 percent). Histologic features — Low grade (grade 1) tumors
have a significantly lower rate of ALN metastases compared to grade 2 or 3 tumors. As
an example, in data derived from the Surveillance, Epidemiology and End Results (SEER)
database, the incidence of ALN disease in patients with grade 1 and grade 3 tumors of
similar size was 3.4 and 21 percent, respectively. The presence of lymphatic invasion
also increases the risk of ALN metastases. 3 Tumors that are associated with a less than
5 percent risk of ALN metastases include those with a single focus of microinvasion,

9.Detection and Diagnosis of Cancer

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It depends upon the histological features of malignant structure.
1. Bone marrow Biopsy (a piece of suspected tissue cut into thin sections) s stained
and examined under microscope by pathologists) and abnormal count of WBCs
in Leukemia.
2. Biopsy of tissue direct or indirect through endoscopy. Also endoscopic
observation. Pap's test (cytological staining) s used to detect cancer of cervix and
other parts of the genital tract.
3. Techniques such as Radiography (use of X-rays), CT (Computed tomography),
MRI (magnetic resonance imaging) are very useful to detect cancers of the
internal organs. In CT, X-rays are used to generate a three dimensional image of
internal organs. In MRI strong magnetic fields and and non-ionizing radiations
are used to detect pathological and physiological changes in the living tissue.
Antibodies against cancer specific antigens are also used for detection of certain
cancers . Techniques of molecular biology can be applied to detect genes in
individuals. Mammography is radiographic examination of breasts for possible
cancer.
4. Monoclonal antibodies coupled to appropriate radioisotopes can detect cancer-
specific antigens and hence cancer.
5. Ames test is for carcinogenic diseases.

10. How Does Cancer cells activate?

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It is well known that cancer is preceded by damaged DNA. Because DNA is
encoded with the instructions for cell behaviour, damaged DNA can alter
cell processes including those that regulate growth and division. This is
supported by the fact that tissues which have a high cell-division rate, such
as bone and lymph, are the most common sites for cancer.

Some genes, encoded on DNA, act as a switch that can be turned on or off
depending on cell needs. Free radicals have the ability to break DNA
strands which can result in some genes being permanently switched on,
such is the case with cancerous cell growth. Although it is often taught that
the DNA mutations that lead to cancer happen at random, research
suggests there are epigenetic triggers that may increase prevalence of DNA
damage.

11. Prevention Steps:

DNA is vital for cell function and the body has mechanisms by which it
protects DNA from being damaged. One of the most important mechanisms

20 | S T U D Y O F C A N C E R
is the one responsible for the production of antioxidants. A major step in
the prevention of DNA damage, and therefore cancer, would be to optimize
antioxidant activity. Research has suggested that this can be achieved
through the adoption of a diet that incorporates antioxidant rich foods or
extracts.

Glutathione plays a major role in the antioxidant activities of the body.

Evidence shows that this molecule alone has the ability to influence cancer
risk in a directly correlative manner. This means that by increasing your
body’s supply of glutathione, you are drastically improving its ability to
control free radicals before they damage cells. There are several ways in
which you can increase your supply of glutathione.

 Doctors have identified several ways of reducing your cancer risk, such as:

 Stop smoking. If you smoke, quit. If you don't smoke, don't start.
Smoking is linked to several types of cancer — not just lung cancer.
Stopping now will reduce your risk of cancer in the future.

 Avoid excessive sun exposure. Harmful ultraviolet (UV) rays from the

sun can increase your risk of skin cancer. Limit your sun exposure by
staying in the shade, wearing protective clothing or applying sunscreen.

 Eat a healthy diet. Choose a diet rich in fruits and vegetables. Select

whole grains and lean proteins.

 Exercise most days of the week. Regular exercise is linked to a lower

risk of cancer. Aim for at least 30 minutes of exercise most days of the
week. If you haven't been exercising regularly, start out slowly and work
your way up to 30 minutes or longer.

 Maintain a healthy weight. Being overweight or obese may increase your

risk of cancer. Work to achieve and maintain a healthy weight through a
combination of a healthy diet and regular exercise.

 Drink alcohol in moderation, if you choose to drink. If you choose to

drink alcohol, limit yourself to one drink a day if you're a woman of any age
or a man older than age 65, or two drinks a day if you're a man 65 years old
or younger.

21 | S T U D Y O F C A N C E R
  Schedule cancer screening exams. Talk to your doctor about what
types of cancer screening exams are best for you based on your risk
factors.

