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Steve Jobs’ Cancer Journey

3 minute read
Alice Park

All patients face difficult choices when they hear the words “You have cancer.” Steve Jobs, who died Oct. 5, was no different, though he tried one thing most people don’t–having his entire genome and that of his cancer decoded. This can expose the tumor’s genetic mutations and help doctors choose anticancer drugs. Yet while this approach already guides the treatment of some cancers, pancreatic cancer isn’t among them.

That doesn’t mean scientists aren’t on the case. Already they are beginning to compile a list of the mutations that commonly occur in pancreatic tumors, hoping to learn how each of these aberrations drives growth. Without that information, it’s difficult to know which molecular processes to target with which drug treatments. Add that to the expense of genomic decoding–Jobs reportedly paid $100,000 for his–and it’s clear that the approach is hardly right for everyone.

In coming years, as more data on the DNA of different tumors accumulates, that will likely change. Jobs, sadly, wasn’t able to take advantage of such a strategy. In this case, as with so many of his best ideas, he may simply have been ahead of his time.

CANCER GENES AT WORK

CURRENT THERAPY

Lung cancer is an especially deadly malignancy, and its course of care is familiar

1 Biopsy

Doctors remove a small portion of tissue from a suspicious mass in the lung

2 Diagnosis

Pathologists study the withdrawn cells, looking for telltale signs of malignant or otherwise abnormal growth

3 Treatment

If cancer is present, patients undergo surgery to remove tumors, followed by chemotherapy to kill remaining cancer cells

DNA-BASED THERAPY

Doctors have identified some genes behind lung cancer, widening treatment options

AT

TA

CG

AT

GG

AT

DNA letter sequence

4 DNA MAPPING

Sequencing the genes in a lung tumor exposes the mutations that drive the cancer and that can be attacked to stop it

5 EGFR tumors

Mutations in the gene regulating epidermal-growth-factor receptors is one lung-cancer trigger. Drugs can inhibit the receptor

[The following text appears within a chart. Please see hardcopy or PDF for actual chart.]

MUTATIONS FOUND SO FAR IN LUNG CANCER

OTHER MUTATIONS

15% EGFR

23% KRAS

42% NONE

6 Combo cancer

If tumors have mutations in both the EGFR gene and the KRAS gene (which regulates a growth protein), they do not respond to an EGFR inhibitor, so chemotherapy is a better option

7 Monitoring

Cancer patients will likely need to have tumor cells mapped periodically to keep track of new growths and resistance to chemotherapy

DECODING CANCER

Breast Cancer

A test on 21 genes predicts recurrence and the need for chemotherapy

Prostate Cancer

A similar test is being developed to treat prostate tumors

Lung Cancer

Tumors with mutations in a growth-factor gene respond to inhibitor drugs

Melanoma

A drug inhibits tumors with mutations in a gene regulating a cancer-linked protein

Multiple Myeloma

The melanoma drug can work against myeloma with the same mutation

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