PROGRAM:
Analysis of the main features of the B2 level of the CEFR

LISTENING
- Understanding of B2 level listening tracks
- Closed answer exercises
GRAMMATICS AND SYNTAX:
- possessive and Saxon genitive
- comparative and superlative degree of adjectives
- relative pronouns
- countable and uncountable nouns
- main prepositions of time and place
- main conjunctions
- main verbs + prepositions (Phrasal Verbs)
- Present Simple / Present Continuous
- Past Simple
- Present Perfect simple and Present Perfect Continuous, Stative verbs
- Present Perfect with for and since
- Use of different forms to express the future (present simple, 'going to', 'will' and 'Present Continuous')
- modal verbs (can, could, must, will, would, should)
- have to, don't need to
- (Past Continuous)
- passive form of verbs
- indirect speech
- verbs with infinitive and gerund
- unreal past, wishes / contrast
- phrasal verbs
LEXICON:
- travel and transport
- hobbies, sport and games
- science and technology
- the media
- people and society
- food and drink
- health and fitness
- education and learning
SPECIFIC MICRO LANGUAGE:
Understanding and discussion of scientific texts (short oral presentation / summary of their content).
Topics and texts will be specifically defined during the course.

Steve Taylore-Knowles, Malcolm Mann, DESTINATION B2 Sb +Key, MacMillan, UK.


NORRIS ROY, READY FOR FIRST 3RD ED COURSEBOOK WITH KEYS, MacMillan, UK. Codice EAN: 9781786327543

Raymond Murphy, English Grammar in Use with Answers: A Self-Study Reference and Practice Book for Intermediate Students of English, Cambridge, UK.

Siti utili per la preparazione:

https://www.englishaula.com/en/mobile/exam-prep-cat-section/2/1/

https://www.englishaula.com/en/mobile/exam-prep-cat-section/2/3/

https://www.cambridgeenglish.org/it/exams-and-tests/first/preparation/

https://www.examenglish.com/B2/index.php

ARTICOLI ESAME ORALE DI INGLESE

1. Chromosomes

Introduction
When a cell divides, one of its main jobs is to make sure that each of the two new cells gets a full, perfect copy of genetic material. Mistakes during copying, or unequal division of the genetic material between cells, can lead to cells that are unhealthy or dysfunctional (and may lead to diseases such as cancer).
But what exactly is this genetic material, and how does it behave over the course of a cell division?
DNA and genomes
DNA (deoxyribonucleic acid) is the genetic material of living organisms. In humans, DNA is found in almost all the cells of the body and provides the instructions they need to grow, function, and respond to their environment.
When a cell in the body divides, it will pass on a copy of its DNA to each of its daughter cells. DNA is also passed on at the level of organisms, with the DNA in sperm and egg cells combining to form a new organism that has genetic material from both its parents.
Physically speaking, DNA is a long string of paired chemical units (nucleotides) that come in four different types, abbreviated A, T, C, and G, and it carries information organized into units called genes. Genes typically provide instructions for making proteins, which give cells and organisms their functional characteristics.





In eukaryotes such as plants and animals, the majority of DNA is found in the nucleus and is called nuclear DNA. Mitochondria, organelles that harvest energy for the cell, contain their own mitochondrial DNA, and chloroplasts, organelles that carry out photosynthesis in plant cells, also have chloroplast DNA. The amounts of DNA found in mitochondria and chloroplasts are much smaller than the amount found in the nucleus. In bacteria, most of the DNA is found in a central region of the cell called the nucleoid, which functions similarly to a nucleus but is not surrounded by a membrane.
A cell’s set of DNA is called its genome. Since all of the cells in an organism (with a few exceptions) contain the same DNA, you can also say that an organism has its own genome, and since the members of a species typically have similar genomes, you can also describe the genome of a species. In general, when people refer to the human genome, or any other eukaryotic genome, they mean the set of DNA found in the nucleus. Mitochondria and chloroplasts are considered to have their own separate genomes.
Chromatin
In a cell, DNA does not usually exist by itself, but instead associates with specialized proteins that organize it and give it structure. In eukaryotes, these proteins include the histones, a group of basic (positively charged) proteins that form “bobbins” around which negatively charged DNA can wrap. In addition to organizing DNA and making it more compact, histones play an important role in determining which genes are active. The complex of DNA plus histones and other structural proteins is called chromatin.


