3 What is prostate cancer?

To understand prostate cancer, it helps to know something about the prostate and nearby structures in the body.

About the prostate

The prostate is a gland found only in males. It is located in front of the rectum and below the urinary bladder. The size of the prostate varies with age. In younger men, it is about the size of a walnut, but it can be much larger in older men.

The prostate's job is to make some of the fluid that protects and nourishes sperm cells in semen, making the semen more liquid. Just behind the prostate are glands called seminal vesicles that make most of the fluid for semen. The urethra, which is the tube that carries urine and semen out of the body through the penis, goes through the center of the prostate.

The prostate starts to develop before birth. It grows rapidly during puberty, fueled by male hormones (called androgens) in the body. The main androgen, testosterone, is made in the testicles. The enzyme 5-alpha reductase converts testosterone intodihydrotestosterone (DHT). DHT is the main hormone that signals the prostate to grow.

The prostate usually stays at about the same size or grows slowly in adults, as long as male hormones are present.

Benign prostatic hyperplasia

The inner part of the prostate (around the urethra) often keeps growing as men get older, which can lead to a common condition called benign prostatic hyperplasia (BPH). In BPH, the prostate tissue can press on the urethra, leading to problems passing urine.

BPH is not cancer and does not develop into cancer. But it can be a serious medical problem for some men. If it requires treatment, medicines can often be used to shrink the size of the prostate or to relax the muscles in it, which usually helps with urine flow. If medicines aren't helpful, some type of surgery, such as a transurethral resection of the prostate (TURP) may be needed. (See the "Surgery for prostate cancer" section for a description of this procedure.)

Prostate cancer

Several types of cells are found in the prostate, but almost all prostate cancers develop from the gland cells. Gland cells make the prostate fluid that is added to the semen. The medical term for a cancer that starts in gland cells isadenocarcinoma.

Other types of cancer can also start in the prostate gland, including sarcomas, small cell carcinomas, and transitional cell carcinomas. But these types of prostate cancer are so rare that if you have prostate cancer it is almost certain to be an adenocarcinoma. The rest of this document refers only to prostate adenocarcinoma.

Some prostate cancers can grow and spread quickly, but most grow slowly. In fact, autopsy studies show that many older men (and even some younger men) who died of other diseases also had prostate cancer that never affected them during their lives. In many cases neither they nor their doctors even knew they had it.

Possible pre-cancerous conditions of the prostate

Some doctors believe that prostate cancer starts out as a pre-cancerous condition, although this is not yet known for sure.

Prostatic intraepithelial neoplasia (PIN)

In this condition, there are changes in how the prostate gland cells look under the microscope, but the abnormal cells don't look like they are growing into other parts of the prostate (like cancer cells would). Based on how abnormal the patterns of cells look, they are classified as:

• Low-grade PIN: the patterns of prostate cells appear almost normal
• High-grade PIN: the patterns of cells look more abnormal

PIN begins to appear in the prostates of some men as early as their 20s. Almost half of all men have PIN by the time they reach 50. Many men begin to develop low-grade PIN at an early age but do not necessarily develop prostate cancer. The importance of low-grade PIN in relation to prostate cancer is still unclear. If a finding of low-grade PIN is reported on a prostate biopsy, the follow-up for patients is usually the same as if nothing abnormal was seen.

If high-grade PIN has been found on your prostate biopsy, there is about a 20% to 30% chance that you also have cancer in another area of your prostate. This is why doctors often watch men with high-grade PIN carefully and may advise them to have a repeat prostate biopsy, especially if the original biopsy did not take samples from all parts of the prostate.

Proliferative inflammatory atrophy (PIA)

This is another finding that may be noted on a prostate biopsy. In PIA, the prostate cells look smaller than normal, and there are signs of inflammation in the area. PIA is not cancer, but researchers believe that PIA may sometimes lead to high-grade PIN, or perhaps to prostate cancer directly.
source : cancer.org

0 WHAT SIGNIFICANT EVENTS HAVE HAPPENED IN CANCER RESEARCH IN THE LAST 25 YEARS?

(1981). Many things have happened since then, of course, and everyone has their favorite list.

