Fatoumata Diallo
Writing for the Sciences
Professor Zayas
Annotated Bibliography
March 24, 2025
Annotated Bibliography
Chippa, V., & Barazi, H. (2023, April 16). Inflammatory breast cancer. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK564324/#article-111445.s2
IBC is an aggressive and rapid spreading form of breast cancer; it accounts for 2-4% of all breast cancers and is responsible for 7% of all breast cancer related deaths. The diagnostic criteria are Edema (swelling), orange peel appearance with no underlying mass, they symptoms should not happen more than 6 months, Erythema(redness) covering, and Pathologist confirming the cancer. There are two subcategories of Inflammatory breast cancer: Primary IBC and secondary IBC. Primary IBC the cancer develops in a healthy breast while in secondary the cancer reoccurs or shows up where a previous breast cancer occurred. Obesity is a huge risk factor for IBC. Most IBC are hormone receptor negative meaning they have shorter disease-free survival; IBC also has excessive amounts of her2 proteins which lead to rapid growth of the tumor. The p53 tumor suppressor gene plays a huge role in IBC, Mutation, or the increase of the p53 tsg happens in 20-50% of all breast cancers including IBC and is linked to hereditary breast cancers syndrome it often associated with larger tumors and higher chance of death. This gets worser when p53 tsg is combined with negative estrogen receptors this only increases the risk of death. In IBC, the RhoC GTPase oncogene in of IBC cases was more amplified in 90% of the cases compared to 38% in other BC forms. While WISP3 is lost in IBC. IBC does not produce elevated levels of inflammatory cytokines like IL-12 or IL-2, Instead it releases VEGF, FGF, IL-6, and IL-8, which has the potential to promote blood vessel growth and tumor growth. IBC needs to be Both clinically and pathologically diagnosed. A core needle is used to verify the invasive carcinoma, while a skin biopsy shows a dermal lymphatic invasion. DLI cannot only confirm IBC because it can be found in other breast cancer. Only 10% of IBC cases are detected through mammograms, many people are often misdiagnosed, they are often told take anti-biotic for mastitis or abscess for non-metastatic stage 3 treatment includes; chemotherapy, surgery, and radiation therapy for metastatic stage 5 the primary treatment is systemic therapy (about 1/3 of all patients are at this stage)
This article is knowledgeable on Inflammatory breast Cancer. It talks about the Patho psychology of IBC such as the genetic mutations (P53, WISP3, RhoC GTPase) and cytokine involvement, it also talks about how the her2, and negative receptors contribute to how aggressive cancer is. The text Highlights the different symptoms (erythema, edema, and orange peel) and different treatments (chemotherapy, radiation, systemic therapy)
“It accounts for about 2% to 4% of breast cancer cases in the United States. Despite its low incidence, IBC contributes to 7% of breast cancer caused mortality” (Chippa, Barazi, 2023).
“P53 gene mutation and nuclear overexpression was associated with the larger tumor size and disseminated disease at the time of diagnosis and had 8.6 fold higher risk of death compared with patients that do not have this mutation … Patients with both ER-negative and a p53 overexpression had an 18 fold higher risk of death compared to 2.8 fold for women with p 53 nuclear overexpression alone”(Chippa ,Barazi, 2023).
“Inflammatory breast cancer is associated with very poor prognosis and a high risk of early recurrence …With the advent of tri-modality treatment, current overall 5-year survival rates range from 30% to 70%” (Chippa, Barazi, 2023).
IBC needs to be Both clinically and pathologically diagnosed. A core needle is used to verify the invasive carcinoma, while a skin biopsy shows a dermal lymphatic invasion (Chippa, Barazi, 2023).