For most of the life of the cell, chromatin is decondensed, meaning that it exists in long, thin strings that look like squiggles under the microscope. In this state, the DNA can be accessed relatively easily by cellular machinery (such as proteins that read and copy DNA), which is important in allowing the cell to grow and function.
Decondensed may seem like an odd term for this state – why not just call it “stringy”? – but makes more sense when you learn that chromatin can also condense. Condensation takes place when the cell is about to divide. When chromatin condenses, you can see that eukaryotic DNA is not just one long string. Instead, it’s broken up into separate, linear pieces called chromosomes. Bacteria also have chromosomes, but their chromosomes are typically circular.

Chromosomes
Each species has its own characteristic number of chromosomes. Humans, for instance, have 46 chromosomes in a typical body cell (somatic cell), while dogs have 78. Like many species of animals and plants, humans are diploid (2n), meaning that most of their chromosomes come in matched sets known as homologous pairs. The 46 chromosomes of a human cell are organized into 23 pairs, and the two members of each pair are said to be homologues of one another (with the slight exception of the X and Y chromosomes; see below).
Human sperm and eggs, which have only one homologous chromosome from each pair, are said to be haploid (1n). When a sperm and egg fuse, their genetic material combines to form one complete, diploid set of chromosomes. So, for each homologous pair of chromosomes in your genome, one of the homologues comes from your mom and the other from your dad.


The sex chromosomes, X and Y, determine a person's biological sex: XX specifies female and XY specifies male. These chromosomes are not true homologues and are an exception to the rule of the same genes in the same places. Aside from small regions of similarity needed during meiosis, or sex cell production, the X and Y chromosomes are different and carry different genes. The 44 non-sex chromosomes in humans are called autosomes.

Chromosomes and cell division


As a cell prepares to divide, it must make a copy of each of its chromosomes. The two copies of a chromosome are called sister chromatids. The sister chromatids are identical to one another and are attached to each other by proteins called cohesins. The attachment between sister chromatids is tightest at the centromere, a region of DNA that is important for their separation during later stages of cell division.
As long as the sister chromatids are connected at the centromere, they are still considered to be one chromosome. However, as soon as they are pulled apart during cell division, each is considered a separate chromosome.

Why do cells put their chromosomes through this process of replication, condensation, and separation? The short answer is: to make sure that, during cell division, each new cell gets exactly one copy of each chromosome.

2. Phases of mitosis
How a cell divides to make two genetically identical cells. Prophase, metaphase, anaphase, and telophase.

Introduction
What do your intestines, the yeast in bread dough, and a developing frog all have in common? Among other things, they all have cells that carry out mitosis, dividing to produce more cells that are genetically identical to themselves.
Why do these very different organisms and tissues all need mitosis? Intestinal cells have to be replaced as they wear out; yeast cells need to reproduce to keep their population growing; and a tadpole must make new cells as it grows bigger and more complex.
What is mitosis?
Mitosis is a type of cell division in which one cell (the mother) divides to produce two new cells (the daughters) that are genetically identical to itself. In the context of the cell cycle, mitosis is the part of the division process in which the DNA of the cell's nucleus is split into two equal sets of chromosomes.
The great majority of the cell divisions that happen in your body involve mitosis. During development and growth, mitosis populates an organism’s body with cells, and throughout an organism’s life, it replaces old, worn-out cells with new ones. For single-celled eukaryotes like yeast, mitotic divisions are actually a form of reproduction, adding new individuals to the population.
In all of these cases, the “goal” of mitosis is to make sure that each daughter cell gets a perfect, full set of chromosomes. Cells with too few or too many chromosomes usually don’t function well: they may not survive, or they may even cause cancer. So, when cells undergo mitosis, they don’t just divide their DNA at random and toss it into piles for the two daughter cells. Instead, they split up their duplicated chromosomes in a carefully organized series of steps.
Phases of mitosis
Mitosis consists of four basic phases: prophase, metaphase, anaphase, and telophase. Some textbooks list five, breaking prophase into an early phase (called prophase) and a late phase (called prometaphase). These phases occur in strict sequential order, and cytokinesis - the process of dividing the cell contents to make two new cells - starts in anaphase or telophase.

