Malignancy (from
the Latin roots mal- = "bad" and -ignis =
"fire") is the tendency of a medical condition, especially tumors, to
become progressively worse and to potentially result in death. It is
characterized by the properties of anaplasia, invasiveness, and metastasis.[1] Malignant is
a corresponding adjectival medical term used to describe a severe and
progressively worsening disease. The term is most familiar as a description
of cancer.
A malignant tumor may be contrasted with a non-cancerous benign tumor in that a malignancy is not
self-limited in its growth, is capable of invading into adjacent tissues, and
may be capable of spreading to distant tissues (metastasizing), while abenign tumor has none of those
properties. Malignant tumor is synonymous with cancer. Uses of"malignant" in oncology:
§ Malignant ascites
Non-oncologic
disorders referred to as "malignant":
Cancers are classified by the type of cell that resembles the tumor and, therefore, the tissue presumed
to be the origin of the tumor. These are the histology and the location,
respectively. Examples of general categories include:
§ Carcinoma: Malignant tumors derived from epithelial cells. This group represents the most common cancers,
including the common forms of breast, prostate, lung and colon cancer.
§ Germ cell tumor: Tumors derived from totipotent cells. In adults most often
found in the testicleand ovary; in fetuses, babies,
and young children most often found on the body midline, particularly at the
tip of the tailbone; in horses most often found at the poll (base of the
skull).
§ Blastic tumor or blastoma: A tumor (usually malignant) which resembles an immature or
embryonic tissue. Many of these tumors are most common in children.
Malignant tumors (cancers) are usually named using -carcinoma, -sarcoma or -blastoma as
a suffix, with the Latin or Greek word for the organ of origin as the root. For
instance, a cancer of the liver is called hepatocarcinoma; a cancer of the fat cells
is called liposarcoma. For common cancers, the English organ name
is used. For instance, the most common type of breast cancer is called ductal carcinoma of the
breast or mammary ductal carcinoma. Here, the
adjective ductal refers to the appearance of the cancer under
the microscope, resembling normal breast ducts.
Benign tumors (which are not cancers) are named
using -oma as a suffix with the organ name as the root. For
instance, a benign tumor of the smooth muscle of the uterus is called leiomyoma (the
common name of this frequent tumor is fibroid). Unfortunately, some
cancers also use the -omasuffix, examples being melanoma and seminoma.
Roughly, cancer symptoms can be divided into three groups:
§ Local symptoms: unusual lumps or swelling (tumor),hemorrhage (bleeding), pain and/or ulceration. Compression of surrounding tissues may cause
symptoms such as jaundice (yellowing the eyes and skin).
§ Symptoms
of metastasis (spreading): enlarged lymph nodes, cough and hemoptysis, hepatomegaly (enlargedliver), bone pain, fracture of affected bones andneurological symptoms. Although advanced cancer may cause pain, it is often not the
first symptom.
§ Systemic symptoms: weight loss, poor appetite, fatigueand cachexia (wasting), excessive sweating (night sweats), anemia and specific paraneoplastic
phenomena, i.e. specific conditions that are due to an active
cancer, such as thrombosis or hormonal changes.
Every symptom in the above list can be caused by a variety of
conditions (a list of which is referred to as the differential diagnosis). Cancer may be a common or uncommon cause of
each item.
Causes
Cancers are primarily an environmental disease with 90-95% of
cases due to lifestyle and environmental factors and 5-10% due to genetics.[4] Common environmental factors that lead to cancer death
include: tobacco (25-30%), diet and obesity (30-35%), infections (15-20%), radiation, radonexposure, stress, lack of physical activity, environmental
pollutants.[4] The virtual absence of cancerous malignancies in ancient
human remains suggests that cancer is mainly a man-made disease of the Industrial Age caused by environmental changes and the
modern diet.[6]
Chemicals
Further
information: Carcinogen
The incidence of lung
cancer is highly correlated with smoking. Source:NIH.
Cancer pathogenesis is traceable back to DNA mutationsthat impact cell growth and metastasis.
