The document is a biology investigatory project focused on cancer, detailing its definition, causes, types, and treatment options. It emphasizes the differences between cancerous and normal cells, as well as the importance of early detection for better prognosis. It also explores various cancer treatment methods, including surgery, chemotherapy, radiation therapy, and emerging immunotherapies.

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BIOLOGY INVESTIGATORY PROJECT
A I S C E - 2 0 2 3
TOPIC – STUDY OF A GENETICAL DISEASE
CANCER
CLASS – XII
BOARD ROLL NUMBER - SUBMITTED BY – Archisman Chakraborty

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ACKNOWLEGDEMENT
There are times when “silence speak so much more louder than words”
of praise to only as good as belittle a person, whose words do not express,
but only put a veneer over true feelings, which are of gratitude at this
point of time.
I hereby acknowledge my deep sense of gratitude and indebtedness to my
parents and my biology teacher and our principal whose immense help,
genius guidance, encouragement , necessary suggestions, enthusiasm and
inspiration made this work a master project and a joint enterprise.

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CERTIFICATE
This is to certify that ARCHISMAN CHAKRABORTY of class 12th has
satisfactorily completed his biology investigatory project as prescribed
by the CBSE course during the academic year 2022 – 2023
I further certify that this work is his own work and is certainly not
published or submitted to anywhere else.
SIGNATURE( TEACHER ) SIGNATURE ( EXAMINER )
SIGNATURE ( PRINCIPAL )

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INDEX
TOPICS / SUBTOPICS
PAGE
NO.
Introduction 5
What is cancer ? 6
What are cancer cells ? 6
Differences between cancer cell and normal cell 7
What is tumour ? 7
Types of tumours 8
How does cancer develop ? 9
Causes of cancer 10
Types of cancer 10
Various stages of cancer 14
Cancer detection and diagnosis 15
Treatment of cancer 16
Goals of cancer treatment 17
Various tools for cancer treatment 18
Case Study - 1 20
Case Study - 2 23
Bibliography 27

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INTRODUCTION
Cancer is a disease in which some of the body’s cells grow uncontrollably
and spread to other parts of the body.
Cancer can start almost anywhere in the human body, which is made up
of trillions of cells. Normally, human cells grow and multiply (through a
process called cell division) to form new cells as the body needs them.
When cells grow old or become damaged, they die, and new cells take
their place.
You are made up of trillions of cells that over your lifetime normally
grow and divide as needed. When cells are abnormal or get old, they
usually die. Cancer starts when something goes wrong in this process
and your cells keep making new cells and the old or abnormal ones don't
die when they should. As the cancer cells grow out of control, they
can crowd out normal cells. This makes it hard for your body to work
the way it should.
For many people, cancer can be treated successfully. In fact, more
people than ever before lead full lives after cancer treatment.

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WHAT IS CANCER ?
Cancer is one of the most dreaded diseases of human being and is a major
cause of death all over the globe. More than a million Indians suffer from
cancer and a large number of them die from it annually. The mechanisms
that underlie development of cancer or oncogenic transformation of
cells, its treatment and control have been some of the most intense areas
of research in biology and medicine.
WHAT ARE CANCER CELLS ?
In our body, cell growth and differentiation is highly controlled and
regulated. In cancer cells, there is breakdown of these regulatory
mechanisms. Normal cells show a property called contact inhibition by
virtue of which contact with other cells inhibits their uncontrolled
growth. Cancer cells appears to have lost this property. As a result of
this, cancerous cells just continue to divide giving rise to masses of cells
called tumors.