You can remember the order of the phases with the famous mnemonic: [Please] Pee on the MAT. But don’t get too hung up on names – what’s most important to understand is what’s happening at each stage, and why it’s important for the division of the chromosomes.

Let’s start by looking at a cell right before it begins mitosis. This cell is in interphase (late G_22start subscript, 2, end subscript phase) and has already copied its DNA, so the chromosomes in the nucleus each consist of two connected copies, called sister chromatids. You can’t see the chromosomes very clearly at this point, because they are still in their long, stringy, decondensed form.
This animal cell has also made a copy of its centrosome, an organelle that will play a key role in orchestrating mitosis, so there are two centrosomes. (Plant cells generally don’t have centrosomes with centrioles, but have a different type of microtubule organizing center that plays a similar role.)

In early prophase, the cell starts to break down some structures and build others up, setting the stage for division of the chromosomes.
• The chromosomes start to condense (making them easier to pull apart later on).
• The mitotic spindle begins to form. The spindle is a structure made of microtubules, strong fibers that are part of the cell’s “skeleton.” Its job is to organize the chromosomes and move them around during mitosis. The spindle grows between the centrosomes as they move apart.
• The nucleolus (or nucleoli, plural), a part of the nucleus where ribosomes are made, disappears. This is a sign that the nucleus is getting ready to break down.

In late prophase (sometimes also called prometaphase), the mitotic spindle begins to capture and organize the chromosomes.
• The chromosomes finish condensing, so they are very compact.
• The nuclear envelope breaks down, releasing the chromosomes.
• The mitotic spindle grows more, and some of the microtubules start to “capture” chromosomes.

Microtubules can bind to chromosomes at the kinetochore, a patch of protein found on the centromere of each sister chromatid. (Centromeres are the regions of DNA where the sister chromatids are most tightly connected.)
Microtubules that bind a chromosome are called kinetochore microtubules. Microtubules that don’t bind to kinetochores can grab on to microtubules from the opposite pole, stabilizing the spindle. More microtubules extend from each centrosome towards the edge of the cell, forming a structure called the aster.

In metaphase, the spindle has captured all the chromosomes and lined them up at the middle of the cell, ready to divide.
• All the chromosomes align at the metaphase plate (not a physical structure, just a term for the plane where the chromosomes line up).
• At this stage, the two kinetochores of each chromosome should be attached to microtubules from opposite spindle poles.
Before proceeding to anaphase, the cell will check to make sure that all the chromosomes are at the metaphase plate with their kinetochores correctly attached to microtubules. This is called the spindle checkpoint and helps ensure that the sister chromatids will split evenly between the two daughter cells when they separate in the next step. If a chromosome is not properly aligned or attached, the cell will halt division until the problem is fixed.

In anaphase, the sister chromatids separate from each other and are pulled towards opposite ends of the cell.
• The protein “glue” that holds the sister chromatids together is broken down, allowing them to separate. Each is now its own chromosome. The chromosomes of each pair are pulled towards opposite ends of the cell.
• Microtubules not attached to chromosomes elongate and push apart, separating the poles and making the cell longer.
All of these processes are driven by motor proteins, molecular machines that can “walk” along microtubule tracks and carry a cargo. In mitosis, motor proteins carry chromosomes or other microtubules as they walk.

In telophase, the cell is nearly done dividing, and it starts to re-establish its normal structures as cytokinesis (division of the cell contents) takes place.
• The mitotic spindle is broken down into its building blocks.
• Two new nuclei form, one for each set of chromosomes. Nuclear membranes and nucleoli reappear.
• The chromosomes begin to decondense and return to their “stringy” form.

Cytokinesis, the division of the cytoplasm to form two new cells, overlaps with the final stages of mitosis. It may start in either anaphase or telophase, depending on the cell, and finishes shortly after telophase.
In animal cells, cytokinesis is contractile, pinching the cell in two like a coin purse with a drawstring. The “drawstring” is a band of filaments made of a protein called actin, and the pinch crease is known as the cleavage furrow. Plant cells can’t be divided like this because they have a cell wall and are too stiff. Instead, a structure called the cell plate forms down the middle of the cell, splitting it into two daughter cells separated by a new wall.

When cytokinesis finishes, we end up with two new cells, each with a complete set of chromosomes identical to those of the mother cell. The daughter cells can now begin their own cellular “lives,” and – depending on what they decide to be when they grow up – may undergo mitosis themselves, repeating the cycle.