Substances that cause DNA mutations are known as mutagens, and mutagens that
cause cancers are known as carcinogens. Particular substances have been linked
to specific types of cancer. Tobacco smoking is associated with many forms of cancer,[7] and causes 90% of lung cancer.[8] Prolonged exposure to asbestos fibers is associated withmesothelioma.[9][10]
Many mutagens are also carcinogens, but some carcinogens are not mutagens. Alcohol is an example of a chemical carcinogen that is not a
mutagen.[11] Such chemicals may promote cancers through stimulating the
rate of cell division. Faster rates of replication leaves less time for repair
enzymes to repair damaged DNA duringDNA replication, increasing the likelihood of a mutation.
Decades of research has demonstrated the link between tobacco use and cancer in the lung, larynx, head, neck, stomach, bladder, kidney, oesophagus and pancreas.[12] Tobacco smoke contains over fifty known carcinogens,
including nitrosamines and polycyclic aromatic hydrocarbons.[13] Tobacco is responsible for about one in three of all cancer
deaths in the developed world,[7] and about one in five
worldwide.[13] Indeed, lung cancer death rates in the United States have mirrored smoking patterns, with increases in smoking followed by dramatic
increases in lung cancer death rates and, more recently[when?], decreases in smoking followed by decreases in lung cancer death
rates in men. However, the numbers of smokers worldwide is still rising,
leading to what some organizations have described as the tobacco
epidemic.[14]
Cancer related to ones occupation is believed to represent between
2-20% of all cases.[15]
Ionizing radiation
Sources of ionizing radiation, such as radon gas, can cause
cancer. Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies.[16] One report estimates that approximately 29 000 future
cancers could be related to the approximately 70 million CT scansperformed in the US in 2007.[17] It is estimated that 0.4% of current cancers in the United
States are due to CTs performed in the past and that this may increase to as
high as 1.5-2% with 2007 rates of CT usage.[18]
Non-ionizing radio frequency radiation from mobile phones and other similar RF sources has also been proposed as a cause of cancer, but
there is currently little established evidence of such a link.[19]
Infection
Some cancers can be caused by infection.[20] This is especially true in animals such as birds, but also in humans, with viruses
responsible for up to 20% of human cancers worldwide.[21] These includehuman papillomavirus (cervical carcinoma), human polyomaviruses (mesothelioma, brain tumors),Epstein-Barr virus (B-cell lymphoproliferative disease and nasopharyngeal
carcinoma), Kaposi's
sarcoma herpesvirus (Kaposi's Sarcoma and primary effusion lymphomas), hepatitis B and hepatitis Cviruses (hepatocellular
carcinoma), Human
T-cell leukemia virus-1 (T-cell
leukemias), and Helicobacter pylori (gastric carcinoma).[21]
Experimental and epidemiological data imply a causative role for
viruses and they appear to be the second most important risk factor for cancer
development in humans, exceeded only by tobacco usage.[22] The mode of virally induced tumors can be divided into
two, acutely transforming or slowly transforming.
In acutely transforming viruses, the virus carries an overactive oncogene
called viral-oncogene (v-onc), and the infected cell is transformed as soon as
v-onc is expressed. In contrast, in slowly transforming viruses, the virus
genome is inserted near a proto-oncogene in the host genome. The viral promoter or other transcription regulation elements
then cause overexpression of that proto-oncogene. This induces uncontrolled
cell division. Because the site of insertion is not specific to proto-oncogenes
and the chance of insertion near any proto-oncogene is low, slowly transforming
viruses will cause tumors much longer after infection than the acutely
transforming viruses.
Hepatitis viruses, including hepatitis B and hepatitis C, can induce a chronic viral infection that leads to liver
cancer in 0.47% of hepatitis B patients per year (especially in Asia, less so in North
America), and in 1.4% of hepatitis C carriers per year. Liver cirrhosis, whether from chronic
viral hepatitis infection or alcoholism, is associated with the development
of liver
cancer, and the combination of
cirrhosis and viral hepatitis presents the highest risk of liver
cancer development.
Worldwide, liver
cancer is one of the most
common, and most deadly, cancers due to a huge burden of viral hepatitistransmission and disease.
Advances in cancer research have made a vaccine designed to
prevent cancers available. In 2006, theU.S. Food and Drug Administration approved a human papilloma virus vaccine, called Gardasil. The vaccine protects against
6,11,16,18 strains of HPV, which together cause 70% of cervical cancers and 90%
of genital warts. It also lists vaginal and vulvar cancers as being protected.