 Ask your doctor about immunizations. Certain viruses increase your

risk of cancer. Immunizations may help prevent those viruses, including
hepatitis B, which increases the risk of liver cancer, and human
papillomavirus (HPV), which increases the risk of cervical cancer and other
cancers. Ask your doctor whether immunization against these viruses is
appropriate for you.

22 | S T U D Y O F C A N C E R
12. Development of Cancer

13. Causes of Cancer:

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Study of cancer is called Oncology. Chemical and physical agents that cause
cancer are called Carcinogens, which belong to three categories.

I. Oncogenic Transformations: They are agents or factors which bring

about changes in genetic material. They are of two types, radiations
and chemicals.
II. Tumours Promoters: They promote proliferation of cells which have
undergone oncogenic transformation e.g., some growth factors,
hormones
III. Tumours Viruses: Some viruses are known to be connected with
oncogenic transformations.
Another Classification of carcinogens is as follows :
I. Physical irritants: a) Use of kangri(an earthen pot containing
burning coal) by Kashmiris causes abdominal cancer as these
people keep kangri close to their abdomen during winter.
b)Betel and tobacco chewing causes oral cancer. c)Heavy
smoking causes lung cancer and may also cause cancer of oral
cavity, pharynx(throat) and larynx. d) Jagged teeth may cause
tongue cancer. e) Excessive exposure to sunlight can cause
skin cancer.
II. Chemical agents: Several chemicals are known to cause
cancer. These are Caffeine, Nicotine,, products of combustion
ofcoal and oil and pesticides; constants use of artificial
sweetner can cause cancer. An animal protein-rich diet is
known to cause cancer of large intestine. Breast cancer has
hormonal relationship. Thus , some sex hormones and steroids
if secreted or given in large amounts may cause cancer.
Chimney sweepers develop cancer of scrotum. Dye workers
have a high rate of bladder cancer.

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 III. Radiations : The X-rays, cosmic rays, ultra-violet rays, etc; can
cause cancer. Japanese people exposed to radiations from
world war (ii) nuclear bombing show five times the incidence
of leukemia seen in rest of the population.
IV. Biological agents : Some viruses and other parasites, excessive
secretion of certain hormones are believed to cause cancer.

Some of the facts :

 Tobacco use is the cause of about 33% of cancer deaths.

 Another 10% is due to obesity, poor diet, lack of physical activity,
excessive drinking of alcohol.
 Nearly 20% of cancer cause is due to hepatitis B, hepatitis C and
human papillomavirus.
 Approximately 5-10% of cancer is due to inherited genetic defect
from person’s parents.

14. Treatment of Cancer:

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Cancer is the second-leading cause of death in the world. But survival rates are
improving for many types of cancer, thanks to improvements in cancer screening
and cancer treatment.

 SURGERY :
It involves the removal of the entire cancerous tissue.

 RADIATION THERAPY :
It involves the exposure of the cancerous parts of the body to X-rays
which destroy rapidly growing cells without harming the surrounding
tissues. Radon (Rn-220), Cobalt (Co-60) and Iodine (I-131) are the
radioisotopes which are generally used in radiotherapy.

 CHEMOTHERAPY :
It involves the administration of certain anticancer drugs. These
drugs check cell division by inhabiting DNA synthesis. These drugs
may be more toxic to cancerous cells than normal cells. The

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 Chemotherapeutic drugs kill cancerous cells. Majority of drugs have
side effects like Hair loss, anaemia, etc. A common weed
Catharanthus roseus is the source of two anticancer drugs,
Vincristine and Vinblastine used in treatment of leukemia.

 IMMUNOTHERAPY :
It involves natural anti-cancer immunological defence mechanisms.
The patients are given substances called Biological response
modifiers such as α- interferon which activate the immunity and help
in destroying tumour.

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Most cancers are treated by combination of Surgery, Radiotherapy,
immunotherapy and chemotherapy

Efforts are being made to develop cancer vaccines.

Haraid Zur Hausen shared 2008 nobel prize for physiology and
medicine for finding Human Papilloma Virus(HPV) that causes
Cervical cancer., second most common cancer in women in the
world.

Taxol drug is an anticancer drug for breast and ovarian cancer. It is

obtained from pacific yew (Taxas buccata).

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 THANK YOU!

BIBLIOGRAPHY

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  www.google.com
 www.thoughtco.com
 www.cancer.net
 www.healthtap.com
 www.cancerresearchuk.org
 www.academia.edu
 www.quora.com

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