Molecular biology of cancer

The term Cancer refers to one of the most common diseases that is manifested in about a third of population in some form or other and accounts for more than 20% of all deaths in the developed countries.

Cancer is not a single disease but rather refers to a great variety of malignant tumors.  However, the basic process in all the cases is mainly due to “uncontrolled growth”.

Cell proliferation results in a mass (neoplasm or tumor) that invades neighboring tissues and in some cases distant sites, called “metastasis”.

The Growth is autonomous, increasingly malignant, and , if untreated, invariably fatal.  There are two types of growth namely, benign and malignant.

Benign tumors:  Benign tumors grow more slowly, and retain their response to the intracellular signals which keeps the cells approximately in the right position; they therefore, remain within the natural tissue boundaries.

Malignant tumors:  Malignant tumors grow more rapidly and do not respect boundaries.  They invade other tissues, and some times, malignant tumor cells detach, travel through the tissues and establish fresh colonies far from the original tumor, forming metastases.

Often, if untreated benign tumors may become malignant.   This is one very important aspect of gradual progression of cancer.

Are There Any Common Denominators to the Many Different Types of Cancer?

  • One of the hallmarks of all cancers regardless of where they occur is cell structure change.
  • The earliest event that occurs in the carcinogenic process, is a change in cell structure as determined by a pathologist
  • This variation in cell shape extends through the cell, including the nucleus, nucleolus and the chromosome.

What determines this shape is a dynamic cellular and tissue matrix. This highly dynamic matrix can form self organizing sites within the cell for fixed sites of replication, transcription and splicing events, as well as DNA rearrangement.

Recent studies suggest a specific pattern of transcription/ translation sites in tumor cells !!

The two-hit model and the haploinsufficiency model of tumorigenesis.  (Top) In the two-hit model, both alleles of a tumor suppressor gene (TSG) must be inactivated to trigger tumor formation. (Bottom) In the aploinsufficiency  model, the gene-dosage defect caused by the expression of only one functional allele contributes to tumor formation either by conferring a selective advantage on the tumor cells (gatekeeper genes) or by causing genetic instability (caretaker genes). Alternatively, haploinsufficiency may not result directly in a specific cellular phenotype. Nevertheless, in both haploinsufficient scenarios, additional tumor-promoting events such as oncogenic mutations, loss of other tumor suppressor genes, or epigenetic changes will be necessary to uncover the haploinsufficiency of the original tumor suppressor gene. (Normal cell, brown; initiated cell at increased risk of tumor formation, blue; tumor cell, pink.)

The complex process of carinogenesis: Cancer arises through the accumulation of genetic alterations within a subset of our genes.  Certain of  these  genetic  alterations  can  be  hereditary whereas others alterations arise as a result of expo-sure to carcinogens and certain oncogenic viruses.  It is clear that commonality in exposure does  not lead to common outcomes in terms of cancer development.  Modulators of carcinogenesis include  hormones,  diet,  and  a  range  of  other  host factors.  The impact of exposure to carcinogens as well as the influence of these modulators are in a sense  “filtered”  by  an  individual’s  genes  that  can eliminate,  reduce,  or  enlarge  the  impact  of  a given contributor to the process.  In the figure, this modulation by the individual’s genes is represent- ed  as  elimination,  reduction,  or  enlargement  of  the arrows as they pass through the genetic “filter”. Understanding the process of carcinogenesis will require a much more comprehensive understand- ing  of  gene-environment  interactions  than  existstoday.

Tumor classification

Papilloma: A benign growth of an epithelial tissue.

Carcinoma: A malignant epithelial tumor

Sarcoma: A malignant tumor of connective tissue origin.

Neuroblastoma: A tumor of nervous tissue origin.

Glioblastoma: A tumor of Glial cells

Melanoma: A tumor usually dark in color, derived from a melanocyte that makes skin pigment.

Lymphoma: A tumor of a lymph gland

Leukemia:  A over production of leukocytes, diffused throughout the circulatory system.

Hence, the basic principle in tumor formation is that, a cell, otherwise normal gets converted to a transformed cell.

The second aspect is the formation of the tumor for which, several other cooperative events should takes place.

After all this, set of additional events would allow a transformed cell to become metastatic.

Progression of normal cell to tumor growth

Manifestation of a tumor is a multi step process.  This involves simultaneous cooperativity of both environmental agents and genetic make up.

Each step is guided by aberrations in one or more genes and several of those events lead to formation of the tumor.

The first step towards the transformation of the normal cell is immortalization.

The second step is transformation.

The transformed cells then would proliferate and give a tumor mass.  This requires additional supporting events such as, escape from immune surveillance and new capillary formation for nutrient supply called ” angiogenesis”.


Surely, Cancer can be considered as a genetic disorder, in which the normal control of cell growth is lost.  The basic mechanism in all cancers is mutation, either in the “germline” that predispose or “somatic” that precipitates the tumor initiation.  More often, mutations in the somatic cells is the cause for cancer.

Several genes have been implicated in the overall tumor formation. Examples of some of these genes that were found to be heritable have been presented.

Since, Many factors are involved in the progression of cancer, we may not be able to assign a strict inheritance pattern for such a complex disorder.

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Science Blogger

I’m a life long learner who loves reading, painting, sci-fi and travelling. As the publisher of The Sciencelock, I edits the website Features and writes articles across the publication.

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