But looking back,
have several things, as listed below :


1. Cancer susceptibility genes. In 1981 we
knew that familial clustering of some cancers
occurred, for example, with colon cancer,
but the genes involved in this hadn’t been determined. The APC, BRCA-1,BRCA-2, and p53 inherited mutations, forexample, were not known at that time. Research
in this area has identified a number of genes involved in cancer susceptibility,andwithmoderncloningtechniques,more
are identified every few months.


2. The techniques of modern molecular biology were in their infancy at that time. Polymerase chain reaction (PCR), DNACHARACTERISTICS OF HUMAN CANCER 5microarrays, protein chips, and bioinformatics were not terms in anybody’sdictionary.


3. Genes involved in cancer initiation and
promotion were very poorly defined.  Althoughwe knew that chemicals and irradiation could damage DNA and initiate cancer in animals and humans, the specific genes altered were almost completely unknown. We now know a lot about the genes involved at various stages of a number of cancers. For example, the work of Bert Vogelstein and colleagues has defined a pathway sometimes called the ‘‘Vogelgram’’ for the progression of colon cancer (see Chapter 5). We knew that DNArepairwas important and that heritable conditions of defective DNA repair (e.g., xeroderma pigmentosum) could lead to cancer, but the ideas about the mechanisms of DNA repair were primitive.


4. The identification of oncogenes didn’treally start until the early 1980s. The srcgene was identified in 1976 by Stehelin
et al., and erb, myc, and myb oncogeneswere identified in the late 1970s, but thiswas about the limit of our knowledge(see Chapter 5).


5. The term tumor suppressor gene wasn’t even coined until the early 1980s,
 althoughtheir existence had been impliedfrom the cell fusion experiments ofHenry Harris, (Chapter 5) who showed
that if a normal cell was fused with amalignant cell, the phenotype was usuallynonmalignant. The RB gene was the first one cloned, in 1983 by Cavenee et al.(Chapter 5) p53 was originally thought of as an oncogene. It wasn’t realized until(1989) that wild-type p53 could actually suppress malignant transformation. Anumber of tumor suppressor genes have,of course, been identified since then.


6. Starting in the 1970s, cell cycle checkpoints were identified in yeast by Lee Hartwell and colleagues, but the identification of human homologs of these genes didn’t occur until the late 1980s (seeChapter4).


7. Tumor immunology was still poorly understood in 1981—both the mechanism of the immune response and the ability to manipulate it with cytokines, activated dendritic cells, and vaccines. Such manipulation was not in the treatment armamentarium.


8. The first treatment of a patient with gene therapy occurred in 1990. Several gene therapy clinical trials for cancer are under way and some gene therapy modalities will likely be approved in the next few years.


9. The viral etiology of cancer was still being widely debated in 1981. The involvement of Epstein-Barr virus in Burkitt’s lymphoma and of hepatitis B virus in liver cancer was becoming accepted, but the role of viruses in these diseases and in cervical cancer, Kaposis’ sarcoma, and in certain T-cell lymphomas became clearer much later.


10. Although some growth factors that affect cancer cell replication, such as IGF-1 and IGF-2, FGF, NGF, PDGF, and EGF, were known in 1981, knowledge about their receptors and signal transduction mechanisms was primitive indeed. Tumor growth factor a was known as sarcoma growth factor (SGF), and the existence of its partner, TGF-b, was only implied from what was thought to be a contaminating HPLC peak from the purification procedure. The explosion of knowledge about signal transduction mechanisms and how these pathways interact has been a tremendous boon to our understanding of how cells respond to signals in their environment and communicate with each other.


11. Knowledge about the regulation of gene expression has greatly increased in the past 25 years, on the basis of our current information on the packaging of chromatin, transcription factors, coinducers and corepressors, and inhibitory RNA (siRNA).


12. While not topics discussed in detail in the earlier editions of Cancer Biology, advances in diagnostic imaging such as magnetic resonanceimaging (MRI), computed tomography (CT), and positron emission tomography (PET) have significantly im- 6 CANCER BIOLOGY proved cancer diagnosis. Improved radiation therapy, combined modality therapy, bone marrow transplant, and supportive care have also improved significantly

0 What are the most common types of childhood cancers?

The types of cancers that occur most often in children are different from those seen in adults. The most common cancers of children are:

• Leukemia
• Brain and other nervous system tumors
• Neuroblastoma
• Wilms tumor
• Lymphoma
• Rhabdomyosarcoma
• Retinoblastoma
• Bone cancer

Other types of cancers are rare in children, but they do happen sometimes. In very rare cases, children may even develop cancers that are much more common in adults.