3. Cancer and the cell cycle
How cancer can be linked to overactive positive cell cycle regulators (oncogenes) or inactive negative regulators (tumor suppressors).
Does cell cycle control matter? If you ask an oncologist – a doctor who treats cancer patients – she or he will likely answer with a resounding yes.
Cancer is basically a disease of uncontrolled cell division. Its development and progression are usually linked to a series of changes in the activity of cell cycle regulators. For example, inhibitors of the cell cycle keep cells from dividing when conditions aren’t right, so too little activity of these inhibitors can promote cancer. Similarly, positive regulators of cell division can lead to cancer if they are too active. In most cases, these changes in activity are due to mutations in the genes that encode cell cycle regulator proteins.
Here, we’ll look in more detail at what's wrong with cancer cells. We'll also see how abnormal forms of cell cycle regulators can contribute to cancer.
What’s wrong with cancer cells?
Cancer cells behave differently than normal cells in the body. Many of these differences are related to cell division behavior.
For example, cancer cells can multiply in culture (outside of the body in a dish) without any growth factors, or growth-stimulating protein signals, being added. This is different from normal cells, which need growth factors to grow in culture.
Cancer cells may make their own growth factors, have growth factor pathways that are stuck in the "on" position, or, in the context of the body, even trick neighboring cells into producing growth factors to sustain them^11start superscript, 1, end superscript.

Cancer cells also ignore signals that should cause them to stop dividing. For instance, when normal cells grown in a dish are crowded by neighbors on all sides, they will no longer divide. Cancer cells, in contrast, keep dividing and pile on top of each other in lumpy layers.
The environment in a dish is different from the environment in the human body, but scientists think that the loss of contact inhibition in plate-grown cancer cells reflects the loss of a mechanism that normally maintains tissue balance in the body.
Another hallmark of cancer cells is their "replicative immortality," a fancy term for the fact that they can divide many more times than a normal cell of the body. In general, human cells can go through only about 40-60 rounds of division before they lose the capacity to divide, "grow old," and eventually die.
Cancer cells can divide many more times than this, largely because they express an enzyme called telomerase, which reverses the wearing down of chromosome ends that normally happens during each cell division.
Cancer cells are also different from normal cells in other ways that aren’t directly cell cycle-related. These differences help them grow, divide, and form tumors. For instance, cancer cells gain the ability to migrate to other parts of the body, a process called metastasis, and to promote growth of new blood vessels, a process called angiogenesis (which gives tumor cells a source of oxygen and nutrients). Cancer cells also fail to undergo programmed cell death, or apoptosis, under conditions when normal cells would (e.g., due to DNA damage). In addition, emerging research shows that cancer cells may undergo metabolic changes that support increased cell growth and division.



How cancer develops
Cells have many different mechanisms to restrict cell division, repair DNA damage, and prevent the development of cancer. Because of this, it’s thought that cancer develops in a multi-step process, in which multiple mechanisms must fail before a critical mass is reached and cells become cancerous. Specifically, most cancers arise as cells acquire a series of mutations (changes in DNA) that make them divide more quickly, escape internal and external controls on division, and avoid programmed cell.
How might this process work? In a hypothetical example, a cell might first lose activity of a cell cycle inhibitor, an event that would make the cell’s descendants divide a little more rapidly. It’s unlikely that they would be cancerous, but they might form a benign tumor, a mass of cells that divide too much but don’t have the potential to invade other tissues (metastasize).
Over time, a mutation might take place in one of the descendant cells, causing increased activity of a positive cell cycle regulator. The mutation might not cause cancer by itself either, but the offspring of this cell would divide even faster, creating a larger pool of cells in which a third mutation could take place. Eventually, one cell might gain enough mutations to take on the characteristics of a cancer cell and give rise to a malignant tumor, a group of cells that divide excessively and can invade other tissues.