In March 2007, the USCenters for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices(ACIP) officially recommended that females aged
11–12 receive the vaccine, and indicated that females as young as age 9 and as
old as age 26 are also candidates for immunization. There is a second vaccine
from Cervarix which protects against the more
dangerous HPV 16,18 strains only. In 2009, Gardasil was approved for protection
against genital warts. In 2010, the Gardasil vaccine was approved for
protection against anal cancer for males and reviewers stated there was no
anatomical, histological or physiological anal differences between the genders
so females would also be protected.
In addition to viruses, researchers have noted a connection
between bacteria and certain
cancers. The most prominent
example is the link between chronic infection of the wall of the stomach withHelicobacter pylori and gastric cancer.[23][24] Although only a minority of those infected withHelicobacter go
on to develop cancer, since this pathogen is quite common it is probably
responsible for most of these cancers.[25]
HIV is associated with
a number of malignancies, including Kaposi's sarcoma, non-Hodgkin's lymphoma, and HPV-associated malignancies
such as anal cancer and cervical cancer. AIDS-defining illnesses have
long included these diagnoses. The increased incidence of malignancies in HIV
patients points to the breakdown of immune surveillance as a possible etiology
of cancer.[26] Certain other immune deficiency states (e.g. common variable immunodeficiency and IgA deficiency) are also associated with
increased risk of malignancy.[27]
Heredity
Most forms of cancer are sporadic, meaning that there
is no inherited cause of the cancer. There are, however, a number of
recognised syndromes where there is an inherited predisposition
to cancer, often due to a defect in a gene that protects against tumor formation. Famous examples are:
§ certain inherited mutations in the genes BRCA1 and BRCA2 are associated with an elevated risk ofbreast cancer and ovarian cancer
§ Li-Fraumeni syndrome (various tumors such as osteosarcoma, breast cancer, soft tissue sarcoma,brain tumors) due to mutations of p53
§ Familial adenomatous polyposis an inherited mutation of the APC gene that
leads to early onset ofcolon carcinoma.
§ Hereditary nonpolyposis colorectal cancer (HNPCC, also known as Lynch syndrome) can
include familial cases of colon cancer, uterine cancer, gastric cancer, and ovarian cancer, without a preponderance of colon polyps.
§ Retinoblastoma, when occurring in young children, is due to a
hereditary mutation in the retinoblastoma gene.
§ Down syndrome patients, who have an extra chromosome 21, are known to develop malignancies such
as leukemia and testicular cancer, though the reasons for this difference are not
well understood.
Other causes
Excepting the rare transmissions that occur with pregnancies and
only a marginal few organ donors, cancer is generally not a transmissible disease. The main reason for this is tissue graft
rejection caused by MHC incompatibility.[28] In humans and other vertebrates, the immune system uses MHC
antigens to differentiate between "self" and "non-self"
cells because these antigens are different from person to person. When non-self
antigens are encountered, the immune system reacts against the appropriate cell.
Such reactions may protect against tumour cell engraftment by eliminating
implanted cells. In the United States, approximately 3,500 pregnant women have
a malignancy annually, and transplacental transmission of acute leukaemia, lymphoma, melanoma and carcinoma from mother to fetus has been observed.[28] The development of donor-derived tumors from organ
transplants is exceedingly rare. The main cause of organ transplant associated
tumors seems to be malignant melanoma, that was undetected at the time of organ
harvest.[29] though other cases exist[30] In fact, cancer from one organism will usually grow in
another organism of that species, as long as they share the same histocompatibility genes,[31] proven using mice; however this would never happen in a
real-world setting except as described above.
In non-humans, a few types of transmissible cancer have been described, wherein the cancer
spreads between animals by transmission of the tumor cells themselves. This
phenomenon is seen in dogs with Sticker's sarcoma, also known as canine transmissible venereal
tumor,[32] as well as Devil
facial tumour disease in Tasmanian devils.
Pathophysiology
Main article: Oncogenesis
Cancers are caused by a
series of mutations. Each mutation alters the behavior of the cell somewhat.
