Question

Can cancer really be cured?

Answer 1

First of all, 'cancer' is not one disease. It is a term loosely applied to any uncontrolled proliferation of any type of cell - there are hundreds of different cancers, so it is ridiculous to expect that any one cure could cure them all.

Theoretically, yes, if all the neoplastic cells are killed or die of their own. But in practice that is very, very difficult to achieve.

Answer 2

Blues is quite correct, as ever. It depends on the type but some can be cured. Sadly it's not the case for most types. Plenty of scope for research!

Answer 3

If caught early before it has the chance to metastasize several type of cancers can be surgically removed (not all cases), other more drastic methods are cytostatic drugs as a supplement to chemotherapy which is aimed to destroy malignant neoplasm which has formed in a region. Radiotherapy is a less drastic and selective measure to combat cancer, you basically inject a radioactiveisotope with bound proteins, the proteins has the "cancer" as target cell and the isotopes are delivered to the affected tissue. This isotope will kill most parakrin cells including healthy cells at deliverance, and with luck it will eradicate the cancer.
None of this methods has any garantuees so if you're asking for personal reasons you won't find a miraculous.

Answer 4

Depends on which cancer it is, how hard it is to beat, and how willing you are to fight.

Answer 5

The example I was thinking of is APL (acute promyelocytic leukemia) which has a translocation of the retinoic acid receptor (RARalpha). This subtype of AML can be treated with retinoic acid and another drug once remission is achieved. I suppose even this cancer can't be cured but the discovery of part of the mechanism by which the cells become malignant did offer a new treatment regime and a much better chance of remission.

Answer 6

Thanks!

I was thinking of acute myeloid leukemia. I work on CD117, which is a receptor tyrosine kinase activated by stem cell factor and subject to a variety of mutations which are found in an equally wide variety of cancers. The subset of mutations found in the imatinib resistant form of AML seem to induce subtle changes in the overall structural stability of the kinase which produce or enable big changes in the stability of the activation loop.

It is currently difficult to treat - the structural differences between the mutant(s) and wild type are so small that the wild type binds pretty much whatever kinase inhibitors are thrown at the mutant and are rendered useless by rapid of acquisition of secondary mutations.

There is some talk of kinase inhibitors which depend not on enthalpic binding energy but on entropic binding energy - instead of pandering to the transformed protein's structure and fitting itself so snugly that it doesn't dissociate, it preferentially binds the already slightly unstable mutant form and gets its binding energy by inducing even more disorder in the target.

With added joy that, unlike the current imatinib-esque wonder drugs, entropic inhibitors are theoretically much more resistant to structural changes due to secondary mutations. So perhaps, one day, there might be actually be a drug which approaches a genuine cure for AML...