As a tumor progresses, its cells typically acquire more and more mutations. Advanced-stage cancers may have major changes in their genomes, including large-scale mutations such as the loss or duplication of entire chromosomes. How do these changes arise? At least in some cases, they seem to be due to inactivating mutations in the very genes that keep the genome stable (that is, genes that prevent mutations from occurring or being passed on).
These genes encode proteins that sense and repair DNA damage, intercept DNA-binding chemicals, maintain the telomere caps on the ends of chromosomes, and play other key maintenance roles^99start superscript, 9, end superscript. If one of these genes is mutated and nonfunctional, other mutations can accumulate rapidly. So, if a cell has a nonfunctional genome stability factor, its descendants may reach the critical mass of mutations needed for cancer much faster than normal cells.
Cell cycle regulators and cancer
Different types of cancer involve different types of mutations, and, each individual tumor has a unique set of genetic alterations. In general, however, mutations of two types of cell cycle regulators may promote the development of cancer: positive regulators may be overactivated (become oncogenic), while negative regulators, also called tumor suppressors, may be inactivated.
Oncogenes
Positive cell cycle regulators may be overactive in cancer. For instance, a growth factor receptor may send signals even when growth factors are not there, or a cyclin may be expressed at abnormally high levels. The overactive (cancer-promoting) forms of these genes are called oncogenes, while the normal, not-yet-mutated forms are called proto-oncogenes. This naming system reflects that a normal proto-oncogene can turn into an oncogene if it mutates in a way that increases its activity.
Mutations that turn proto-oncogenes into oncogenes can take different forms. Some change the amino acid sequence of the protein, altering its shape and trapping it in an “always on” state. Others involve amplification, in which a cell gains extra copies of a gene and thus starts making too much protein. In still other cases, an error in DNA repair may attach a proto-oncogene to part of a different gene, producing a “combo” protein with unregulated activity.

Many of the proteins that transmit growth factor signals are encoded by proto-oncogenes. Normally, these proteins drive cell cycle progression only when growth factors are available. If one of the proteins becomes overactive due to mutation, however, it may transmit signals even when no growth factor is around. In the diagram above, the growth factor receptor, the Ras protein, and the signaling enzyme Raf are all encoded by proto-oncogenes.
Overactive forms of these proteins are often found in cancer cells. For instance, oncogenic Ras mutations are found in about 90% of pancreatic cancers. Ras is a G protein, meaning that it switches back and forth between an inactive form (bound to the small molecule GDP) and an active form (bound to the similar molecule GTP). Cancer-causing mutations often change Ras’s structure so that it can no longer switch to its inactive form, or can do so only very slowly, leaving the protein stuck in the “on” state.
Tumor suppressors
Negative regulators of the cell cycle may be less active (or even nonfunctional) in cancer cells. For instance, a protein that halts cell cycle progression in response to DNA damage may no longer sense damage or trigger a response. Genes that normally block cell cycle progression are known as tumor suppressors. Tumor suppressors prevent the formation of cancerous tumors when they are working correctly, and tumors may form when they mutate so they no longer work.
One of the most important tumor suppressors is tumor protein p53, which plays a key role in the cellular response to DNA damage. p53 acts primarily at the G_1 checkpoint (controlling the G_1 to S transition), where it blocks cell cycle progression in response to damaged DNA and other unfavorable conditions.
When a cell’s DNA is damaged, a sensor protein activates p53, which halts the cell cycle at the G_11start subscript, 1, end subscript checkpoint by triggering production of a cell-cycle inhibitor. This pause buys time for DNA repair, which also depends on p53, whose second job is to activate DNA repair enzymes. If the damage is fixed, p53 will release the cell, allowing it to continue through the cell cycle. If the damage is not fixable, p53 will play its third and final role: triggering apoptosis (programmed cell death) so that damaged DNA is not passed on.

In cancer cells, p53 is often missing, nonfunctional, or less active than normal. For example, many cancerous tumors have a mutant form of p53 that can no longer bind DNA. Since p53 acts by binding to target genes and activating their transcription, the non-binding mutant protein is unable to do its job^{14}14start superscript, 14, end superscript.
When p53 is defective, a cell with damaged DNA may proceed with cell division. The daughter cells of such a division are likely to inherit mutations due to the unrepaired DNA of the mother cell. Over generations, cells with faulty p53 tend to accumulate mutations, some of which may turn proto-oncogenes to oncogenes or inactivate other tumor suppressors.
p53 is the gene most commonly mutated in human cancers, and cancer cells without p53 mutations likely inactivate p53 through other mechanisms (e.g., increased activity of the proteins that cause p53 to be recycled).