Cancer is fundamentally a disease of regulation of tissue growth.
In order for a normal cell to transform into a cancer cell, genes which regulate
cell growth and differentiation must be altered.[33] Genetic changes can occur at many levels, from gain or loss
of entire chromosomes to a mutation affecting a single DNA nucleotide. There are two broad categories of genes which are affected by
these changes. Oncogenes may be
normal genes which are expressed at inappropriately high levels, or altered
genes which have novel properties. In either case, expression of these genes
promotes the malignant phenotype of cancer cells. Tumor suppressor genes are genes which inhibit cell division,
survival, or other properties of cancer cells. Tumor suppressor genes are often
disabled by cancer-promoting genetic changes. Typically, changes in many genes
are required to transform a normal cell into a cancer cell.[34]
There is a diverse classification scheme for the various genomic
changes which may contribute to the generation of cancer cells. Most of these
changes are mutations, or changes in the nucleotidesequence of genomic DNA. Aneuploidy, the presence of an abnormal number
of chromosomes, is one genomic change which is not a mutation, and may involve
either gain or loss of one or morechromosomes through errors in mitosis.
Large-scale mutations involve the deletion or gain of a portion of
a chromosome. Genomic amplification occurs when a cell gains many copies
(often 20 or more) of a small chromosomal locus, usually containing one or more
oncogenes and adjacent genetic material.Translocation occurs when two separate chromosomal
regions become abnormally fused, often at a characteristic location. A
well-known example of this is the Philadelphia
chromosome, or translocation of
chromosomes 9 and 22, which occurs in chronic
myelogenous leukemia, and results in
production of the BCR-abl fusion protein, an oncogenic tyrosine kinase.
Small-scale mutations include point mutations, deletions, and
insertions, which may occur in thepromoter of a gene and affect its expression, or may occur in the gene's coding sequence and alter the function or stability of
its protein product. Disruption of a single gene may also result fromintegration of genomic material from a DNA virus or retrovirus, and such an event may also result in the expression of viral
oncogenes in the affected cell and its descendants.
Anything which replicates (living cells) will probabilistically suffer from errors (mutations). Unless
error correction and prevention is properly carried out, the errors will
survive, and might be passed along todaughter cells. Normally, the body safeguards against cancer
via numerous methods, such as:apoptosis, helper
molecules (some DNA polymerases), possibly senescence, etc. However these error-correction methods often fail in small
ways, especially in environments that make errors more likely to arise and
propagate. For example, such environments can include the presence of
disruptive substances called carcinogens, or periodic injury (physical, heat, etc.), or environments that
cells did not evolve to withstand, such as hypoxia[35] (see subsections). Cancer is thus a progressive disease,
and these progressive errors slowly accumulate until a cell begins to act
contrary to its function in the organism.
The errors which cause cancer are often self-amplifying,
eventually compounding at an exponential rate. For example:
§ A mutation in the error-correcting machinery of
a cell might cause that cell and its children to accumulate errors more rapidly
§ A mutation in signaling (endocrine) machinery of the cell can send error-causing signals to nearby
cells
§ A mutation might cause cells to become neoplastic, causing them to migrate and
disrupt more healthy cells
§ A mutation may cause the cell to become immortal
(see telomeres), causing them to disrupt healthy cells forever
Thus cancer often explodes in something akin to a chain reaction caused by a few errors, which compound
into more severe errors. Errors which produce more errors are effectively the
root cause of cancer, and also the reason that cancer is so hard to treat: even
if there were 10,000,000,000 cancerous cells and one killed all but 10 of those
cells, those cells (and other error-prone precancerous cells) could still
self-replicate or send error-causing signals to other cells, starting the
process over again. This rebellion-like scenario is an undesirable survival of the
fittest, where the driving
forces of evolution work against the body's design and
enforcement of order. In fact, once cancer has begun to develop, this same
force continues to drive the progression of cancer towards more invasive
stages, and is called clonal evolution.[36]
Research about cancer causes often falls into the following
categories:
§ Agents (e.g. viruses) and events (e.g.
mutations) which cause or facilitate genetic changes in cells destined to
become cancer.
§ The precise nature of the genetic damage, and
the genes which are affected by it.
