Running head: HEREDITARY CANCER 1
Hereditary Cancer
Heredity-related cancers involve two types of genes: ones that display the inability to
repair cellular damage or are lacking entirely, and others that engage in unmitigated
proliferation. Hereditary cancers are particularly insidious because there is little one can do to
prevent them, unlike avoiding an environmental carcinogen or virus that causes cancer such as
HPV. Examples of such cancers include some types of breast cancer and Lynch Syndrome.
Gene therapy is still a long ways away, so we can only treat these forms of cancers with radiation
and chemotherapy, making the study of hereditary cancers particularly relevant to cancer
researchers. So as we can see, Heredity-related cancers involve inherited defective or lacking
genes, and raise significant ethical and research challenges.
Defective genes interfere with the normal growth of cells. Damaged or mutated tumor
suppressor genes deregulate the progression of the cell cycle as well as interfere with cellular
adhesion (Hesketh, 1997). Oncogenes control signaling pathways when they function normally,
but when they are defective they are similar to a car missing its breaks. Finally, DNA repair
enzymes can also play a role, leading to mutations that can also support cellular instability.
Heredity’s role in genetic cancers was suspected in the late 19th century, when it was
noted cancer could run in families (Mukherjee, 2011). However, it was the mid-twentieth century
when the discoveries of gene abnormalities were implicated in cancer. For example, BRCA 1
and 2 mutations were not discovered until 1994 and 1995, respectively (Jacobs, 2009). Even
though the identification of genetic involvement is still relatively new, it will be demonstrated
that this technology can have far-reaching implications for quality of life and family planning.
Robert Weinberg was the first individual to isolate the ras gene, which is an oncogene, in
1972 at MIT. He did this by meticulously sheering DNA into thousands of pieces, inserting
, Running head: HEREDITARY CANCER 2
these pieces into normal cells, and waiting to see if foci appears (a “focus” of dense, proliferating
cells) (Mukherjee, 2011). Tumor suppressor genes proved more difficult to isolate because they
are significant because of their absence. A clinician named Thad Dryja was able to locate these
deletions because he had a vast store of tissue samples. By looking at small pieces of genes
called probes on the outside of chromosomes, Dryja could find two deletions on the Rb gene on
the same chromosome (Mukherjee, 2011). Because one working, present gene can take up the
slack, so to speak, he knew he had uncovered an absent tumor suppressor gene. In this case, the
cancer caused was retinoblastoma, a devastating cancer that causes eye removal(s) or death at an
early age. It is one thing to see a genetic abnormality in a petri dish, but it is far worse when
these mutations affect living beings with a sense of self-awareness, and worse, the ability to pass
on that legacy in their linage.
A woman being diagnosed with breast and ovarian cancers is a frightening proposition,
evoking images of disfigurement and lost fertility. However, men can inherit these same
defective genes and also develop cancer in their breast tissue. BRCA1 and BRCA2 are in the
tumor suppressor gene category, so they fail to cull mutations that lead to cancer from the body if
they are mutated. Ordinarily, they prevent the development of cancer by stopping unregulated
growth. BRCA mutations can also increase the odds of developing cervical, uterine, pancreatic,
and colon cancer (National Cancer Institute, 2009).
These genes show a dominant vs. recessive inheritance pattern, meaning that only one set
of the defective gene has to be present in order to express itself. However, since everyone
inherits four copies of the gene, individuals can also be carriers. “Epidemiological studies
estimate a twofold risk in close relatives to breast cancer cases, averaged across all ages, and
twin studies suggest a genetic origin” (Borg, p. S5, 2005). A woman’s odds of developing
Hereditary Cancer
Heredity-related cancers involve two types of genes: ones that display the inability to
repair cellular damage or are lacking entirely, and others that engage in unmitigated
proliferation. Hereditary cancers are particularly insidious because there is little one can do to
prevent them, unlike avoiding an environmental carcinogen or virus that causes cancer such as
HPV. Examples of such cancers include some types of breast cancer and Lynch Syndrome.
Gene therapy is still a long ways away, so we can only treat these forms of cancers with radiation
and chemotherapy, making the study of hereditary cancers particularly relevant to cancer
researchers. So as we can see, Heredity-related cancers involve inherited defective or lacking
genes, and raise significant ethical and research challenges.
Defective genes interfere with the normal growth of cells. Damaged or mutated tumor
suppressor genes deregulate the progression of the cell cycle as well as interfere with cellular
adhesion (Hesketh, 1997). Oncogenes control signaling pathways when they function normally,
but when they are defective they are similar to a car missing its breaks. Finally, DNA repair
enzymes can also play a role, leading to mutations that can also support cellular instability.
Heredity’s role in genetic cancers was suspected in the late 19th century, when it was
noted cancer could run in families (Mukherjee, 2011). However, it was the mid-twentieth century
when the discoveries of gene abnormalities were implicated in cancer. For example, BRCA 1
and 2 mutations were not discovered until 1994 and 1995, respectively (Jacobs, 2009). Even
though the identification of genetic involvement is still relatively new, it will be demonstrated
that this technology can have far-reaching implications for quality of life and family planning.
Robert Weinberg was the first individual to isolate the ras gene, which is an oncogene, in
1972 at MIT. He did this by meticulously sheering DNA into thousands of pieces, inserting
, Running head: HEREDITARY CANCER 2
these pieces into normal cells, and waiting to see if foci appears (a “focus” of dense, proliferating
cells) (Mukherjee, 2011). Tumor suppressor genes proved more difficult to isolate because they
are significant because of their absence. A clinician named Thad Dryja was able to locate these
deletions because he had a vast store of tissue samples. By looking at small pieces of genes
called probes on the outside of chromosomes, Dryja could find two deletions on the Rb gene on
the same chromosome (Mukherjee, 2011). Because one working, present gene can take up the
slack, so to speak, he knew he had uncovered an absent tumor suppressor gene. In this case, the
cancer caused was retinoblastoma, a devastating cancer that causes eye removal(s) or death at an
early age. It is one thing to see a genetic abnormality in a petri dish, but it is far worse when
these mutations affect living beings with a sense of self-awareness, and worse, the ability to pass
on that legacy in their linage.
A woman being diagnosed with breast and ovarian cancers is a frightening proposition,
evoking images of disfigurement and lost fertility. However, men can inherit these same
defective genes and also develop cancer in their breast tissue. BRCA1 and BRCA2 are in the
tumor suppressor gene category, so they fail to cull mutations that lead to cancer from the body if
they are mutated. Ordinarily, they prevent the development of cancer by stopping unregulated
growth. BRCA mutations can also increase the odds of developing cervical, uterine, pancreatic,
and colon cancer (National Cancer Institute, 2009).
These genes show a dominant vs. recessive inheritance pattern, meaning that only one set
of the defective gene has to be present in order to express itself. However, since everyone
inherits four copies of the gene, individuals can also be carriers. “Epidemiological studies
estimate a twofold risk in close relatives to breast cancer cases, averaged across all ages, and
twin studies suggest a genetic origin” (Borg, p. S5, 2005). A woman’s odds of developing