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DIFFERENCES BETWEEN CANCER CELLS
AND NORMAL CELLS
Cancer cells differ from normal cells in many ways. For instance, cancer
cells:
• grow in the absence of signals telling them to grow. Normal cells
only grow when they receive such signals.
• ignore signals that normally tell cells to stop dividing or to die (a
process known as programmed cell death, or apoptosis).
• invade into nearby areas and spread to other areas of the body.
Normal cells stop growing when they encounter other cells, and
most normal cells do not move around the body.
• tell blood vessels to grow toward tumours. These blood vessels
supply tumors with oxygen and nutrients and remove waste
products from tumors.
• hide from the immune system. The immune system normally
eliminates damaged or abnormal cells.
• trick the immune system into helping cancer cells stay alive and
grow. For instance, some cancer cells convince immune cells to
protect the tumor instead of attacking it.
• accumulate multiple changes in their chromosomes, such as
duplications and deletions of chromosome parts. Some cancer
cells have double the normal number of chromosomes.
• rely on different kinds of nutrients than normal cells. In addition,
some cancer cells make energy from nutrients in a different way
than most normal cells. This lets cancer cells grow more quickly.
WHAT IS A TUMOR ?
A tumor is a lump or growth. Some lumps are cancer, but many are not.
• Lumps that are not cancer are called benign
• Lumps that are cancer are called malignant

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What makes cancer different is that it can spread to other parts of the
body while benign tumors do not. Cancer cells can break away from the
site where the cancer started. These cells can travel to other parts of
the body and end up in the lymph nodes or other body organs causing
problems with normal functions.
TYPES OF TUMORS
Benign tumors normally remain confined to their original location and do
not spread to other parts of the body and cause little damage. The
malignant tumors, on the other hand are a mass of proliferating cells
called neoplastic or tumor cells. These cells grow very rapidly, invading
and damaging the surrounding normal tissues. As these cells actively
divide and grow they also starve the normal cells by competing for vital
nutrients. Cells sloughed from such tumors reach distant sites through
blood, and wherever they get lodged in the body, they start a new tumor
there. This property called metastasis is the most feared property of
malignant tumors.

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HOW DOES CANCER DEVELOP?
Cancer is caused
by certain
changes to
genes, the basic
physical units of
inheritance.
Genes are
arranged in long
strands of tightly
packed DNA
called
chromosomes.
Cancer is a genetic disease—that is, it is caused by changes to genes that
control the way our cells function, especially how they grow and divide.
Genetic changes that cause cancer can happen because:
• of errors that occur as cells divide.
• of damage to DNA caused by harmful substances in the
environment, such as the chemicals in tobacco smoke
and ultraviolet rays from the sun.
• they were inherited from our parents.
The body normally eliminates cells with damaged DNA before they turn
cancerous. But the body’s ability to do so goes down as we age. This is
part of the reason why there is a higher risk of cancer later in life.
Each person’s cancer has a unique combination of genetic changes. As
the cancer continues to grow, additional changes will occur. Even within
the same tumor, different cells may have different genetic changes.

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CAUSES OF CANCER
Transformation of normal cells into cancerous neoplastic cells may be
induced by physical, chemical or biological agents. These agents are
called carcinogens. Ionising radiations like X-rays and gamma rays and
non-ionizing radiations like UV cause DNA damage leading to neoplastic
transformation. The chemical carcinogens present in tobacco smoke have
been identified as a major cause of lung cancer. Cancer causing viruses
called oncogenic viruses have genes called viral oncogenes. Furthermore,
several genes called cellular oncogenes (c-onc) or proto oncogenes have
been identified in normal cells which, when activated under certain
conditions, could lead to oncogenic transformation of the cells.
Diagnosis, treatment, and prognosis for childhood cancers are different
than for adult cancers. The main differences are the survival rate and the
cause of the cancer. The overall five-year survival rate for childhood
cancer is about 80%, while in adult cancers the survival rate is 68%. This
difference is thought to be because childhood cancer is more responsive
to therapy and a child can tolerate more aggressive therapy.
Childhood cancers often occur or begin in the stem cells, which are simple
cells capable of producing other types of specialized cells that the body
needs. A sporadic (occurs by chance) cell change or mutation is usually
what causes childhood cancer. In adults, the type of cell that becomes
cancerous is usually an epithelial cell. Epithelial cells line the body cavity
and cover the body surface. Cancer occurs from environmental exposures
to these cells over time. Adult cancers are sometimes referred to as
acquired for this reason.
TYPES OF CANCER
There are more than 100 types of cancer. Types of cancer are usually
named for the organs or tissues where the cancers form. For example,
lung cancer starts in the lung, and brain cancer starts in the brain.
Cancers also may be described by the type of cell that formed them, such
as an epithelial cell or a squamous cell.

