English: Anatomy of a crab, exemplified by Can...

Cancer is a broad group of various diseases involving unregulated cell growth. It is medically known as a malignant neoplasm. In cancer, cells divide and grow uncontrollably and invade nearby parts of the body. The cancer may also spread to more distant parts of the body through the lymphatic system or bloodstream, it is called metastasis. However, not all tumors are cancerous. Some tumors do not grow uncontrollably, do not invade neighboring tissues, and do not spread throughout the body which are called Benign tumors.

There are more than 100 types of Cancers. Follow the link to know more:

Main sites of metastases for some common cance...

Main sites of metastases for some common cancer types. Primary cancers are denoted by “…cancer” and their main metastasis sites are denoted by “…metastases”. List of included entries and references is found on main image page in Commons: (Photo credit: Wikipedia)

Classification of Cancers:

There are five broad groups that are used to classify cancer.

  1. Carcinomas: These are characterized by cells that cover internal and external parts of the body such as lung, breast, and colon cancer.
  2. Sarcomas:These are characterized by cells that are located in bone, cartilage, fat, connective tissue, muscle, and other supportive tissues.
  3. Lymphomas:These are cancers that begin in the lymph nodes and immune system tissues.
  4. Leukemias:These are cancers that begin in the bone marrow and often accumulate in the bloodstream.
  5. Adenomas:These are cancers that arise in the thyroid, the pituitary gland, the adrenal gland, and other glandular tissues.


  • Hereditary (about 5-10%)
  • Environmental (90-95% of cases) factors e.g.,
    • Tobacco (25-30%) – about 70% of the lung cancers are due to tobacco habit
    • Infections (15-20%)
    • Radiation (both ionizing and non-ionizing, up to 10%)
    • Obesity (30-35%) and
    • Pollutants,Sedentary life, poor diet etc., are likely to cause cancer.

These can directly damage genes or combine with existing genetic faults within cells to cause the disease. It appears that DNA methylation plays a crucial role in the development of nearly all types of cancer. Therefore, it is important to understand DNA methylation and its role in gene regulation and disease.

Interestingly, most of the environmental influences are preventable, e.g.,


  • Tobacco (about 30%): if you wish you can quit Tobacco consumption today itself (it is never late) – do this good favor to yourself and to your neighbors. In fact it would be your great service to the passive-smokers – in return, you will get respect and will save lots of money, health of your loved-ones and your health too.
  • Radiation (about 10%): minimize exposure to radiation where possible. Don’t worry about the things which are beyond our control, but  make an effort to avoid where it is possible to avoid.
  • Infections (about 20%): this can be prevented by maintaining proper hygienic conditions and can be controlled immediately with the available antibiotics and can be prevented by timely recommended vaccinations.
  • Obesity (about 30%): Obesity and other diet related factors can be controlled with little effort, i.e., Daily physical activity, Meditation (proper, rhythmic breathing exercises etc.) Fresh Indigenous Food, i.e., adopt DMF as a Good Health Practice

Infect-obesity (infections that contribute to human obesity): There appears to be an increasing interest to understanding the etiology of obesity due to rapid increase in obesity. Of the several etiological factors, infection has recently started receiving greater attention. In the last two decades, 10 adipogenic pathogens were reported, including human and nonhuman viruses, scrapie agents, bacteria, and gut microflora. Some of these pathogens are associated with human obesity says one study (2007).

Following is a recent review (2011) on Infect-obesity which says that “a comprehensive understanding of the causative factors of obesity might provide more effective management approaches”.

Another study (2012) reviewed the literature concerning the role of adenovirus 36 (AD-36) which says that AD-36 is the most widely studied infectious agent in animals and humans, because of its potential association with childhood obesity. The available evidence suggests that more studies are needed to evaluate whether or not the association between the presence of AD-36 antibodies and obesity is simply unrelated, and to verify whether there are subjects that have greater tendency to become obese because more easily susceptible to AD-36 infection or with a predisposition to suffer from persistent viral infection more easily leading to the development of obesity.

If it is demonstrated that AD-36 does play a role in obesity, it will be important to investigate possible vaccines against the infection itself or antiviral drugs capable of inhibiting disease progression.