§ The consequences of those genetic changes on the
biology of the cell, both in generating the defining properties of a cancer
cell, and in facilitating additional genetic events which lead to further
progression of the cancer.
Prevention
Cancer prevention is defined as active measures to decrease the
incidence of cancer.[37] Greater than 30% of cancer is preventable via avoiding risk
factors including: tobacco, overweight or obesity, low fruit and vegetable intake, physical inactivity, alcohol, sexually transmitted infection, air pollution.[38]This can be accomplished by avoiding carcinogens or altering their metabolism, pursuing a lifestyle or diet that modifies cancer-causing
factors and/or medical intervention (chemoprevention, treatment of pre-malignant lesions). The epidemiological concept of "prevention" is
usually defined as either primary prevention, for people who have not been diagnosed with a
particular disease, or secondary prevention, aimed at reducing recurrence or complications
of a previously diagnosed illness.
But the EPIC study published in 2010, tracking the eating habits
of 478,000 Europeans suggested that consuming lots of fruits and vegetables has
little if any effect on preventing cancer.[39]
Modifiable factors
See also: Alcohol and cancer
The vast majority of cancer risk factors are environmental or
lifestyle-related, leading to the claim that cancer is a largely preventable
disease.[40] Examples of modifiable cancer risk factors include alcoholconsumption
(associated with increased risk of oral, esophageal, breast, and other
cancers), smoking (80% of women with lung cancer have smoked in the past, and
90% of men[41]), physical inactivity (associated with increased risk of colon,
breast, and possibly other cancers), and being overweight /obese (associated with colon, breast,
endometrial, and possibly other cancers). Based on epidemiologic evidence, it
is now thought that avoiding excessive alcohol consumption may contribute to
reductions in risk of certain cancers; however, compared with tobacco exposure,
the magnitude of effect is modest or small and the strength of evidence is
often weaker. Other lifestyle and environmental factors known to affect cancer
risk (either beneficially or detrimentally) include certain sexually
transmitted diseases (such as those conveyed by the human papillomavirus), the use of exogenous hormones, exposure
to ionizing radiation and ultraviolet radiation from the sun or fromtanning beds, and certain occupational and chemical exposures.
Every year, at least 200,000 people die worldwide from cancer
related to their workplace.[42] Millions of workers run the risk of developing cancers such
as lung cancer and mesothelioma from inhalingasbestos fibers and tobacco smoke, or leukemia from exposure to benzene at their workplaces.[42]Currently, most cancer deaths caused by occupational risk factors
occur in the developed world.[42] It is estimated that approximately 20,000 cancer deaths and
40,000 new cases of cancer each year in the U.S. are attributable to occupation.[43]
Diet
Main article: Diet and cancer
The consensus on diet and cancer is that obesity increases the risk of developing cancer. Particular dietary
practices often explain differences in cancer incidence in different countries
(e.g. gastric canceris more common in Japan, while colon cancer is more common in the United States. In this example the
preceding consideration of Haplogroups are excluded). Studies have
shown that immigrants develop the risk of their new country, often within one
generation, suggesting a substantial link between diet and cancer.[44] Whether reducing obesity in a population also reduces cancer
incidence is unknown.
Despite frequent reports of particular substances (including
foods) having a beneficial or detrimental effect on cancer risk, few of these
have an established link to cancer. These reports are often based on studies in
cultured cell media or animals. Public health recommendations cannot be made
based on these studies until they have been validated in an observational (or
occasionally a prospective interventional) trial in humans.
Proposed dietary interventions for primary cancer risk reduction
generally gain support from epidemiological association studies. Examples of
such studies include reports that reduced meat consumption is associated with
decreased risk of colon cancer,[45] and reports that consumption
of coffee is associated with a reduced risk of liver cancer.[46] Studies have linked consumption of grilled meat to an
increased risk of stomach cancer,[47] colon cancer,[48] breast cancer,[49] and pancreatic cancer,[50] a phenomenon which could be due to the presence of
carcinogens such as benzopyrene in
foods cooked at high temperatures.
