Learner Reviews & Feedback for Introduction to the Biology of Cancer by Johns Hopkins University

🙏🙏❤

great

Great

ótimo

Good

good

Good

Good

good

good

good

Good

good

good

nice

good

good

nice

....

Gud

..

.

.

My personal interest in this subject is primarily the fact that my mum died of lung cancer two years ago after 4.5 years after diagnosis. She had received chemotherapy, radiation as well as alternative therapy. And I was very much involved in her decisions. Concerning the course, although the content was really good, I need to make some comments in order to improve the course. Except from the first doctor, all the other speakers spoke very very fast and it was difficult to follow as a non native speaker even though my English is very good. It would have been better to talk a little bit slower. Also, I would make the course a little bit longer, a few more steps in between the lessons, slower meaning more explaining. Also, I would have appreciated if the lecturers were speaking facing the screen a bit more, not just showing slides. I would have also given some case studies. The course lacked case studies. For example I would have given at the end a whole week of cases studies, ie 6 case studies of people who had cancer, what type of treatment they had, others that did not have treatment as well. I would also have a quiz on these. Furthermore, I would have given some examples of alternative therapies too as working as complementary for example to treatment of cancer. I would have also given some examples of incidence and treatment of cancer in a selected other countries. I would have made this topic for an extra week as well. I would definitely be interested in taking a more advanced course as well.

Nice introductory course. Maybe the weak part were the hallmarks in relation to the cell-cycle. Cell-cycle checkpoints can be found in S, G2 and M-phases. Upon checkpoint-dependent cell-cycle arrest, cells do not exit the cell-cycle and, thus, they do not re-enter the cell-cycle once checkpoints have been satisfied. That is, they stay within the cell-cycle. Exit would entail senescence, which is theoretically irreversible (although it can be overcome). Hence, after arrest, cells could not exit the cell-cycle (Cyclins and Cdks are kept in check, for example, by p21 upon activation of the DNA-damage response to double strand breaks [ATM/Chk2/p53/p21). Speaking of senescence, fates stemming from p53 activation can be apoptosis but also senescence. Thus, avoiding cell-death is critical, but so is avoiding senescence (p53/p21-dependent). Finally, G0 is quiescence, not senescence. Quiescence is a reversible withdrawal from the cell-cycle whilst senescence is not. PD-L1/2 upregulation exhausts cytotoxic T-cells within the tumor microenvironment by activating PD-1. Howbeit, the activation of CTLA4 also inhibit T-cell function outside of the tumor microenvironment in a previous stage. CTLA4 inhibitory antibodies are under intense research and such research preceded that of PD-1 inhibitory antibodies. I feel CTLA4 should be mentioned.