Search

Text Color

Margin Size

Font Type

Enable Dyslexic Font

Unit 12: Cancer

Last updated

May 14, 2022
Save as PDF
- 11.13: Metagenomics
- 12.1: Cancer in General

$\newcommand{\vecs}[1]{\overset { \scriptstyle \rightharpoonup} {\mathbf{#1}} }$

$\newcommand{\vecd}[1]{\overset{-\!-\!\rightharpoonup}{\vphantom{a}\smash {#1}}}$

$\newcommand{\id}{\mathrm{id}}$ $\newcommand{\Span}{\mathrm{span}}$

( \newcommand{\kernel}{\mathrm{null}\,}\) $\newcommand{\range}{\mathrm{range}\,}$

$\newcommand{\RealPart}{\mathrm{Re}}$ $\newcommand{\ImaginaryPart}{\mathrm{Im}}$

$\newcommand{\Argument}{\mathrm{Arg}}$ $\newcommand{\norm}[1]{\| #1 \|}$

$\newcommand{\inner}[2]{\langle #1, #2 \rangle}$

$\newcommand{\Span}{\mathrm{span}}$

$\newcommand{\id}{\mathrm{id}}$

$\newcommand{\Span}{\mathrm{span}}$

$\newcommand{\kernel}{\mathrm{null}\,}$

$\newcommand{\range}{\mathrm{range}\,}$

$\newcommand{\RealPart}{\mathrm{Re}}$

$\newcommand{\ImaginaryPart}{\mathrm{Im}}$

$\newcommand{\Argument}{\mathrm{Arg}}$

$\newcommand{\norm}[1]{\| #1 \|}$

$\newcommand{\inner}[2]{\langle #1, #2 \rangle}$

$\newcommand{\Span}{\mathrm{span}}$ $\newcommand{\AA}{\unicode[.8,0]{x212B}}$

$\newcommand{\vectorA}[1]{\vec{#1}} % arrow$

$\newcommand{\vectorAt}[1]{\vec{\text{#1}}} % arrow$

$\newcommand{\vectorB}[1]{\overset { \scriptstyle \rightharpoonup} {\mathbf{#1}} }$

$\newcommand{\vectorC}[1]{\textbf{#1}}$

$\newcommand{\vectorD}[1]{\overrightarrow{#1}}$

$\newcommand{\vectorDt}[1]{\overrightarrow{\text{#1}}}$

$\newcommand{\vectE}[1]{\overset{-\!-\!\rightharpoonup}{\vphantom{a}\smash{\mathbf {#1}}}}$

$\newcommand{\vecs}[1]{\overset { \scriptstyle \rightharpoonup} {\mathbf{#1}} }$

$\newcommand{\vecd}[1]{\overset{-\!-\!\rightharpoonup}{\vphantom{a}\smash {#1}}}$

$\newcommand{\avec}{\mathbf a}$

$\newcommand{\bvec}{\mathbf b}$

$\newcommand{\cvec}{\mathbf c}$

$\newcommand{\dvec}{\mathbf d}$

$\newcommand{\dtil}{\widetilde{\mathbf d}}$

$\newcommand{\evec}{\mathbf e}$

$\newcommand{\fvec}{\mathbf f}$

$\newcommand{\nvec}{\mathbf n}$

$\newcommand{\pvec}{\mathbf p}$

$\newcommand{\qvec}{\mathbf q}$

$\newcommand{\svec}{\mathbf s}$

$\newcommand{\tvec}{\mathbf t}$

$\newcommand{\uvec}{\mathbf u}$

$\newcommand{\vvec}{\mathbf v}$

$\newcommand{\wvec}{\mathbf w}$

$\newcommand{\xvec}{\mathbf x}$

$\newcommand{\yvec}{\mathbf y}$

$\newcommand{\zvec}{\mathbf z}$

$\newcommand{\rvec}{\mathbf r}$

$\newcommand{\mvec}{\mathbf m}$

$\newcommand{\zerovec}{\mathbf 0}$

$\newcommand{\onevec}{\mathbf 1}$

$\newcommand{\real}{\mathbb R}$

$\newcommand{\twovec}[2]{\left[\begin{array}{r}#1 \\ #2 \end{array}\right]}$

$\newcommand{\ctwovec}[2]{\left[\begin{array}{c}#1 \\ #2 \end{array}\right]}$

$\newcommand{\threevec}[3]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \end{array}\right]}$

