How do mutated oncogenes and tumor suppressor genes cause cancer?

  title={How do mutated oncogenes and tumor suppressor genes cause cancer?},
  author={Dan Grandér},
  journal={Medical Oncology},
In recent decades we have been given insight into the process that transforms a normal cell into a malignant cancer cell. It has been recognised that malignant transformation occurs through successive mutations in specific cellular genes, leading to the activation of oncogenes and inactivation of tumor suppressor genes. The further study of these genes has generated much of its excitement from the convergence of experiments addressing the genetic basis of cancer, together with cellular pathways… 


The results suggest that some other genetically linked mechanisms may play a role in CRC development and progression, and hence K-ras and p53 mutations cannot be considered to be universal genetic markers for CRC.

Apoptosis and cell growth inhibition as antitumor effector functions of interferons

This reviews is written with a focus on two anticellular effects of IFN, inhibition of proliferation and induction of apoptosis, possible mechanisms underlying the antitumor action ofIFN.

Theories of cancer origin

  • R. Paduch
  • Biology
    European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation
  • 2015
The theories discussed are divided into epigenetic and genetic ones, with the latter further classified into gene-based and genome-based hypotheses.

Tumor and endothelial cell invasion of basement membranes. The matrigel chemoinvasion assay as a tool for dissecting molecular mechanisms.

  • A. Albini
  • Biology, Medicine
    Pathology oncology research : POR
  • 1998
An assay developed over ten years ago, the matrigel "chemoinvasion" assay, has been a useful tool for studying the mechanisms involved in tumor and endothelial cell invasion of basement membranes and for the screening of anti-invasive agents.


The hypothesis that tumors may originate from a rare population of cancer stem cells (CSCs) has gained tremendous popularity in recent years and is supported extensively by several pioneering works.

Identification of candidate genes encoding tumor-specific neoantigens in early- and late-stage colon adenocarcinoma.

The mutational spectra of COAD-overexpressed genes are investigated to define clinically relevant diagnostic/prognostic signatures and to unmask functional relationships with both tumor-infiltrating immune cells and regulatory miRNAs.



A cell cycle regulator potentially involved in genesis of many tumor types.

Findings suggest that MTS1 mutations are involved in tumor formation in a wide range of tissues.

Perturbation of cell cycle regulators in human cancer.

Inhibitors of this pathway have considerable promise as therapeutic agents as they form part of a common pathway, and as they are generally mutually exclusive.

G1 events and regulation of cell proliferation.

This work has shown that switches in and out of G1 are the main determinants of post-embryonic cell proliferation rate and are defectively controlled in cancer cells.

Cell cycle control in mammalian cells: role of cyclins, cyclin dependent kinases (CDKs), growth suppressor genes and cyclin-dependent kinase inhibitors (CKIs).

In this review, the mechanisms by which the mammalian cell cycle engine integrates intracellular and extracellular signals of different nature are discussed.

Cell differentiation in acute myeloid leukemia

With differentiation therapy, the leukemic cell mass is reduced to allow restoration of normal hematopoiesis and clinical remission, but the disease is not cured, however, initial reduction of the cell mass by maturation can increase the probability for cure with chemotherapy.

Apoptosis and carcinogenesis.

The possibility that defective apoptosis may permit the persistence of damaged, mutated cells that would otherwise have been deleted is explored, with particular reference to cancer.

Cell-cell and cell-stromal interactions in breast cancer invasion and metastasis (review).

There is evidence that both integrin and possibly E-cadherin mediated signalling can modulate expression of matrix degrading proteases, which would further influence invasive and metastatic behaviour.

Control of normal cell differentiation and the phenotypic reversion of malignancy in myeloid leukaemia

A cell system has been developed to determine and dissect the controls that regulate normal myeloid cell growth, differentiation and malignancy, and to suggest a novel approach to the therapy of

Telomeres and telomerase in aging and cancer.