Some cell biology questions (cancer & lactose intolerance)

[aychamo]

Hey guys!

I'm taking a pretty basic cell biology class this semester, our book is "The World of the Cell", 5th edition, by Becker, Kleinsmith, and Hardin.

My prof assigned a little homework assignment, it's pretty easy, but I think I'm reading to deep into it. The problem is called "Disorders at the Organelle Level." We are supposed to read the little thing and tell what organelle or structure is involved and indicate if it is overactive or underactive. The organelles we've covered so far are: nucleus, mitochondrion, the rER, sER, Golgi, secretory vessicles, lysosomes, peroxisomes, riboesomes, cytoskeleton (cytosol, cytoplasm), and the different filaments.

The first one I question is this:

A smoker develops lung cancer and is told that the cause of the problem is a population of cells in her lungs (I love how the book made it a female smoker) that are undergoing mitosis at a much greater rate than is normal for lung cells.

For the answer, I put that the cytoskeleton is over-active, because our book says that the cytoskeleton plays an important role in cell division. However, I always thought that cancer was caused by a mutation in DNA that made the cell divide uncontrolably. I guess I never thought how DNA would control cell division? Would the correct answer be that the nucleus is overactive, or the cytoskeleton?

For the second question it is:

"A young child is placed on a milk-free diet because the mucosal cells that line his small intestine do not secrete the enzyme necessary to hydrolyze lactose, the disaccharide present in milk"

I answered it like this:
Since the mucosal cells are not secreting the necessary enzyme, there are three possible problems. The first possibility is that the rough ER is not properly synthesizing secretory proteins. The second possibility is that the Golgi complex is not correctly packaging the secretory proteins. The third possibility is that the secretory vesicles are not properly completing the process of exocytosis.

I put those as the possibilities because those are three of the main cell organelles that we have learned so far, and they all seem to be linked in the process of secreting an enzyme from a cell.

However, isn't the problem with lactose intolerance genetic? I thought it was that they had a mutated gene that coded for the enzyme to hydrolyze lactose? Would the above answer be "correct", but the ultimate cause is genetic?

Also, regarding lactose, my book says that mammals lack the enzyme that can hydrolyze Beta(1-4) bonds, that's why they can't utilize cellulose as food. But, it shows that lactose is a disaccharide of B-D-galactose and B-d-glucose, linked by a Beta(1-4) bond. How can any people digest lactose if humans lack the enzyme to hydrolize that type of bond?

I appreciate your insight and help with these questions, I'm just trying to achieve a more fundamental understanding of the topics that we are covering.

For those in the US, enjoy your labor day :)

Aychamo

 

[Moonbear]

Aychamo, I think you need to email your prof and ask just what you asked us here. I can see your reasoning for each of the answers, and you could probably list reasons for every organelle being involved. However, I don't know if that's what your prof intends for you to get out of this lesson or not. You might know too much for your own good Anyway, your question is totally valid as to how much depth he/she wants you to go into with your answers, and asking him/her directly is the only way you'll know. This is more important than just this one homework assignment. This is going to be important in understanding his/her question style for when you take exams in the course too. So, for the lactose intolerance example, you need to know whether your prof wants you to read "do not secrete the enzyme" to mean literally a secretory problem involving the secretory vesicles/exocytosis, or more generally to mean there could have been a problem in any step of the path from gene to RNA to protein to secretion.

Trust me, it's refreshing for a prof to get a question from a student that shows the student is actually thinking about an assignment and understanding the material.

 

[arildno]

aychamo:
"For the answer, I put that the cytoskeleton is over-active, because our book says that the cytoskeleton plays an important role in cell division. However, I always thought that cancer was caused by a mutation in DNA that made the cell divide uncontrolably. I guess I never thought how DNA would control cell division? Would the correct answer be that the nucleus is overactive, or the cytoskeleton?"