Leukemia

Leukemias are the most common childhood cancers. They account for about 34% of all cancers in children. The most common types in children are acute lymphocytic leukemia (ALL) and acute myelogenous leukemia (AML). Leukemia may cause bone and joint pain, weakness, bleeding, fever, weight loss, and other symptoms.

.

Brain and nervous system tumors

Brain and other nervous system tumors are the second most common cancers in children, and make up about 27% of childhood cancers. There are many types of brain tumors, and the treatment and outlook for each is different. Most brain tumors in children start in the lower parts of the brain, such as the cerebellum or brain stem. They can cause headaches, nausea, vomiting, blurred or double vision, dizziness, and trouble walking or handling objects. Adults are more likely to develop cancers in upper parts of the brain. Spinal cord tumors are less common than brain tumors in both children and adults.

.

Neuroblastoma

Neuroblastoma is a form of cancer that starts in certain types of nerve cells found in a developing embryo or fetus. It accounts for about 7% of childhood cancers. This type of cancer occurs in infants and young children. It is rarely found in children older than 10. This tumor can start anywhere but is usually in the belly (abdomen) and is noticed as swelling. It can also cause bone pain and fever.

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Wilms tumor

Wilms tumor is a cancer that starts in one, or rarely, both kidneys. It is most often found in children about 3 years old, and is uncommon in children older than age 6. It can show up as a swelling or lump in the belly (abdomen). Sometimes the child may have other symptoms, like fever, pain, nausea, or poor appetite. Wilms tumor accounts for about 5% of childhood cancers.

.

Lymphoma

These are cancers that start in lymph tissues, like the lymph nodes, tonsils, and thymus. They may spread to bone marrow and other organs, which can cause different symptoms depending on where the cancer is growing. Lymphomas can cause fever, sweats, weakness, and swollen lymph nodes in the neck, armpit, or groin.

There are 2 main types of lymphoma: Hodgkin lymphoma (sometimes called Hodgkin disease) and non-Hodgkin lymphoma. Both types can occur in both children and adults.

Hodgkin lymphoma accounts for about 4% of childhood cancers. It is more common, though, in 2 age groups: early adulthood (age 15 to 40, usually people in their 20s) and late adulthood (after age 55). Hodgkin lymphoma is rare in children younger than 5 years of age. This is one type of cancer that is very similar in children and adults, including which types of treatment work best.

Non-Hodgkin lymphoma also makes up about 4% of childhood cancers. It is more likely to occur in younger children than is Hodgkin lymphoma, but it is still rare in children younger than 3. The most common types of non-Hodgkin lymphoma in children are different from those in adults. These cancers often grow quickly and require intensive treatment, but they also tend to respond better to treatment than most non-Hodgkin lymphomas in adults.

Rhabdomyosarcoma

Rhabdomyosarcoma starts in cells that normally develop into skeletal muscles. (These are the muscles that we control to move parts of our body.) It can happen in the head and neck, groin, belly (abdomen), pelvis, or in an arms or leg. It may cause pain, swelling (a lump), or both. This is the most common type of soft tissue sarcoma in children. It makes up about 3% of childhood cancers.

.

Retinoblastoma

Retinoblastoma is a cancer of the eye. It accounts for about 3% of childhood cancers. It usually occurs in children around the age of 2, and is seldom found in children older than 6. Retinoblastomas are usually found because a parent or doctor notices a child's eye looks unusual. Normally when you shine a light in a child's eye, the pupil (the dark spot in the center of the eye) looks red because of the blood in vessels in the back of the eye. In an eye with retinoblastoma, the pupil often looks white or pink. This white glare of the eye may be noticed after a flash picture is taken.

For more information see our document called .

Bone cancers

Primary bone cancers (cancers that start in the bones) occur most often in older children and teens, but they can develop at any age.

Primary bone cancer is different from metastatic bone cancer, which is cancer that started somewhere else in the body and has spread to the bone. Metastatic bone cancer is more common than primary bone cancer because many types of cancer (including many cancers in adults) can spread to the bone.