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Here are some categories of cancers that begin in specific types of
cells:
CARCINOMA
Carcinomas are the most common type of cancer. They are formed by
epithelial cells, which are the cells that cover the inside and outside
surfaces of the body. There are many types of epithelial cells, which
often have a column-like
shape when viewed under a
microscope.
Carcinomas that begin in
different epithelial cell
types have specific names:
Adenocarcinoma is a cancer
that forms in epithelial cells
that produce fluids or
mucus. Tissues with this
type of epithelial cell are sometimes called glandular tissues. Most
cancers of the breast, colon, and prostate are adenocarcinomas.
Basal cell carcinoma is a cancer that begins in the lower or basal (base)
layer of the epidermis, which is a person’s outer layer of skin.
Squamous cell carcinoma is a cancer that forms in squamous cells, which
are epithelial cells that lie just beneath the outer surface of the skin.
Squamous cells also line many other organs, including the stomach,
intestines, lungs, bladder, and kidneys. Squamous cells look flat, like fish
scales, when viewed under a microscope. Squamous cell carcinomas are
sometimes called epidermoid carcinomas.
Transitional cell carcinoma is a cancer that forms in a type of epithelial
tissue called transitional epithelium, or urothelium. This tissue, which is
made up of many layers of epithelial cells that can get bigger and smaller,
is found in the linings of the bladder, ureters, and part of the kidneys

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(renal pelvis), and a few other organs. Some cancers of the bladder,
ureters, and kidneys are transitional cell carcinomas.
SARCOMA
Sarcomas are cancers that form in bone and
soft tissues, including muscle, fat, blood
vessels, lymph vessels, and fibrous tissue
(such as tendons and ligaments).
Osteosarcoma is the most common cancer
of bone. The most common types of soft
tissue sarcoma are leiomyosarcoma, Kaposi
sarcoma, malignant fibrous
histiocytoma, liposarcoma,
and dermatofibrosarcoma protuberans.
LEUKEMIA
Cancers that begin in the blood-forming tissue of the bone marrow are
called leukaemia. These cancers do not form solid tumors. Instead, large
numbers of abnormal white blood cells (leukaemia cells and leukemic
blast cells) build up in the blood and bone marrow, crowding out normal
blood cells. The low level of normal blood cells can make it harder for
the body to get oxygen to its tissues, control bleeding, or fight
infections.
There are four common
types of leukaemia, which
are grouped based on how
quickly the disease gets
worse (acute or chronic) and
on the type of blood cell the
cancer starts in
(lymphoblastic or myeloid).
Acute forms of leukaemia

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grow quickly and chronic forms grow more slowly.
LYMPHOMA
Lymphoma is cancer that
begins in lymphocytes (T
cells or B cells). These are
disease-fighting white
blood cells that are part of
the immune system. In
lymphoma, abnormal
lymphocytes build up
in lymph nodes and lymph
vessels, as well as in other
organs of the body.
There are two main types
of lymphoma:
Hodgkin lymphoma – People with this disease have abnormal lymphocytes
that are called Reed-Sternberg cells. These cells usually form from B
cells.
Non-Hodgkin lymphoma – This is a large group of cancers that start in
lymphocytes. The cancers can grow quickly or slowly and can form from
B cells or T cells.
MELANOMA
Melanoma is cancer that begins in cells that become melanocytes, which
are specialized cells that make melanin (the pigment that gives skin its
colour). Most melanomas form on the skin, but melanomas can also form
in other pigmented tissues, such as the eye.