$\newcommand{\cthreevec}[3]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \end{array}\right]}$

$\newcommand{\fourvec}[4]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}$

$\newcommand{\cfourvec}[4]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}$

$\newcommand{\fivevec}[5]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}$

$\newcommand{\cfivevec}[5]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}$

$\newcommand{\mattwo}[4]{\left[\begin{array}{rr}#1 \amp #2 \\ #3 \amp #4 \\ \end{array}\right]}$

$\newcommand{\laspan}[1]{\text{Span}\{#1\}}$

$\newcommand{\bcal}{\cal B}$

$\newcommand{\ccal}{\cal C}$

$\newcommand{\scal}{\cal S}$

$\newcommand{\wcal}{\cal W}$

$\newcommand{\ecal}{\cal E}$

$\newcommand{\coords}[2]{\left\{#1\right\}_{#2}}$

$\newcommand{\gray}[1]{\color{gray}{#1}}$

$\newcommand{\lgray}[1]{\color{lightgray}{#1}}$

$\newcommand{\rank}{\operatorname{rank}}$

$\newcommand{\row}{\text{Row}}$

$\newcommand{\col}{\text{Col}}$

$\renewcommand{\row}{\text{Row}}$

$\newcommand{\nul}{\text{Nul}}$

$\newcommand{\var}{\text{Var}}$

$\newcommand{\corr}{\text{corr}}$

$\newcommand{\len}[1]{\left|#1\right|}$

$\newcommand{\bbar}{\overline{\bvec}}$

$\newcommand{\bhat}{\widehat{\bvec}}$

$\newcommand{\bperp}{\bvec^\perp}$

$\newcommand{\xhat}{\widehat{\xvec}}$

$\newcommand{\vhat}{\widehat{\vvec}}$

$\newcommand{\uhat}{\widehat{\uvec}}$

$\newcommand{\what}{\widehat{\wvec}}$

$\newcommand{\Sighat}{\widehat{\Sigma}}$

$\newcommand{\lt}{<}$

$\newcommand{\gt}{>}$

$\newcommand{\amp}{&}$

$\definecolor{fillinmathshade}{gray}{0.9}$

A cancer is an uncontrolled proliferation of cells. In some the rate is fast; in others, slow; but in all cancers the cells never stop dividing. This distinguishes cancers — malignant tumors — from benign growths like moles where their cells eventually stop dividing (usually). Even more important, benign growths differ from malignant ones in not producing metastases; that is, they do not seed new growths elsewhere in the body.