Two main types of primary bone cancers occur in children:

Osteosarcoma accounts for about 3% of all new childhood cancer cases in the United States. It is most common in teens, and usually develops in areas where the bone is growing quickly, such as near the ends of the long bones in the legs or arms. It often causes no pain or symptoms until swelling starts, but sometimes there is bone pain that gets worse at night or with activity.
Ewing sarcoma is a less common primary bone cancer, which can also cause bone pain. It is most often found in young teens. The most common places for it to start are the bones in the pelvis, the chest wall (such as the ribs or shoulder blades), or in the middle of the long leg bones. Ewing sarcoma accounts for about 1% of childhood cancers.
source : cancer.org

0 CANCER TYPES >>>

1. Adrenal Cortical Cancer
2. Advanced Cancer
3. Anal Cancer
4. Aplastic Anemia
5. Bile Duct Cancer
6. Bladder Cancer
7. Bone Cancer
8. Bone Metastasis
9. Brain/CNS Tumors In Adults
10. Brain/CNS Tumors In Children
11. Breast Cancer
12. Breast Cancer In Men
13. Cancer in Children
14. Cancer of Unknown Primary
15. Castleman Disease
16. Cervical Cancer
17. Colon/Rectum Cancer
18. Endometrial Cancer
19. Esophagus Cancer
20. Ewing Family Of Tumors
21. Eye Cancer
22. Gallbladder Cancer
23. Gastrointestinal Carcinoid Tumors
24. Gastrointestinal Stromal Tumor (GIST)
25. Gestational Trophoblastic Disease
26. Hodgkin Disease
27. Kaposi Sarcoma
28. Kidney Cancer
29. Laryngeal and Hypopharyngeal Cancer
30. Leukemia - Acute Lymphocytic (ALL) in Adults
31. Leukemia - Acute Myeloid (AML)
32. Leukemia - Chronic Lymphocytic (CLL)
33. Leukemia - Chronic Myeloid (CML)
34. Leukemia - Chronic Myelomonocytic (CMML)
35. Leukemia in Children
36. Liver Cancer
37. Lung Cancer - Non-Small Cell
38. Lung Cancer - Small Cell
39. Lung Carcinoid Tumor
40. Lymphoma of the Skin
41. Malignant Mesothelioma
42. Multiple Myeloma
43. Myelodysplastic Syndrome
44. Nasal Cavity and Paranasal Sinus Cancer
45. Nasopharyngeal Cancer
46. Neuroblastoma
47. Non-Hodgkin Lymphoma
48. Non-Hodgkin Lymphoma In Children
49. Oral Cavity and Oropharyngeal Cancer
50. Osteosarcoma
51. Ovarian Cancer
52. Pancreatic Cancer
53. Penile Cancer
54. Pituitary Tumors
55. Prostate Cancer
56. Retinoblastoma
57. Rhabdomyosarcoma
58. Salivary Gland Cancer
59. Sarcoma - Adult Soft Tissue Cancer
60. Skin Cancer - Basal and Squamous Cell
61. Skin Cancer - Melanoma
62. Small Intestine Cancer
63. Stomach Cancer
64. Testicular Cancer
65. Thymus Cancer
66. Thyroid Cancer
67. Uterine Sarcoma
68. Vaginal Cancer
69. Vulvar Cancer
70. Waldenstrom Macroglobulinemia
71. Wilms Tumor

source : cancer.org

0 What is cancer?

What is cancer?

Cancer begins when cells in a part of the body start to grow out of control. There are many kinds of cancer, but they all start because of out-of-control growth of abnormal cells. To learn more about how cancer forms and grows, see our document called ?

Cancer is the second leading cause of death in the United States. About one-half of all men and one-third of all women in the US will develop cancer during their lifetimes. Today, millions of people are living with cancer or have had cancer.

Oldest descriptions of cancer

Human beings have had cancer throughout recorded history. So it’s no surprise that from the dawn of history people have written about cancer. Some of the earliest evidence of cancer is found among fossilized bone tumors, human mummies in ancient Egypt, and ancient manuscripts. Growths suggestive of the bone cancer called osteosarcoma have been seen in mummies. Bony skull destruction as seen in cancer of the head and neck has been found, too.

Our oldest description of cancer (although the word cancer was not used) was discovered in Egypt and dates back to about 3000 BC. It is called the Edwin Smith Papyrus, and is a copy of part of an ancient Egyptian textbook on trauma surgery. It describes 8 cases of tumors or ulcers of the breast that were treated by cauterization, with a tool called the fire drill. The writing says about the disease, “There is no treatment.”