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VARIOUS STAGES OF CANCER

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CANCER DETECTION AND DIAGONOSIS
Early detection of cancers is essential as it allows the disease to be
treated successfully in many cases.
Physical examination
Your doctor may feel areas of your body for lumps that may indicate
cancer. During a physical exam, your doctor may look for abnormalities,
such as changes in skin color or enlargement of an organ, that may
indicate the presence of cancer.
Laboratory tests ( Bone Marrow Test )
Laboratory tests, such as urine and blood tests, may help your doctor
identify abnormalities that can be caused by cancer. For instance, in
people with leukemia, a common blood test called complete blood count
may reveal an unusual number or type of white blood cells.
Imaging tests
Imaging tests allow your doctor to
examine your bones and internal
organs in a noninvasive way. Imaging
tests used in diagnosing cancer may
include a computerized tonography
(CT) scan, bone tests, magnetic
resonance imaging (MRI), positron
emission tomography (PET) scan,
ultrasound and X-ray, among others.

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Biopsy
During a biopsy, your doctor collects a sample of cells for testing in the
laboratory. There are several
ways of collecting a sample.
Which biopsy procedure is right
for you depends on your type of
cancer and its location. In most
situations, a biopsy is the only
way to definitively diagnose
cancer.
In the laboratory, doctors look
at cell samples under the
microscope. Normal cells look uniform, with similar sizes and orderly
organization. Cancer cells look less orderly, with varying sizes and
without apparent organization.
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 with inherited susceptibility to certain
cancers. Identification of such genes, which predispose an individual to
certain cancers, may be very helpful in prevention of cancers. Such
individuals may be advised to avoid exposure to particular carcinogens to
which they are susceptible (e.g., tobacco smoke in case of lung cancer).
TREATMENT OF CANCER
Many cancer treatments are available. Your treatment options will
depend on several factors, such as the type and stage of your cancer,
your general health, and your preferences. Together you and your doctor
can weigh the benefits and risks of each cancer treatment to determine
which is best for you.
.

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GOALS OF CANCER TREATMENT
Cancer treatments have different objectives, such as:
Cure
The goal of treatment is to achieve a cure for your cancer, allowing you
to live a normal life span. This may or may not be possible, depending
on your specific situation.
Primary treatment
The goal of a primary treatment is to completely remove the cancer
from your body or kill the cancer cells.
Any cancer treatment can be used as a primary treatment, but the most
common primary cancer treatment for the most common cancers is
surgery. If your cancer is particularly sensitive to radiation therapy or
chemotherapy, you may receive one of those therapies as your primary
treatment.
Adjuvant treatment
The goal of adjuvant therapy is to kill any cancer cells that may remain
after primary treatment in order to reduce the chance that the cancer
will recur.
Any cancer treatment can be used as an adjuvant therapy. Common
adjuvant therapies include chemotherapy, radiation therapy and
hormone therapy.
Palliative treatment
Palliative treatments may help relieve side effects of treatment or signs
and symptoms caused by cancer itself. Surgery, radiation,
chemotherapy and hormone therapy can all be used to relieve
symptoms and control the spread of cancer when a cure isn't possible.
Medications may relieve symptoms such as pain and shortness of breath.
Palliative treatment can be used at the same time as other treatments
intended to cure your cancer.

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VARIOUS TOOLS OF CANCER
TREATMENT
Doctors have many tools when it comes to treating cancer. Cancer
treatment options include:
SURGERY.
The goal of surgery is to remove the cancer or as much of the cancer as
possible.
CHEMOTHERAPY.
Chemotherapy uses drugs to kill cancer cells.
RADIATION THERAPY.
Radiation therapy uses high-powered energy beams, such as X-rays and
protons, to kill cancer cells. Radiation treatment can come from a
machine outside your body (external beam radiation), or it can be placed
inside your body (brachytherapy).
BONE MARROW TRANSPLANT.
Bone marrow transplant is also known as a stem cell transplant. Your bone
marrow is the material inside your bones that makes blood cells. A bone
marrow transplant can use your own cells or cells from a donor.
A bone marrow transplant allows your doctor to use higher doses of
chemotherapy to treat your cancer. It may also be used to replace
diseased bone marrow.
IMMUNOTHERAPY.
Immunotherapy, also known as biological therapy, uses your body's
immune system to fight cancer. Cancer can survive unchecked in your

