Cloned an­ti­bod­ies may be used to bat­tle can­cer

CityPress - - News - ZINHLE MAPUMULO zinhle.mapumulo@city­press.co.za

Im­munother­apy, a med­i­cal pro­ce­dure that uses an­ti­bod­ies cloned in lab­o­ra­to­ries to fight can­cer, is emerg­ing as a pos­si­ble so­lu­tion to treat­ing and cur­ing the dis­ease that kills more than 8 mil­lion peo­ple world­wide ev­ery year.

A num­ber of local and in­ter­na­tional stud­ies that have been re­search­ing this pro­ce­dure are show­ing pos­i­tive re­sults in terms of treat­ment and sur­vival of can­cer pa­tients. How­ever, on­col­o­gists are warn­ing that it is too early to re­joice.

Speak­ing in Cape Town on Fri­day, Dr Daniel Voro­biof, di­rec­tor of the Sand­ton On­col­ogy Cen­tre in Jo­han­nes­burg, said that, while im­munother­apy was show­ing promis­ing re­sults, it would take some time be­fore on­col­o­gists could safely say that this was the so­lu­tion to can­cer treat­ment and pos­si­ble cure.

“We are see­ing ex­cit­ing clin­i­cal ev­i­dence from a num­ber of stud­ies. But we still have a lot of work to do in this re­gard,” he em­pha­sised.

“What we know right now is that im­munother­apy boosts the body’s own im­mune re­sponse to de­stroy can­cer cells. This treat­ment also has fewer side-ef­fects than con­ven­tional chemo­ther­apy, which works by poi­son­ing the can­cer­ous cells,” he said.

Im­munother­apy is an ac­tive area of can­cer re­search. Sci­en­tists and doc­tors around the world have been study­ing ways to use im­munother­apy to treat can­cer for years.

It works by ac­ti­vat­ing and boost­ing the body’s own im­mune re­sponse sys­tem, which will then de­stroy can­cer cells. The im­mune sys­tem has the abil­ity to iden­tify and de­stroy cells in­fected with viruses or cells that are dam­aged or ab­nor­mal, such as can­cer cells.

In the case of can­cer, T-cells (part of the white blood cells) are the main fighters. For T-cells to get into ac­tion, a check­point pro­tein, known as PD-1, on their sur­face must be ac­ti­vated. This pro­tein is like a “reg­u­la­tor but­ton” and helps keep the T-cells from at­tack­ing nor­mal cells that have a PD-L1 pro­tein on their sur­face. The rea­son for a Tcell to at­tack a nor­mal cell with a PD-L1 is that some can­cer cells have large amounts of PD-L1 pro­tein.

To pre­vent nor­mal cells from be­ing at­tacked by T-cells, the check­point pro­tein (PD-1) binds to PD-L1. Can­cer cells that have PD-L1 seem to know and take ad­van­tage of this cover, thereby evad­ing at­tacks from T-cells.

With this in mind, sci­en­tists de­vel­oped new drugs called pem­brolizumab, nivolumab and ip­il­i­mumab, which block this bind­ing and boost the im­mune re­sponse against can­cer cells. Th­ese drugs have been shown to be help­ful in treat­ing sev­eral can­cer types, in­clud­ing that of the skin, lungs, kid­neys, blad­der, and head and neck.

Ip­il­i­mumab was ap­proved by the Medicines Con­trol Coun­cil for stage-four melanoma can­cer two years ago. A woman in Jo­han­nes­burg who had a stage-four melanoma was suc­cess­fully treated with ip­il­i­mumab by Voro­biof as part of the phase-three clin­i­cal trial in 2005.

Voro­biof said: “Ten years later, the pa­tient re­mains free of can­cer.”

Since then, Voro­biof said, more drugs had en­tered the in­ter­na­tional mar­ket, though, in South Africa, only one (ip­il­i­mumab) is reg­is­tered.

“The one [drug] that seems to be more ac­tive and durable is pem­brolizumab. Clin­i­cal ev­i­dence from the 2015 Keynote 006 study shows that the long-term safety pro­file for pem­brolizumab re­mains favourable, sug­gest­ing and con­firm­ing pem­brolizumab as a stan­dard of care for ad­vanced melanoma,” he said.

Asked if im­munother­apy is the fu­ture of skin can­cer treat­ment, Voro­biof said: “Im­munother­apy con­tin­ues to grow in im­por­tance in the care of pa­tients with melanoma.

“Com­bi­na­tion strate­gies, in­clud­ing im­munother­apy, are be­ing eval­u­ated. How­ever, it’s too early to say that im­munother­apy will be the ul­ti­mate can­cer treat­ment be­cause more re­search still needs to be done.”

Daniel Voro­biof

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