Chainitikun, S., Saleem, S., Lim, B., Valero, V., & Ueno, N. T. (2021). Update on systemic treatment for newly diagnosed inflammatory breast cancer. Journal of Advanced Research, 29, 1–12. https://doi.org/10.1016/j.jare.2020.08.014
IBC is a rare and aggressive form of BC that is responsible for 8-10% of all BC deaths. Black women and younger women have a higher chance of getting IBC.IN addition black women had the lowest chance of survival while Asian women had the highest. IBC has low survival rates compared to other BC and is considered a high-risk disease. The characteristic of IBC is rapid appreance of an orange peel appearance, erythema, edema that affects 1/3 of the breast, and those symptoms should not happen more than 6 months. The way to Treat IBC is trimodality treatment which Involves systemic treatments, surgery, and radiation. Previously systemic treatment for IBC were developed from non-IBC treatments like a mastectomy because there were not enough IBC clinical trials. Chemotherapy is an important systemic treatment because it shrinks the tumor before surgery. Neoadjuvant Chemotherapy can lead to pCR( pathological complete response) which in return increases survival rates. Anthracycline- and taxane-based chemotherapy is the standard treatment for IBC. By adding paclitaxel to the chemotherapy, it benefits the pCR and Er-negative patients. In addition, Mixing HDCT (high dose chemotherapy) with AHSCT (Autologous Hematopoietic Stem Cell Transplantation) has been a failure due to toxicity and lack of survival. There has been limited data on targeted therapy for IBC. Trastuzumab, a standard anti-her2+ therapy is a key treatment because of HER2 overexpression, they are Higher levels of HER2 in IBC than other BC. Trastuzumab plus chemotherapy have increased overall survival rate in a 5-year span. Pertuzumab works as HER2 and HER3 dimerization blocker, thus enhances trastuzumab. The NeoSphere clinical trial tested THP (trastuzumab, pertuzumab, and chemotherapy) and showed that THP had the best pCR results. The Tryphena clinical trial tested the safety of dual anti-HER2 therapy, and results were 50% pCR and low cardiac toxicity. The overmoyer study concentrated neoadjuvant weekly paclitaxel + pertuzumab + trastuzumab, it revealed that 56% pCR and had low levels of toxicity. Lapatinib blocks Her2 and EGFR (epidermal growth factor receptor regulates growth). The main clinical trials of lapatinib are the GeparQuinto and NeoALTTO, but studies have shown that lapatinib has harsh side effects and is recommended against the use of it.
“subgroup analysis in IBC showed that the addition of trastuzumab increased the 5-year event-free survival rate (64% vs. 24%, hazard ratio = 0.34, 95% CI 0.15–0.80) and 5-year OS rate (74% vs. 44%, hazard ratio = 0.38, 95% CI 0.15–0.95) without any serious cardiac events” (Chainitikun et al., 2021).
“NeoSphere reported promising pCR rates: 45.8%, the highest, in the THP arm; 29.0% for docetaxel plus trastuzumab; 16.8% for trastuzumab and pertuzumab without docetaxel; and 24.0% for pertuzumab plus docetaxel” (Chainitikun et al., 2021).
“At the 5-year follow-up, NeoSphere [61] reported progression-free survival rates of 81% for docetaxel plus trastuzumab, 86% for THP, 73% for trastuzumab and pertuzumab without docetaxel, and 73% for pertuzumab plus docetaxel” (Chainitikun et al., 2021).
“The combination of pembrolizumab and chemotherapy showed significant improvement in pCR rate compared with placebo plus chemotherapy (64.8% vs. 51.2%, P < 0.001)” (Chainitikun et al., 2021)
“The pCR rate was significantly higher for the TCHP regimen than for T-DM1 plus pertuzumab (56% vs. 44%, respectively; p = 0.016)” (Chainitikun et al., 2021)
“ExteNET study showed benefit from adjuvant neratinib for 1 year after completion of adjuvant trastuzumab, with an invasive DFS rate of 90.2% compared with 87.7% from placebo (hazard ratio = 0.73, 95% CI 0.57–0.92, p = 0.008) [76]” (Chainitikun et al., 2021)