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body because your immune system doesn't recognize it as an intruder.
Immunotherapy can help your immune system "see" the cancer and attack
it.
HORMONE THERAPY
Some types of cancer are fueled by your body's hormones. Examples
include breast cancer and prostate cancer. Removing those hormones
from the body or blocking their effects may cause the cancer cells to stop
growing.
TARGETED DRUG THERAPY
Targeted drug treatment focuses on specific abnormalities within cancer
cells that allow them to survive.
CLINICAL TRIALS
Clinical trials are studies to investigate new ways of treating cancer.
Thousands of cancer clinical trials are underway.
BIOLOGICAL MODIFIERS
Tumor cells have been shown to avoid detection and destruction by
immune system. Therefore, the patients are given substances called
biological response modifiers such as α-interferon which activates their
immune system and helps in destroying the tumor.

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CASE STUDY - 1
CASE REPORT OF METASTATIC LUNG ADENOCARCINOMA WITH LONG-TERM SURVIVAL FOR OVER
11 YEARS
CASE REPORT
ABSTRACT
RATIONALE:
This is the first known report in the English literature to describe a case of metastatic non-small
cell lung cancer that has been controlled for >11 years.
PATIENT CONCERNS:
A 71-year-old man visited our hospital because of dry cough.
DIAGNOSIS:
Chest computed tomography revealed a tumour on the left lower lobe with pleural effusion, and
thoracic puncture cytology indicated lung adenocarcinoma.
INTERVENTIONS:
Four cycles of carboplatin and docetaxel chemotherapy reduced the size of the tumour;
however, it increased in size after 8 months, and re-challenge chemotherapy (RC) with the same
drugs was performed. Repeated RC controlled disease activity for 6 years. After the patient
failed to respond to RC, erlotinib was administered for 3 years while repeating a treatment
holiday to reduce side effects. The disease progressed, and epidermal growth factor receptor
(EGFR) gene mutation analysis of cells from the pleural effusion detected the T790 M mutation.
Therefore, Osimertinib was administered, which has been effective for >1 year.
OUTCOMES:
The patient has survived for >11 years since the diagnosis of lung cancer.
LESSONS:
Long-term survival may be implemented by actively repeating cytotoxic chemotherapy and
EGFR-tyrosine kinase inhibitor administration.