A recent study analysed the correlation between many factors and
cancer and concluded that the major contributory dietary factor was animal
protein, whereas plant protein did not have an effect. Animal studies confirmed
the mechanism by showing that reducing the proportion of animal protein
switched off both the initiation and promotion stages. [51]
A 2005 secondary prevention study showed that consumption of a
plant-based diet and lifestyle changes resulted in a reduction in cancer
markers in a group of men with prostate cancer who were using no conventional
treatments at the time.[52] These results were amplified by a 2006 study. Over 2,400
women were studied, half randomly assigned to a normal diet, the other half
assigned to a diet containing less than 20% calories from fat. The women on the
low fat diet were found to have a markedly lower risk of breast cancer
recurrence, in the interim report of December, 2006.[53]
Recent[when?] studies
have also demonstrated potential links between some forms of cancer and high
consumption of refined sugars and other simple carbohydrates.[54][55][56][57][58] Although the degree of correlation and the degree of
causality is still debated,[59][60][61] some organizations have in fact begun to recommend reducing
intake of refined sugars and starches as part of their cancer prevention
regimens.[62][63][64]
In November 2007, the American Institute for Cancer Research (AICR), in conjunction with the World
Cancer Research Fund (WCRF),
published Food, Nutrition, Physical Activity and the
Prevention of Cancer: a Global Perspective, "the most current and comprehensive
analysis of the literature on diet, physical activity and cancer".[65] The WCRF/AICR Expert Report lists 10 recommendations that
people can follow to help reduce their risk of developing cancer, including the
following dietary guidelines: (1) reducing intake of foods and drinks that
promote weight gain, namely energy-dense foods and sugary drinks, (2) eating
mostly foods of plant origin, (3) limiting intake of red meat and avoiding
processed meat, (4) limiting consumption of alcoholic beverages, and (5)
reducing intake of salt and avoiding mouldy cereals (grains) or pulses (legumes).[66][67]
Some mushrooms offer an anti-cancer effect, which is thought to be
linked to their ability to up-regulate the immune system. Some mushrooms known
for this effect include, Reishi,[68][69] Agaricus blazei,[70] Maitake,[71] and Trametes versicolor.[72] Research suggests the compounds in medicinal mushrooms most responsible for up-regulating the
immune system and providing an anti-cancer effect, are a diverse collection
of polysaccharide compounds, particularly beta-glucans. Beta-glucans are known as "biological response
modifiers", and their ability to activate the immune system is well
documented. Specifically, beta-glucans stimulate the innate branch of the immune system. Research has
shown beta-glucans have the ability to stimulate macrophage, NK cells, T cells, and immune system cytokines. The mechanisms in which beta-glucans stimulate the immune system
is only partially understood. One mechanism in which beta-glucans are able to
activate the immune system, is by interacting with the Macrophage-1 antigen (CD18) receptor on immune cells.[73]
Vitamins
As of 2010 vitamins have not been found to be effective at preventing cancer.[74] While low levels ofvitamin D is correlated with increased cancer risk.[75][76] Whether this relationship is causal and vitamin D
supplementation is protective is yet to be determined.[77] Beta-carotene supplementation has been found to increase
slightly, but not significantly risks of lung cancer.[78] Folic acidsupplementation has not been found effective in
preventing colon cancer and may increase colon polyps.[79]
Chemoprevention
The concept that medications could be used to prevent cancer is an
attractive one, and many high-quality clinical trials support the use of such
chemoprevention in defined circumstances.
Daily use of tamoxifen, a selective estrogen receptor modulator (SERM), typically for 5 years, has
been demonstrated to reduce the risk of developing breast cancer in high-risk women by about 50%. A recent[when?] study reported that the selective estrogen receptor modulator raloxifene has similar benefits to tamoxifen in preventing breast cancer in
high-risk women, with a more favorable side effect profile.[80]
Raloxifene is a SERM like tamoxifen; it has been shown (in the STAR
trial) to reduce the risk of breast cancer in high-risk women equally as well
as tamoxifen. In this trial, which studied almost 20,000 women, raloxifene had fewer side effects
than tamoxifen, though it did permit more DCIS to form.[80]
Finasteride, a 5-alpha-reductase
inhibitor, has been shown to
lower the risk of prostate cancer, though it seems to mostly prevent low-grade
tumors.[81] The effect of COX-2
inhibitors such as rofecoxib andcelecoxib upon the risk of colon polyps have been studied in familial adenomatous polyposispatients[82] and in the general population.[83][84] In both groups, there were significant reductions incolon polyp incidence, but this came at the price of increased
cardiovascular toxicity.