Study (2012) by Korean scientists suggests that Ad-36 seems to be strongly associated with overweight, but not obese, Korean adults.


Presence of certain signs and symptoms, screening tests including medical imaging etc. can be used.


Cancer can be diagnosed by microscopic examination of a tissue sample called biopsy.

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Cancer is usually treated with chemotherapy, radiation therapy and surgery.


Survival depends greatly by the type and location of the cancer and the extent of disease at the start of treatment. The risk of developing cancer generally increases with age.

Young People with Cancer, visit the following link for details:

For Types of Childhood Cancer, visit the following link:

For common medical procedures, visit the following link:

Signs and Symptoms

Initially there will be no signs and symptoms but only appearing as the mass that continues to grow or ulcerates. The findings that result depends on the type and location of the cancer. For example,

Mass effects from Lung Cancer – can cause blockage of the bronchus resulting in cough (coughing up blood if there is ulceration) or pneumonia.

Oesophageal Cancer – can cause narrowing of the esophagus making it difficult or painful to swallow.

Colorectal Cancermay lead to changes in bowel habits and bleeding leading to anemia.

General symptoms may include:

  • Unintentional weight loss,
  • Fever,
  • Being excessively tired,
  • Changes to the skin,
  • Leukemias, and
  • Persistent fever due to Cancers of the liver or kidney.



Metastatic cancer is cancer that has spread from the place where it first started to another place in the body. A tumor formed by metastatic cancer cells is called a metastatic tumor or a metastasis. The process by which cancer cells spread to other parts of the body is also called metastasis.

Metastatic cancer has the same name and the same type of cancer cells as the original, or primary, cancer. For example, breast cancer that spreads to the lung and forms a metastatic tumor is metastatic breast cancer, not lung cancer.

Under a microscope, metastatic cancer cells generally look the same as cells of the original cancer. Moreover, metastatic cancer cells and cells of the original cancer usually have some molecular features in common, such as the expression of certain proteins or the presence of specific chromosome changes.

Although some types of metastatic cancer can be cured with current treatments, most cannot. Nevertheless, treatments are available for all patients with metastatic cancer. In general, the primary goal of these treatments is to control the growth of the cancer or to relieve symptoms caused by it. In some cases, metastatic cancer treatments may help prolong life. However, most people who die of cancer die of metastatic disease.


Cancer type Main sites of metastasis*
Bladder Bone, liver, lung
Breast Bone, brain, liver, lung
Colorectal Liver, lung, peritoneum
Kidney Adrenal gland, bone, brain, liver, lung
Lung Adrenal gland, bone, brain, liver, other lung
Melanoma Bone, brain, liver, lung, skin/muscle
Ovary Liver, lung, peritoneum
Pancreas Liver, lung, peritoneum
Prostate Adrenal gland, bone, liver, lung
Stomach Liver, lung, peritoneum
Thyroid Bone, liver, lung
Uterus Bone, liver, lung, peritoneum, vagina

*In alphabetical order. Brain includes the neural tissue of the brain (parenchyma) and the leptomeninges (the two innermost membranes—arachnoid mater and pia mater—of the three membranes known as the meninges that surround the brain and spinal cord; the space between the arachnoid mater and the pia mater contains cerebrospinal fluid). Lung includes the main part of the lung (parenchyma) as well as the pleura (the membrane that covers the lungs and lines the chest cavity).

How does cancer spread?

Cancer cell metastasis usually involves the following steps:

  • Local invasion: Cancer cells invade nearby normal tissue.
  • Intravasation: Cancer cells invade and move through the walls of nearby lymph vessels or blood vessels.
  • Circulation: Cancer cells move through the lymphatic system and the bloodstream to other parts of the body.
  • Arrest and extravasation: Cancer cells arrest, or stop moving, in small blood vessels called capillaries at a distant location. They then invade the walls of the capillaries and migrate into the surrounding tissue (extravasation).
  • Proliferation: Cancer cells multiply at the distant location to form small tumors known as micrometastases.
  • Angiogenesis: Micrometastases stimulate the growth of new blood vessels to obtain a blood supply. A blood supply is needed to obtain the oxygen and nutrients necessary for continued tumor growth.
Metastasis. Cancer cells invade lymph nodes and blood vessels near a tumor and spread to other parts of the body.