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DETAILED ANALYSIS OF THE CASE
A 71-year-old Japanese man experienced dry cough for 2 weeks and visited the Department of
Respiratory Medicine at our hospital in August 2007. Enhanced chest-abdomen computed
tomography revealed a tumour with a 3-cm diameter in the left lower lobe and left pleural
effusion (Fig. 1). A 5-mm nodule, considered to be lung metastasis, was detected in the left upper
lobe. Cytological analysis of the left pleural effusion by thoracic puncture led to the diagnosis of
lung adenocarcinoma. Gadolinium-enhanced brain magnetic resonance imaging and bone
scintigraphy did not reveal any other metastases. The tumour
was classified as clinical T4N0M1, stage IV according to the TNM classification of the Union of
International Cancer Control (UICC), 6th edition. According to the UICC 8th edition, it was
classified as clinical T4N0M1a, stage IV A. The patient had a history of hypertension and was a
past smoker (60 pack-years) and a company employee. The Eastern Cooperative Oncology Group
performance status (ECOG-PS) at the time of admission was 1. The carcinoembryonic antigen
(CEA) level was 97.4 ng/mL (normal, 0–5 ng/ml).
Beginning in August 2007, the patient received carboplatin
(CBDCA) and docetaxel (DTX). After 4 cycles, the tumour was
reduced to 1 cm in diameter. The 5-mm nodule and pleural
effusion had also decreased. According to the Response
Evaluation Criteria in Solid Tumours version 1.1, partial
response was achieved, but he experienced progressive disease
(PD) after 8 months. Six cycles of re-challenge chemotherapy
(RC) using the same regimen were started in August 2008 and
were effective. Thereafter, at each recurrence of PD, 4 to 6
cycles of RC were administered, and by 2013, 38 cycles had
been completed over 6 years of treatment (Fig. 2A). However, we could no longer control disease
activity using the same chemotherapy regimen. Moreover, primary tumour size evaluation became
difficult owing to massive pleural effusion; although not standard, we estimated the effect of
treatment using the increase and decrease of CEA as an index. CEA increased from a minimum of
4.6 ng/ml to 33.3 ng/ml in October 2013 during repeated cytotoxic chemotherapy. Although
his EGFR mutation status was unknown, we initiated erlotinib administration and the CEA level
decreased. After 8 weeks, the patient developed grade 3 acneiform rash, assessed using the
Common Terminology Criteria for Adverse Events version 5.0, and erlotinib administration was
discontinued for 6 weeks.
Patient's treatment course. (A) Treatment course using cytotoxic chemotherapy.
Chemotherapy with a combination of carboplatin (CBDCA) and docetaxel (DTX) was
performed beginning in August 2007. The tumours and pleural effusion repeatedly
decreased and increased in size. After each increase, 4 to 6 cycles of the same regimen
were performed until 2013, for a total of 38 cycles over 6 years. Each arrow indicates one
cycle. (B) Treatment course using epidermal growth factor receptor-tyrosine kinase
inhibitors (EGFR-TKIs). Administration of erlotinib began in October 2013. Skin disorders
interrupted its administration. The patient interrupted and resumed treatment
repeatedly. Because of the detection of the T790 M mutation in exon 20 in malignant
cells from the pleural effusion, erlotinib was changed to osimertinib in January 2017, and
the administration of the latter is ongoing.
Chest computed tomography (CT)
in August 2007. Chest CT scan
showing a nodule in the left lower
lobe with left pleural effusion.

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REFERENCES
[1]. Non-Small Cell Lung Cancer Collaborative Group. Chemotherapy and supportive care versus supportive
care alone for advanced non-small cell lung cancer. Cochrane Database Syst Rev 2010;12:CD007309.
[2]. Zhao D, Chen X, Qin N, et al. The prognostic role of EGFR-TKIs for patients with advanced non-small cell
lung cancer. Sci Rep 2017;12:40374.
[3]. Lin JJ, Cardarella S, Lydon CA, et al. Five-year survival in EGFR-mutant metastatic lung adenocarcinoma
treated with EGFR-TKIs. J Thorac Oncol 2016;11:556–65.
[4]. Kaira K, Takahashi T, Murakami H, et al. Long-term survivors of more than 5 years in advanced non-small
cell lung cancer. Lung Cancer 2010;67:120–3.
[5]. Kempf E, Planchard D, Le Chevalier T, et al. 10-year long-term survival of a metastatic EGFR-mutated
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[6]. Petrelli F, Coinu A, Cabiddu M, et al. Platinum rechallenge in patients with advanced NSCLC: a pooled
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Cancer 2010;69:315–8.
[8]. Giroux Leprieur E, Lavole A, Ruppert AM, et al. Factors associated with long-term survival of patients with
advanced non-small cell lung cancer. Respiratology 2012;17:134–42.
[9]. Van Damme V, Govaerts E, Nackaerts K, et al. Clinical factors predictive of long-term survival in advanced
non-small cell lung cancer. Lung Cancer 2013;79:73–6.
[10]. Ardizzoni A, Boni L, Tiseo M, et al. Cisplatin- versus carboplatin-based chemotherapy in first-line
treatment of advanced non-small-cell lung cancer: an individual patient data meta-analysis. J Natl Cancer
Inst 2007;99:847–57.
[11]. Fossella F, Pereira JR, von Pawel J, et al. Randomized, multinational, phase III study of docetaxel plus
platinum combinations versus vinorelbine plus cisplatin for advanced non-small-cell lung cancer: the TAX
326 study group. J Clin Oncol 2003;21:3016–24.
[12]. Yeo WL, Riely GJ, Yeap BY, et al. Erlotinib at a dose of 25 mg daily for non-small cell lung cancers with
EGFR mutations. J Thorac Oncol 2010;5:1048–53.
[13]. Yamada K, Aono H, Hosomi Y, et al. A prospective, multicenter phase II trial of low-dose erlotinib in non-
small cell lung cancer patients with EGFR mutations pretreated with chemotherapy: Thoracic Oncology
Research Group 0911. Eur J Cancer 2015;51:1904–10.
[14]. Hata A, Fujita S, Kaji R, et al. Dose reduction or intermittent administration of erlotinib: which is better
for patients suffering from intolerable toxicities? Intern Med 2013;52:599–603.
[15]. Mok TS, Wu Y-L, Ahn M-J, et al. Osimertinib or platinum-pemetrexed in EGFR T790M-positive lung cancer.
N Engl J Med 2017;376:629–40.
[16]. Zhou C, Wu YL, Chen G, et al. Final overall survival results from a randomized, phase III study of erlotinib
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(OPTIMAL, CTONG-0802). Ann Oncol 2015;26:1877–83.

