THE WEEK · JULY 29, 2018 29HEALTHcancer cells manually. I was shocked to imag-
ine myself in that state, to allow myself to be in
a slaughterhouse.”
Fernandes had been doing his own research
on the internet and had read about immuno-
therapy—the buzzword in cancer treatment.
“People think if you have cancer, it's the end.
It's not! So I asked the doctor about immuno-
therapy. I was told it was not possible in India,”
he says.
Not one to give up hope, Fernandes asked
around—many even told him about quacks
who did such procedures—and was directed to
the famed Tata Memorial Hospital. Here, Fer-
nandes met Dr Jyoti Bajpai, medical oncolo-
gist, who told him that the treatment was pos-
sible. “He had recurrent metastatic melanoma,
meaning that the cancer had now spread in the
body, and was in its advanced stage,” says Ba-
jpai. “Before immunotherapy came in, mela-
noma was a death sentence of sorts. Patients
would not survive for long.”
Like several oncologists around the world,
Bajpai is also excited about immunotherapy.
The principle on which it works is simple—
in an ideal world, our immune system would
fi ght cancer cells, just like it recognises other
“foreign” invader cells and kills them.
In cancer, however, something else happens in
the body. The cancer cells trick, even weaken
the immune system's army of soldiers, espe-
cially T-cells, and continue their rampage. Im-
munotherapy strengthens this army by several
means and allows it to kill the cancer cells.
The immune system recognises foreign cells
via “checkpoints”—molecules on certain im-
mune cells that are activated (or inactivated) to
start an immune response.
One of these checkpoints is a protein called
PD 1 (programmed death) on the T-cells. Ac-
cording to the American Cancer Society, PD 1
acts as a type of “off switch” that helps keep
the T-cells from attacking other cells. It does
this by attaching to PD-L1, a protein on some
normal as well as cancer cells. When PD-1
binds to PD-L1, it tells the T-cells to leave the
other cells alone.
Some cancer cells have large amounts of PD-
L1, which helps them evade an immune at-
tack. Monoclonal antibodies that target PD 1
or PD-L1, or CLTA-4 (a protein receptor), can
block this binding, and let the immune cells at-
tack the cancer cells.
For Fernandes, the answer lay in two drugs—
ipilimumab, which was the fi rst to extend
advanced melanoma patient survival, and
nivolumab (sold as Opdivo). These “check-
point inhibitors” have proven to be extremely
successful for advanced stage melanoma.
For about six months, Fernandes would fl y
down to Mumbai every three weeks, and get
himself injected with these. “His scans started
showing positive results after a few doses,”