Because cancers of the lymphatic system or the blood system are already present inside lymph vessels, lymph nodes, or blood vessels, not all of these steps are needed for their metastasis. Also, the lymphatic system drains into the blood system at two locations in the neck.

The ability of a cancer cell to metastasize successfully depends on its individual properties; the properties of the noncancerous cells, including immune system cells, present at the original location; and the properties of the cells it encounters in the lymphatic system or the bloodstream and at the final destination in another part of the body. Not all cancer cells, by themselves, have the ability to metastasize. In addition, the noncancerous cells at the original location may be able to block cancer cell metastasis. Furthermore, successfully reaching another location in the body does not guarantee that a metastatic tumor will form. Metastatic cancer cells can lie dormant (not grow) at a distant site for many years before they begin to grow again, if at all.


English: Main symptoms of cancer metastasis. S...

Symptoms of metastasis include:

  • Enlarged lynph nodes which can be felt or sometimes seen under the skin and are typically hard),
  • Enlarged liver or spleen which can be felt in the abdomen,
  • Pain or fracture of affected bones, and
  • Neurological symptoms.

It is nearly impossible to prove what caused a cancer in any individual, because most cancers have multiple possible causes. For example, lung cancer could be due to tobacco habbit or could be a result of air pollution or radiation.




Cancer’s Origins Revealed: Signatures of mutational processes in human cancer

Leukemia ‘Eradicated’ in Mice

Epigenetics in cancer: implications for early detection and prevention (Related articles)

DNA methylation and cancer (Related A, B, )

Oestrogen and the colon: potential mechanisms for cancer prevention

Strategies for discovering novel cancer biomarkers through utilization of emerging technologies

Innovative proteomic approaches for cancer biomarker discovery

Emerging biomarker technologies

Biomarker discovery in lung cancer–promises and challenges of clinical proteomics

New cancer biomarkers deriving from NCI early detection research

New Developments

Cancer’s Origins Revealed: Signatures of mutational processes in human cancer

All cancers are caused by somatic (ACQUIRED) mutations; however, understanding of the biological processes generating these mutations is limited. The catalogue of somatic mutations from a cancer genome bears the signatures of the mutational processes that have been operative. Here we analysed 4,938,362 mutations from 7,042 cancers and extracted more than 20 distinct mutational signatures. Some are present in many cancer types, notably a signature attributed to the APOBEC family of cytidine deaminases, whereas others are confined to a single cancer class. Certain signatures are associated with age of the patient at cancer diagnosis, known mutagenic exposures or defects in DNA maintenance, but many are of cryptic origin. In addition to these genome-wide mutational signatures, hypermutation localized to small genomic regions, ‘kataegis’, is found in many cancer types. The results reveal the diversity of mutational processes underlying the development of cancer, with potential implications for understanding of cancer aetiology, prevention and therapy.

Molecular Biomarkers for Cancer Detection and Management

This report, from  Insight Pharma Reports, focuses on recent progress and new directions in this highly dynamic diagnostic field.

Significant highlights of the report include:

  • Basic research conducted in both academic and commercial settings divided into three segments: disease detection, prognosis, and companion diagnostics.
    • 42 detailed descriptions of copmanies (including GenomeDx Biosciences, Genomic Health, Life Technologies, Foundation Medicine, Roche Molecular Systems, and many more!).
  • Commercial activity in the three foregoing sectors, and the perspective of market dynamics.
  • Focuses on trends and conclusions.
  • Data depicted across 15 tables and figures.