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CASE STUDY - 2
CASE REPORT OF A 60-YEAR-OLD MALE WITH PROSTATE CANCERRT
CASE REPORT
ABSTRACT
Prostate cancer is a common cancer in elderly men and it frequently metastasizes to regional
lymph nodes and sometimes to bone. Very rarely in some of the cases it also shows involvement
of non-regional lymph nodes like supra-diaphragmatic lymph nodes. In our report, we present a
60-year-old male, initially misdiagnosed as Chronic Obstructive Pulmonary Disease (COPD) with
cervical lymph node involvement may be due to infective region or inflammatory pathology, which
was later found to have prostatic adenocarcinoma metastatic to supraclavicular lymph nodes.
Very less case reports are present which have shown similar presentations. So we would like to
highlight that prostatic carcinoma can be present in an atypical form also.
DETAILED ANALYSIS OF THE CASE
A 60-year-old male was referred to medicine department, initially for difficulty in breathing with
palpable painless left cervical mass, a chest X-ray was done, which showed COPD changes. He
also complained of eight kg weight loss, anorexia and weakness for approximately four months.
He denied any other subjective complaints including difficulty in swallowing, bone pain or urinary
symptoms. Physical examination was unremarkable except for an approximately 2 cm nontender,
firm mass in left cervical region, fixed to underlying structures. Patient’s past history was
unremarkable for any other surgical history or malignancy. His family history was non
contributory. During initial evaluation Digital Rectal Examination (DRE) and serum Prostate
Specific Antigen (PSA) was not done. Subsequently HRCT thorax and CECT whole abdomen was
done which showed possibility of skeletal metastasis and left hydroureteronephrosis [Table/Fig-
1]. USG guided FNAC of left supraclavicular node was done which showed possibility of
adenocarcinoma [Table/Fig-2,,3]3] which was immunohistochemically positive for PSA staining.
Subsequently patient was referred to our department of urology and DRE and PSA was done. DRE
showed bilateral hard, fixed and enlarged lobes of prostate. Serum PSA was >100 ng/ml. Biopsy
of prostate was done which revealed moderately differentiated carcinoma of prostate with
Gleason grade 4+3=7 [Table/Fig-4,,55].