Genetic testing
Genetic testing for high-risk individuals is already
available for certain cancer-related genetic mutations. Carriers of genetic
mutations that increase risk for cancer incidence can undergo enhanced
surveillance, chemoprevention, or risk-reducing surgery. Early identification
of inherited genetic risk for cancer, along with cancer-preventing
interventions such as surgery or enhanced surveillance, can be lifesaving for
high-risk individuals.
Gene
|
Cancer types
|
Availability
|
Breast, ovarian, pancreatic
|
Commercially available for clinical specimens
|
|
Colon, uterine, small bowel, stomach, urinary
tract
|
Commercially available for clinical specimens
|
Vaccination
Prophylactic vaccines have been developed to prevent infection by oncogenic
infectious agents such as viruses, and therapeutic vaccines are in development
to stimulate an immune response against cancer-specific epitopes.[85]
As reported above, a preventive human
papillomavirus vaccine exists
that targets certain sexually transmitted strains of human papillomavirus that are associated with the development
of cervical cancer and genital warts. The only two HPV vaccines on the market as of
October 2007 are Gardasiland Cervarix.[85] There is also a hepatitis B vaccine, which prevents infection with the hepatitis B
virus, an infectious agent that can cause liver cancer.[85] A canine melanoma vaccine has also been developed.[86][87]
Screening
Main article: Cancer screening
Cancer screening is an attempt to detect unsuspected
cancers in an asymptomatic population. In this sense screening is not a means
of prevention. Whereas prevention is designed to reduce the incidence of
cancer, screening is designed to increase the incidence of early cancer which,
it is argued, should be more effectively treatable. Screening tests suitable
for large numbers of healthy people must be relatively affordable, safe,
noninvasive procedures with acceptably low rates of false
positive results. If signs
of cancer are detected, more definitive and invasive follow up tests are
performed to confirm the diagnosis.
Screening for cancer can lead to earlier diagnosis in specific
cases. Early diagnosis may lead to extended life, but may also falsely prolong
the lead time to death through lead time bias or length time bias.[88]
A number of different screening tests have been developed for
different malignancies. Breast cancer screening can be done by breast
self-examination, though this approach
was discredited by a 2005 study in over 300,000 Chinese women. Screening for breast cancer
with mammograms has been shown to reduce the average stage
of diagnosis of breast cancer in a population. Stage of diagnosis in a country
has been shown to decrease within ten years of introduction of mammographic
screening programs. Colorectal cancer can be detected through fecal occult blood
testing and colonoscopy, which reduces both colon cancer incidence and mortality,
presumably through the detection and removal of pre-malignant polyps.
Similarly, cervical cytology testing (using the Pap smear) leads to the identification and excision of precancerous
lesions. Over time, such testing has been followed by a dramatic reduction
of cervical cancer incidence and mortality. Testicular
self-examination is recommended for
men beginning at the age of 15 years to detect testicular cancer. Prostate cancer can be screened using a digital rectal exam along with prostate
specific antigen (PSA) blood
testing, though some authorities (such as the US Preventive Services Task Force) recommend against routinely screening all men.
Screening for cancer is controversial in cases when it is not yet
known if the test actually saves lives. The controversy arises when it is not
clear if the benefits of screening outweigh the risks of follow-up diagnostic
tests and cancer treatments. For example: when screening for prostate cancer, the PSAtest
may detect small cancers that would never become life threatening, but once
detected will lead to treatment. This situation, called overdiagnosis, puts men
at risk for complications from unnecessary treatment such as surgery or
radiation. Follow up procedures used to diagnose prostate cancer (prostate biopsy) may cause side effects, including bleeding and
infection. Prostate cancer treatment may cause incontinence (inability to control urine flow)
and erectile dysfunction (erections inadequate for intercourse).