First of all, I'm walking on VERY thin ice here (or speaking from scant knowledge), however something bugged me about this:
My impression is that one of the primary factors in cancer development is a mutation in genes "whose proteins" are crucial in the regulation system of cell division.
(I'm thinking of the p53 gene,in particular, which I believe codes for an inhibitor protein).
Hence, although the cyto-skeleton will be "trivially" over-active since the cells divide at a sickly rate, I am quite convinced that the "cause" of cancer should be assigned to an inadequate inhibition of the production of "cell division"-proteins.
(That is, an over-active nucleus if you like, since that's where the commands (RNA-strands) to produce various proteins come from)

 

[aychamo]

Hey guys

Thank you for the information and suggestions. I will definitley contract the professor and ask exactly what he is looking for.

 

[aychamo]

Hey guys!

Just for my own information,

Is it right that lactose intolerance is caused by a mutated gene that codes for the enzyme to hydrolyze lactose?

Also, regarding lactose, my book says that mammals lack the enzyme that can hydrolyze Beta(1-4) bonds, that's why they can't utilize cellulose as food. But, it shows that lactose is a disaccharide of B-D-galactose and B-D-glucose, linked by a Beta(1-4) bond. How can any people digest lactose if humans lack the enzyme to hydrolize that type of bond?

And with cancer (at least some cancers?), like Arildno mentioned above, cancer is caused by an overproduction of a protein that controls cell division? Or is it the mutation of the inhibitor protein? Or it could be either (and the inhibitor fails to keep-up?) Perhaps it's that the overproduction is there because the inhibitor is mutated?

 

[indoubt]

hello!

i think you have thought too deep about a matter. this will make you very confused. it is better that you just focuse on what should be learned and read by now and then leave the rest till you come to it. what you are talking about must be read with time and it is definitely in the end of the book .

don't be impatient, because time goes very quickly and suddenly you have come to those pages you are now asking about

best luck to you!

 

[Moonbear]

Regarding lactose intolerance, this says it far better than I could:

Am J Pharmacogenomics. 2004;4(4):239-45.
Genetic variation and lactose intolerance : detection methods and clinical implications.
Sibley E.
The maturational decline in lactase activity renders most of the world's adult human population intolerant of excessive consumption of milk and other dairy products. In conditions of primary or secondary lactase deficiency, the lactose sugars in milk pass through the gastrointestinal tract undigested or are partially digested by enzymes produced by intestinal bacterial flora to yield short chain fatty acids, hydrogen, carbon dioxide, and methane. The undigested lactose molecules and products of bacterial digestion can result in symptoms of lactose intolerance, diarrhea, gas bloat, flatulence, and abdominal pain. Diagnosis of lactose intolerance is often made on clinical grounds and response to an empiric trail of dietary lactose avoidance. Biochemical methods for assessing lactose malabsorption in the form of the lactose breath hydrogen test and direct lactase enzyme activity performed on small intestinal tissue biopsy samples may also be utilized. In some adults, however, high levels of lactase activity persist into adulthood. This hereditary persistence of lactase is common primarily in people of northern European descent and is attributed to inheritance of an autosomal-dominant mutation that prevents the maturational decline in lactase expression.Recent reports have identified genetic polymorphisms that are closely associated with lactase persistence and nonpersistence phenotypes. The identification of genetic variants associated with lactase persistence or nonpersistence allows for molecular detection of the genetic predisposition towards adult-onset hypolactasia by DNA sequencing or restriction fragment length polymorphism analysis. The role for such genetic detection in clinical practice seems limited to ruling out adult-onset hypolactasia as a cause of intolerance symptoms but remains to be fully defined. Attention should be paid to appropriate interpretation of genetic detection in order to avoid potentially harmful reduction in dairy intake or misdiagnosis of secondary lactase deficiency.

Regarding cancer, yes. It can be overproduction of something that increases cell division, underproduction or mutation of an inhibitor of cell division, and a number of other things. This is why it's so hard to find a cure for cancer...it's not just one thing. There are a lot of different ways a cancer can form. Back before I knew what I wanted to do when I grew up, I took an entire semester's course on cancer biology, and that just scratched the surface of the field.