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Detailed discussion with the patient was done and he declined any further investigations (bone
scan) and opted for surgical treatment (bilateral orchidectomy). In addition to this, patient was
also treated with tab bicalutamide 50 mg once daily. Patient was followed up at regular intervals.
His symptoms subsided and PSA decreased to <1 ng/ml. At 12 months follow up he remains
asymptomatic on androgen blockade.
DISCUSSION
Prostate cancer is the second most frequently diagnosed cancer of men after lung cancer and
the fifth most common cancer worldwide . The axial skeleton, the nodes of the pelvis and the
retroperitoneum are the most frequent sites of metastasis . Cervical lymph node involvement
can be due to various reasons like inflammation, lymphoma or metastasis. Prostatic carcinoma
generally metastasizes to regional lymph nodes and bone however in some cases it can present
[Table/Fig-2]:
FNAC specimen of neck mass (lymph node)
under low magnification (10 x) showing
malignant appearing cells.
[Table/Fig-3]:
FNAC specimen of neck mass (lymph node) under
high magnification (40 x) showing malignant
appearing cells.
[Table/Fig-4]:
Histopathological specimen showing moderately well
differentiated adenocarcinoma of prostate (10 x).
[Table/Fig-1]:
Coronal CT scan showing left
hydronephrosis and vertebral
lesion (curved arrow showing
hydronephrosis and straight
arrow showing vertebral lesion);
[Table/Fig-5]:
Histopathological specimen showing moderately well
differentiated adenocarcinoma of prostate (40 x).

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in many forms and one of the aspect is presentation in the form of neck mass as shown in this
report. Cervical lymphadenopathy can be the initial presentation of prostatic carcinoma in very
rare cases. The aim of our case report was to share our experience and focus on an unusual
presentation of prostate cancer.
Many theories suggest the mechanism of metastasis to the supradiaphragmatic lymph nodes
from genito-urinary malignancy. It has been suggested that cancer cells can lodge in the nodes,
near to entry of thoracic duct into left subclavian vein by retrograde spread and this mechanism
may be responsible for supra-diaphragmatic spread of prostatic cancer . Haematogenous spread
via the vertebral venous plexus fails to explain the predilection of this carcinoma to metastasize
to the left cervical region, whilst right side involvement is extremely uncommon . Prostate
carcinoma can also present in various atypical forms like huge abdominal lump, osteolytic bone
metastasis, peritoneal metastasis, malignant ascites . Rarely, it can also manifest its initial
presentation in the form of pneumothorax or anejaculation . However, asymptomatic neck mass
is more common atypical presentation and some of the case reports had presented these kind of
manifestation .
In the present report, patient had left supraclavicular lymphadenopathy with bone metasatsis
without having any other lymph node involvement. Unilateral involvement of cervical
lymphnode is more favorable of lymphatic spread in contrast to hematogenous spread in which
bilateral involvement is more common. It was suggested that prognosis of such kind of cases is
generally poor but Wang et al., followed such cases for 16 months and in their series none of
the cases showed progression. Similarly, we also did follow up for 12 month and in this period
our patient was clinical and biochemically quiescent. However, this can be one of the
limitations because carcinoma prostate is slow growing disease and if patient is followed for a
long duration then results can change. Serum PSA and DRE are the two most important methods
for diagnosis of prostatic carcinoma and in our report PSA and DRE was done after the FNAC of
neck mass, not at the initial stage. So our case report again highlights the fact that Serum PSA
and DRE should be considered in patients that present with such manifestations.
CONCLUSION
Prostate carcinoma is considered to be a disease of old age and can surprise clinicians by its
various manifestations. So any patient (specially elderly) presenting with a asymptomatic neck
mass with an unknown primary even in the absence of urinary symptoms should be considered as
a potential candidate for DRE and PSA estimation. Despite the rare presentation of prostatic
carcinoma in such forms, clinicians should have high index of suspicion coupled with having low
threshold for investigations for early and proper diagnosis of this disease and timely
management.

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BIBLIOGRAPHY
➢ Class 12 NCERT Textbook
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