This situation was summarised in an editorial commenting on recent randomised
controlled trials. [89]. Similarly, for breast cancer, there have recently[when?] been
criticisms that breast screening programs in some countries cause more problems
than they solve. This is because screening of women in the general population
will result in a large number of women with false positive results which
require extensive follow-up investigations to exclude cancer, leading to having
a high number-to-treat (or number-to-screen) to prevent or catch a single case
of breast cancer early.[90]
One difficulty with demonstrating the benefits of mammography
screening is that proof of benefit requires not only a reduction in breast
cancer mortality among women offered screening compared with those in the
control group in randomised controlled trials, but also a reduction in deaths
from all causes.[91]. In most screening trials the observed reduction in deaths from
the particular cancer was accompanied by a comparable increase in deaths from
other causes, presumably as a result of harm caused by post-screening
treatments, giving no significant reduction in deaths from all causes.[92]Even in the large breast and prostate cancer screening trials the
power of the trials is inadequate to confirm the significance of the lack of
reduction in overall deaths. Despite the reduction in harm caused by
post-screening treatments in recent years there is still a significant number
of deaths due to treatment. [93]
Cervical cancer screening via the Pap smear has the best cost-benefit profile of all the forms of cancer
screening from a public health perspective as, largely caused by a virus, it
has clear risk factors (sexual contact), and the natural progression of
cervical cancer is that it normally spreads slowly over a number of years
therefore giving more time for the screening program to catch it early.
Moreover, the test is easy to perform and relatively cheap.
For these reasons, it is important that the benefits and risks of
diagnostic procedures and treatment be taken into account when considering
whether to undertake cancer screening.
Use of medical imaging to search for cancer in people without
clear symptoms is similarly marred with problems. There is a significant risk
of detection of what has been recently[when?] called
anincidentaloma - a benign lesion that may be interpreted
as a malignancy and be subjected to potentially dangerous investigations.
Recent[when?] studies
of CT scan-based screening for lung cancerin smokers have had equivocal results, and systematic screening is
not recommended as of July 2007. Randomized
clinical trials of
plain-film chest X-rays to screen for lung cancer in smokers have
shown no benefit for this approach.
Canine cancer
detection has shown promise,
but is still in the early stages of research.
Diagnosis
Chest x-ray showing lung
cancer in the left lung.
Most cancers are initially recognized either because signs or
symptoms appear or through screening. Neither of these lead to a definitive
diagnosis, which usually requires the opinion of a pathologist, a type of physician (medical doctor) who
specializes in the diagnosis of cancer and other diseases. People with
suspected cancer are investigated with medical tests. These commonly includeblood tests, X-rays, CT scans and endoscopy.
Pathology
A cancer may be suspected for a variety of reasons, but the
definitive diagnosis of most malignancies must be confirmed by histological examination of the cancerous cells by a pathologist. Tissue can be obtained from abiopsy or surgery. Many biopsies (such as those of the skin, breast or liver) can
be done in a doctor's office. Biopsies of other organs are performed underanesthesia and require surgery in an operating room.
The tissue diagnosis given by the pathologist indicates the type of cell that is
proliferating, itshistological grade, genetic abnormalities, and other features of
the tumor. Together, this information is useful to evaluate the prognosis of the patient and to choose the best treatment. Cytogenetics andimmunohistochemistry are other types of testing that the
pathologist may perform on the tissue specimen. These tests may provide
information about the molecular changes (such as mutations,fusion genes, and numerical chromosome changes) that has happened in the cancer cells, and may thus
also indicate the future behavior of the cancer (prognosis) and best treatment.
13. Therapy Target. Researchers
are working on therapies that target the way ovarian cancers grow. A process
called angiogenesis involve the formation of new blood vessels to feed tumors.
A drug called Avastin blocks this process, causing tumors to shrink or stop
growing (seen in the illustration here). Avastin is approved for other cancers,
but ovarian cancer researchers are still testing therapy, which can have
serious side effects.
S8. Breast Biopsy. The
only sure way determine whether a lump is cancer is to do a biopsy. This
involve taking a tissue sample for further examination in the lab, sometimes
through a small needle. Sometimes surgery is done to take part of or the entire
lump for testing. The results will show whether the lump is cancer, and if so,
what tipe. There are several forms of breast cancer, and treatments are
carefully matched to the tipe of cancer.
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