Basic Properties of Cancer Cells

Basic Properties of Cancer Cells

• Cancer is characterized by uncontrolled growth, proliferation, and sometimes metastasis.
• Approximately 30% of deaths are attributed to cancer.
• A neoplasm is an abnormal mass of tissue growing and dividing excessively.
• Neoplasms can be benign (non-cancerous) or malignant (cancerous).
• Proliferation, when unregulated, leads to malignant tumors that invade surrounding healthy tissue.
• Metastasis occurs when cancer cells detach from the primary tumor and spread to distant sites, creating secondary tumors often resistant to treatment.
• The TNM score (Tumor, Node, Metastasis) classifies the stage of cancer based on tumor size, lymph node involvement, and metastasis.
• Cancer is genetic, but not always inherited; mutations can be somatic (acquired) or germline (inherited).
• Lung cancer is the most lethal type, followed by prostate and breast cancers.

Cancer Statistics: Distribution & Gender

• Cancer types are evenly distributed (liver, lung, bone, colon, brain, rectal, pancreatic, kidney, bladder, blood) across genders except for the following:

• Male-specific: testicular and prostate cancer.

• Female-specific: cervical, ovarian, and breast cancer (although can occur in males).

Histological Types of Cancer

• Adenocarcinoma: originates in glandular tissue.
• Carcinoma: originates in epithelial cells.
• Sarcoma: originates in connective tissue.
• Lymphoma: originates in lymphatic tissue.
• Leukemia: originates in white blood cells.
• Glioma: originates in nerve tissue.
• Myeloma: originates in plasma cells.

Basic Properties of a Cancer Cell

• Malignant cells ignore stop signals.
• Growth and division capacity are similar for cancer and normal cells.
• Normal cells stop growing when growth factors are absent or cell contact occurs; malignant cells continue growing.
• Normal cells form monolayers; malignant cells form clumps.
• Cancer cells proliferate independently of external growth factors.
• Cancer cells exhibit an abnormal chromosome complement (aneuploidy); extra or missing chromosomes.

Causes of Cancer

• The exact causes are largely unknown, but mutagenic agents (carcinogenic chemicals, radiation, viruses), DNA/RNA tumor viruses, and alterations in the genome are implicated.
• Migratory factors, including geographic relocation to different climate zones or regions, do play a role.
• Common carcinogens include asbestos, nicotine (associated with oral and lung cancers), papovaviruses (HPV), herpes (Epstein-Barr virus).
• Adenovirus, Hepatitis B virus, are also biological carcinogens

Genetics of Cancer

• Tumorigenesis (malignant tumor development) is a multi-step process involving cumulative genetic alterations.
  • Starts with benign tumor with uncontrolled proliferation, but no metastasis.
• Cancer arises from the uncontrolled proliferation of a single cell.
• Specific gene products (e.g., cell cycle regulation, cell adhesion, DNA repair) influence the sequence of genetic alterations in tumor development.
• The initiation, promotion, and progression phases characterize the development of cancer.

Cancer Stem Cells

• Tumours stem from tissue stem cells or progenitor cells.
• Cancer stem cells (CSCs) self-replicate and generate all tumor cell types.
• CSCs are often resistant to chemotherapy and radiation therapy.

Cancer Progression

• Histological changes accompany genetic changes in tumor progression.
• Initially, pre-cancerous cells/ abnormal cells appear.
• They possess some cancer properties but lack the ability to invade tissues or metastasize.
• Cervical cancer's progression takes years, showing increasingly abnormal cells with larger nuclei.
• Pre-cancerous cervical lesions (e.g., cervical intraepithelial neoplasia, cervical dysplasia) represent uncontrolled growth.

Benign vs. Malignant Tumors

• Benign tumors grow locally and do not spread.
• Malignant tumors invade surrounding tissue and metastasize.

Oncogenes

• Proto-oncogenes are normal genes that regulate cell growth and signaling; mutations convert them into oncogenes.
• Oncogenes are activated by gain-of-function mutations (e.g., gene duplication, amplification, rearrangement).
• Uncontrolled proliferation and transformation ensue from oncogene activation.
• Oncogenes can encode growth factors, receptors, cytoplasmic protein kinases, nuclear transcription factors, proteins modifying chromatin, and metabolic enzymes.
• Examples:
  • Simian sarcoma virus (sis oncogene, PDGF)
  • Altered EGF receptor (erbB oncogene)
  • Raf protein kinase (MAPK cascade)
  • Src tyrosine kinase, impacting cell signaling, cytoskeleton, and adhesion
• Oncogenes function dominantly; only one copy needs to be mutated.

Tumor Suppressor Genes

• Tumor suppressor genes encode proteins that restrain cell growth; they are like the brakes.
• Examples include APC, BRCA1/2, MSH/MLH1, INK4a, and Rb.
• Most tumor suppressor gene products are negative regulators of cell proliferation.
• The retinoblastoma (RB) gene is a widely studied tumor suppressor gene.
• Mutated RB genes contribute to retinoblastoma (eye cancer).
• pRB regulates the G1 to S phase transition of the cell cycle, preventing uncontrolled cell division.
• Loss of both alleles is necessary for cancer development.

p53

• P53 is a crucial tumor suppressor known as the "guardian of the genome."

• It maintains genomic stability and suppresses tumor formation.

• P53 function is sensitive to mutations in its DNA-binding domain, impacting DNA binding and conformation.

• Upon DNA damage, p53 concentration increases, halting cell division and initiating DNA repair.

• Cells with irreparable damage are then programmed for apoptosis.

New Cancer Combating Strategies

• Current treatments (surgery, chemotherapy, radiation) lack specificity, causing harmful side effects to healthy cells.
• Targeted therapies, immunotherapy, and techniques to block angiogenesis or use Oncolytic viruses, are emerging strategies.
• Immunotherapy: Passive immunotherapy utilizes patient antibodies against tumor cells (e.g., Herceptin, Rituxan).
• Targeting Cancer Proteins: Blocking cancer-promoting proteins (e.g., using Zelboraf to target mutant BRAF).
• Blocking Angiogenesis: Compounds like Avastin disrupt blood vessel formation to deprive tumors of nutrients (Targeting VEGF-R).
• Oncolytic viruses: Engineered viruses selectively infect and destroy cancer cells.

Specific factors in some cancers

• Prostate cancer: Calcium /vitamin D, IGF-I theories implicated in heightened risk.

Explore the fundamental characteristics of cancer cells, including their uncontrolled growth, types of neoplasms, and the process of metastasis. Understand key statistics related to cancer prevalence and the significance of the TNM score in staging cancer. This quiz delves into both genetic factors and the most common forms of cancer.