Tumor Epigenetics

That human tumors display both genetic mutations and epigenetic alterations—for example, in DNA methylation—has been known for many years; with the completion of cancer genome sequencing projects, possible causal links between the two have come into sharper focus. The discovery of recurrent tumor-associated mutations in genes that encode chromatin-modifying enzymes or DNA methyltransferases represents a clear link between tumor genotype and “epigenotype.” Emerging evidence suggests that a link can be subtle, as illustrated by two studies describing consistent epigenetic alterations in tumors with mutations in the gene encoding the metabolic enzyme succinate dehydrogenase (SDH). Killian et al. find that gastrointestinal stromal tumors harboring SDH mutations are characterized by dramatic and widespread DNA hypermethylation, whereas Letouzé et al. report that SDH-mutant paragangliomas display DNA hypermethylation that is associated with the silencing of genes involved in neuroendocrine cell differentiation. Both groups hypothesize that the hypermethylation phenotype is due to the aberrant accumulation of an oncometabolite that inhibits DNA-demethylating enzymes, with succinate being a strong candidate. Cancer Discov. 3, 648 (2013); Cancer Cell 23, 739 (2013).

The present and future of prostate cancer urine biomarkers


In order to successfully cure patients with prostate cancer (PCa), it is important to detect the disease at an early stage. The existing clinical biomarkers for PCa are not ideal, since they cannot specifically differentiate between those patients who should be treated immediately and those who should avoid over-treatment. Current screening techniques lack specificity, and a decisive diagnosis of PCa is based on prostate biopsy. Although PCa screening is widely utilized nowadays, two thirds of the biopsies performed are still unnecessary. Thus the discovery of non-invasive PCa biomarkers remains urgent. In recent years, the utilization of urine has emerged as an attractive option for the non-invasive detection of PCa. Moreover, a great improvement in high-throughput “omic” techniques has presented considerable opportunities for the identification of new biomarkers. Herein, authors reviewed the most significant urine biomarkers described in recent years, as well as some future prospects in that field. (Related articles)

Mass spectrometry-based proteomics in molecular diagnostics: discovery of cancer biomarkers using tissue culture.


Accurate diagnosis and proper monitoring of cancer patients remain a key obstacle for successful cancer treatment and prevention. Therein comes the need for biomarker discovery, which is crucial to the current oncological and other clinical practices having the potential to impact the diagnosis and prognosis. In fact, most of the biomarkers have been discovered utilizing the proteomics-based approaches. Although high-throughput mass spectrometry-based proteomic approaches like SILAC, 2D-DIGE, and iTRAQ are filling up the pitfalls of the conventional techniques, still serum proteomics importunately poses hurdle in overcoming a wide range of protein concentrations, and also the availability of patient tissue samples is a limitation for the biomarker discovery. Thus, researchers have looked for alternatives, and profiling of candidate biomarkers through tissue culture of tumor cell lines comes up as a promising option. It is a rich source of tumor cell-derived proteins, thereby, representing a wide array of potential biomarkers. Interestingly, most of the clinical biomarkers in use today (CA 125, CA 15.3, CA 19.9, and PSA) were discovered through tissue culture-based system and tissue extracts. This paper tries to emphasize the tissue culture-based discovery of candidate biomarkers through various mass spectrometry-based proteomic approaches.

Continuous Aging of the Human DNA Methylome Throughout the Human Lifespan:


DNA methylation plays an important role in development of disease and the process of aging. In this study we examine DNA methylation at 476,366 sites throughout the genome of white blood cells from a population cohort (N = 421) ranging in age from 14 to 94 years old. Age affects DNA methylation at almost one third (29%) of the sites (Bonferroni adjusted P-value <0.05), of which 60.5% becomes hypomethylated and 39.5% hypermethylated with increasing age. DNA methylation sites that are located within CpG islands (CGIs) more often become hypermethylated compared to sites outside an island. CpG sites in promoters are more unaffected by age, whereas sites in enhancers more often becomes hypo- or hypermethylated. Hypermethylated sites are overrepresented among genes that are involved in DNA binding, transcription regulation, processes of anatomical structure and developmental process and cortex neuron differentiation (P-value down to P = 9.14*10−67). By contrast, hypomethylated sites are not strongly overrepresented among any biological function or process. Our results indicate that the 23% of the variation in DNA methylation is attributed chronological age, and that hypermethylation is more site-specific than hypomethylation. It appears that the change in DNA methylation partly overlap with regions that change histone modifications with age, indicating an interaction between the two major epigenetic mechanisms. Epigenetic modifications and change in gene expression over time most likely reflects the natural process of aging and variation between individuals might contribute to the development of age-related phenotypes and diseases such as type II diabetes, autoimmune and cardiovascular disease


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