It is both, a and b. The JAK-STAT-Pathway sits below the Erb-receptor and is therefore giving the signal from mutated Erb down the signalling cascade. Besides that a permanent active version of Jak2 has been found which also permanently activates this pathway. Both are contributing to cancer. See this two articles:

• Molecular Pathways: JAK/STAT Pathway: Mutations, Inhibitors, and Resistance
• Mining for JAK-STAT mutations in cancer.

The role of the MAP Kinase pathway in cancer is even more prominent. Mutations in different proteins of the cascade are know, like BRAF V6600E in melanoma, mutations in NRAS, KRAS, MEK and MEK2. Most of these are activating mutations which lead to a permanent activation of this signalling cascade and also a changed gene expression. See this figure from the MAP Kinase paper mentioned below:

See these papers for more details:

• MAP kinase signalling pathways in cancer
• Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

p53 is not a signalling pathway, but a single protein which plays an important role in the regulation of the cell cycle and is important in the prevention of tumors. It is also called a "tumor suppressor gene" and is often mutated or deactivated in cancer. For more details on p53 see here.

The answer is b, as the mutation constantly activates the RAS protein. RAS is part of the MAP-Kinase pathway, constant signaling of it permanently activates this pathway and leads to changes in gene expression. See the image below:

If you are interested in more details, have a look at these papers:

• RAS oncogenes: weaving a tumorigenic web
• RAS mutations and oncogenesis: not all RAS mutations are created equally

It is both, a and b. The JAK-STAT-Pathway sits below the Erb-receptor and is therefore giving the signal from mutated Erb down the signalling cascade. Besides that a permanent active version of Jak2 has been found which also permanently activates this pathway. Both are contributing to cancer. See this two articles:

• Molecular Pathways: JAK/STAT Pathway: Mutations, Inhibitors, and Resistance
• Mining for JAK-STAT mutations in cancer.

The role of the MAP Kinase pathway in cancer is even more prominent. Mutations in different proteins of the cascade are know, like BRAF V6600E in melanoma, mutations in NRAS, KRAS, MEK and MEK2. Most of these are activating mutations which lead to a permanent activation of this signalling cascade and also a changed gene expression. See this figure from the MAP Kinase paper mentioned below:

See these papers for more details:

• MAP kinase signalling pathways in cancer
• Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

It is both, a and b. The JAK-STAT-Pathway sits below the Erb-receptor and is therefore giving the signal from mutated Erb down the signalling cascade. Besides that a permanent active version of Jak2 has been found which also permanently activates this pathway. Both are contributing to cancer. See this two articles:

• Molecular Pathways: JAK/STAT Pathway: Mutations, Inhibitors, and Resistance
• Mining for JAK-STAT mutations in cancer.

The role of the MAP Kinase pathway in cancer is even more prominent. Mutations in different proteins of the cascade are know, like BRAF V6600E in melanoma, mutations in NRAS, KRAS, MEK and MEK2. Most of these are activating mutations which lead to a permanent activation of this signalling cascade and also a changed gene expression. See this figure from the MAP Kinase paper mentioned below:

See these papers for more details:

• MAP kinase signalling pathways in cancer
• Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

p53 is not a signalling pathway, but a single protein which plays an important role in the regulation of the cell cycle and is important in the prevention of tumors. It is also called a "tumor suppressor gene" and is often mutated or deactivated in cancer. For more details on p53 see here.