Origin of the word cancer

The origin of the word cancer is credited to the Greek physician Hippocrates (460-370 BC), who is considered the “Father of Medicine.” Hippocrates used the terms carcinos and carcinoma to describe non-ulcer forming and ulcer-forming tumors. In Greek, these words refer to a crab, most likely applied to the disease because the finger-like spreading projections from a cancer called to mind the shape of a crab. The Roman physician, Celsus (28-50 BC), later translated the Greek term intocancer, the Latin word for crab. Galen (130-200 AD), another Roman physician, used the word oncos (Greek for swelling) to describe tumors. Although the crab analogy of Hippocrates and Celsus is still used to describe malignant tumors, Galen’s term is now used as a part of the name for cancer specialists — oncologists.

source : cancer.org

0 Modern knowledge and cancer cause

Modern knowledge and cancer cause

By the middle of the 20th century, scientists had the instruments they needed to work on some of the complex problems of chemistry and biology that remained unsolved. James Watson and Francis Crick, who received a Nobel Prize in 1962 for their work, had discovered the exact chemical structure of DNA, the basic material in genes.

DNA was found to be the basis of the genetic code that gives orders to all cells. After learning how to translate this code, scientists were able to understand how genes worked and how they could be damaged by mutations (changes or mistakes in genes). These modern techniques of chemistry and biology answered many complex questions about cancer.

Scientists already knew that cancer could be caused by chemicals, radiation, and viruses, and that sometimes cancer seemed to run in families. But as the understanding of DNA and genes increased, they learned that it was the damage to DNA by chemicals and radiation, or the introduction of new DNA sequences by viruses that often led to the development of cancer. It became possible to pinpoint the exact site of the damage on a specific gene.

Scientists discovered that sometimes defective genes are inherited, and sometimes these inherited genes are defective at the same points that chemicals exerted their effect. In other words, most of the things that caused cancer (carcinogens) caused genetic damage (mutations), these mutations led to abnormal groups of cells (called clones), the mutant clones evolved to even more malignant clones over time, and the cancer progressed by more and more genetic damage and mutations. Normal cells with damaged DNA die; cancer cells with damaged DNA do not. The discovery of this critical difference answered many questions that had troubled scientists for many years.

Oncogenes and tumor suppressor genes

During the 1970s, scientists discovered 2 particularly important families of genes related to cancer: oncogenes and tumor suppressor genes.

Oncogenes are mutated forms of genes that cause normal cells to grow out of control and become cancer cells. They are mutations of certain normal genes of the cell called proto-oncogenes. Proto-oncogenes are the genes that normally control how often a cell divides and the degree to which it differentiates (or specializes).

Tumor suppressor genes are normal genes that slow down cell division, repair DNA errors, and tell cells when to die (a process known as apoptosis or programmed cell death). When tumor suppressor genes don’t work properly, cells can grow out of control, which can lead to cancer.

It may be helpful to think of a cell as a car. For it to work properly, there need to be ways to control how fast it goes. A proto-oncogene normally functions in a way that is similar to a gas pedal — it helps the cell grow and divide. An oncogene could be compared to a gas pedal that is stuck down, which causes the cell to divide out of control. A tumor suppressor gene is like the brake pedal on a car. It normally keeps the cell from dividing too quickly just as a brake keeps a car from going too fast. When something goes wrong with the gene, such as a mutation, cell division can get out of control.

Slowly, medical scientists are identifying the oncogenes and tumor suppressor genes that are damaged by chemicals or radiation and those that, when inherited, can lead to cancer. For example, the 1990s discovery of 2 genes that cause some breast cancers, BRCA1 and BRCA2, represents considerable promise because these genes can be used to identify people who have a higher probability of developing breast cancer.

Other genes have been discovered that are associated with some cancers that run in families, such as cancers of the colon, rectum, kidney, ovary, thyroid, pancreas, and skin melanoma. Familial cancer is not nearly as common as spontaneous cancer. It is less than 15% of all cancers. Still, it is important to understand these cancers because with continued research in genetics we may be able to identify people at very high risk.

Once researchers recognized the importance of specific genetic changes in cancer, they soon began working to developtargeted therapies (drugs or substances that interfere with specific molecules) to overcome the effects of these changes in tumor suppressor genes and oncogenes.

source : cancer.org