Crowdly

Researchers develop a therapy that improves

tumour clearance by enhancing the activity of tumour-infiltrating lymphocytes

rather than directly targeting tumour cells.

Which microenvironmental target is

most likely involved?

B-cell regulatory

pathways that reduce antibody-mediated immunity within the tumour

microenvironment

Immune

checkpoint pathways that regulate the activation state of cytotoxic T cells

within the tumour microenvironment

Angiogenic pathways

that stimulate tumour blood vessel formation within the tumour microenvironment

Extracellular matrix

synthesis pathways that increase tumour structural integrity within the tumour

microenvironment

After treatment with antibodies

targeting PD-1, tumour-infiltrating lymphocytes show increased proliferation

and enhanced tumour-cell killing.

Which mechanism BEST explains this

therapeutic effect?

Direct induction of

DNA damage within tumour cells

Blocking

communication between tumour cells and stromal fibroblasts

Inhibition of

growth-factor signalling between tumour cells

Disruption

of an immune checkpoint interaction that normally suppresses cytotoxic T-cell

responses against tumour cells

A mutation causes a signalling protein

to activate downstream proliferation pathways continuously, even without ligand

stimulation. In this case only one allele of the gene carries the mutation.

Which explanation BEST accounts for

this effect?

A recessive loss-of-function

mutation that disables both alleles of a proto-oncogene

Gene amplification

leading to increased transcription of an inactive signalling protein

dominant gain-of-function mutation that activates a proto-oncogene and promotes

oncogenic signalling

Deletion of a tumour

suppressor gene that normally inhibits cell proliferation

During cerebellar development, granule

cell precursors proliferate extensively within the external granular layer

(EGL) before migrating inward to form the internal granular layer. A paediatric

brain tumour is found to arise from cells that remain highly proliferative

within the EGL.

Which pathological event BEST explains

the origin of this tumour?

Uncontrolled

expansion of granule cell precursor populations normally located in the

external granular layer

Increased

differentiation of supportive Bergmann glial cells that guide neuronal

migration

Overproduction of

Purkinje neurons that regulate cerebellar signalling

Accelerated migration

of granule cells into the internal granular layer

In a tumour sample, genomic analysis

reveals that a cell initially carried one mutated allele and one normal allele

of a tumour suppressor gene. Sequencing of the advanced tumour weeks later reveals

that the remaining functional allele has been deleted through a chromosomal cross-over

event, leaving the cell without any functional copies of the gene.

Which concept BEST describes this

genetic event?

somatic event that removes the remaining functional allele of a tumour

suppressor gene

A mutation that

inactivates both alleles of a tumour suppressor gene

Amplification of a

growth-promoting oncogene leading to increased signalling activity

A germline mutation

that activates a proto-oncogene

During tumour progression, epithelial

cancer cells acquire the ability to detach from neighbouring cells, invade

surrounding tissues, and migrate toward blood vessels. Molecular analysis shows

suppression of proteins that normally maintain epithelial cell adhesion.

Which molecular change most directly

explains this phenotype?

Loss

of E-cadherin that normally maintains epithelial tissue architecture

Up-regulation of

telomerase that extends telomeres and prevents cellular senescence

Increased expression

of VEGF that stimulates new blood vessel formation

Activation of

Cytochrome C involved in apoptosis signalling

In a breast cancer cell line with HER2

gene amplification, strong downstream signalling through the MAPK and PI3K

pathways occurs despite low concentrations of extracellular growth factors.

Researchers conclude that in the breast cancer cell line the HER2 receptor

contributes to signalling by facilitating receptor dimerisation independent of

ligand binding.

Which structural property of this

receptor BEST explains this behaviour?

The HER2 receptor is

expressed exclusively in tumour cells and therefore bypasses normal regulatory

mechanisms

The HER2 receptor cannot

participate in receptor dimerisation and signals through an alternative pathway

The HER2 receptor lacks the ability to bind extracellular ligand but readily forms

signalling-competent dimers with other HER family receptors

The HER2 receptor lacks

intrinsic tyrosine kinase activity and therefore depends on other receptors for

phosphorylation

A mutation is introduced into a

signalling protein that prevents RAS from binding GTP while leaving its

GDP-bound form intact. Cells expressing this mutant protein show dramatically

reduced proliferation.

Which step in the activation of B-RAF

is most directly disrupted?

The assembly of B-RAF

with SOS at the membrane to activate downstream MAPK signalling

The binding of B-RAF

to inactive RAS-GDP followed by phosphorylation by SOS

The

recruitment of B-RAF to active RAS-GTP at the membrane and the formation of RAF

dimers required for kinase activation

The activation of

B-RAF through direct phosphorylation by RAS after receptor stimulation

A dermatology study compares mutation

patterns across different skin cancers. One tumour type shows a very high

mutation burden associated with UV exposure, frequent p53 disruption, and slow

but persistent local growth rather than aggressive metastasis.

Which cancer type BEST fits this

profile?

common epithelial skin cancer that arises from basal keratinocytes and

typically expands locally rather than metastasising

A tumour arising from

neuroendocrine cells that rapidly spreads systemically

A malignancy of

pigment-producing cells that frequently metastasises early and spreads

aggressively

A vascular tumour

associated with immunosuppression and viral infection