12.1: Cancer in General
This page discusses cancer as a disease of uncontrolled cell proliferation, distinct from benign growths due to its ability to metastasize. Originating from mutated cells, cancers involve genetic diversity and are driven by cancer stem cells. Common causes include DNA-damaging agents and viruses, although cancer itself is not contagious. Notably, certain viral infections can elevate cancer risk.
12.2: Cancer Cells in Culture
This page examines mouse fibroblasts, highlighting the contrast between normal cells with contact inhibition and transformed 3T3 cells that lack this feature. It notes that while transformed cells can form tumors in test subjects despite not being cancerous, normal cells require specific nutrients and maintain a normal karyotype. In contrast, transformed and cancer cells can survive on simpler media and often exhibit abnormal karyotypes with irregular chromosome structures.
12.3: Oncogenes
This page explains oncogenes, which are mutated genes that lead to cancer by causing uncontrolled cell division. Normal cells require growth factors to regulate mitosis through activated signaling pathways. Oncogenes can emerge from mutations in these pathways, heightening mutation rates. Additionally, genes that inhibit apoptosis or repair DNA can also become oncogenic. Unlike oncogenes, tumor-suppressor genes must have both alleles mutated to encourage cell division.
12.4: Tumor Suppressor Genes
This page covers the role of tumor suppressor genes, such as RB and p53, in regulating cell division and preventing tumor formation. It details how inherited and sporadic mutations lead to conditions like familial retinoblastoma. The page also discusses the impact of increasing p16INK4a levels with age and loss of heterozygosity (LOH) on tumorigenesis.
12.5: BCL-2
This page discusses BCL-2, a proto-oncogene on chromosome 18 involved in cancer by inhibiting apoptosis in B-cells. Its translocation with chromosome 14 (t(14;18)) results in Bcl-2 overexpression, aiding evasion of programmed cell death, thus promoting cancer. However, this translocation alone does not guarantee cancer, as many carriers remain healthy; other mutations, such as c-myc translocation, also play a role in B-cell malignancies.
12.6: Burkitt's Lymphoma
This page discusses Burkitt's lymphoma, a B lymphocyte tumor caused by genetic alterations, mainly involving the c-myc proto-oncogene. In about 90% of cases, c-myc is translocated from chromosome 8 to chromosome 14, resulting in excessive transcription factor production that drives uncontrolled cell division.
12.7: Chronic Myelogenous Leukemia (CML)
This page discusses leukemia, focusing on Chronic Myelogenous Leukemia (CML), which arises from mutated bone marrow stem cells of the myeloid lineage and may lead to a "blast crisis." CML is associated with the Philadelphia chromosome due to a translocation of chromosomes 9 and 22. Imatinib mesylate (Gleevec) is a key treatment that can effectively control CML progression and shows promise for other cancers.
12.8: Fighting Cancer with Inhibitors of Angiogenesis
This page discusses the role of angiogenesis in cancer growth, highlighting the ability of tumors to both promote and inhibit new blood vessel formation. It notes the potential of angiogenesis inhibitors, like angiostatin and endostatin, in treating tumors, as well as emerging therapies such as Vitaxin and Bevacizumab that seek to target angiogenesis. However, it also advises caution, as increased blood supply might be necessary for certain cancers.
12.9: Immunotherapy of Cancer
This page discusses advancements in cancer treatment, emphasizing targeted therapies that utilize the immune system to minimize damage to healthy cells. Key strategies include immunostimulants, monoclonal antibodies, and adoptive cell therapy, particularly using T cells. Successful treatments for melanoma and B-cell lymphomas are highlighted, alongside patient-specific vaccines.
12.10: Cancer- The Causes and Prevention of Cancer
This page discusses how oxidative damage from metabolic by-products significantly influences aging and contributes to diseases like cancer. It highlights that antioxidants from fruits and vegetables can help mitigate this damage, but many people don't consume enough. It also notes major cancer risk factors such as smoking and poor diet.
12.11: Estimating Cancer Risks
This page discusses the complex relationship between dose and response for mutagens and carcinogens, indicating that low doses may have no effect or even reduce cancer risk, contradicting the linear no-threshold model. Evidence varies regarding cancer incidence linked to radiation exposure, with some areas showing high background radiation without increased cancer rates.
12.12: The LD50 test
This page discusses the LD50, a key metric for assessing chemical toxicity, defined as the dose needed to kill 50% of test animals. A lower LD50 signifies higher toxicity, but results can vary by administration method and species differences. Ethical concerns about animal testing have led to ongoing efforts since 2000 to replace LD50 testing with alternatives that minimize animal deaths.
12.13: Dioxin
This page discusses dioxin, especially TCDD, a toxic contaminant in agent orange linked to cancer and birth defects in animals, with potential human risks according to the EPA. While exposure has dropped since the mid-80s, trace levels persist in human blood. Notably, some research suggests TCDD might offer protective effects against certain diseases, as it can suppress allergic encephalomyelitis in mice.
12.14: Magnetic Fields and Cancer
This page discusses studies from the late 1970s linking high-voltage power lines to childhood leukemia, especially acute lymphoblastic leukemia (ALL). A substantial 1997 National Cancer Institute study found no solid evidence for this association and concluded that only one of five epidemiological standards was met.

Thumbnail: This is a photograph of a basal cell carcinoma on the back taken by me. Basal cell carcinoma is the most common skin cancer. (Public Domain; John Hendrix).

Support Center

How can we help?