The DOI matches its Crossref record; 176 of the 176 references it cites were found in a registry or an index; 14 of the 192 sources its claims cite were checked for support.
Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance
Open accessAbstract
Immune checkpoint inhibitors (ICIs) have made an indelible mark in the field of cancer immunotherapy. Starting with the approval of anti-cytotoxic T lymphocyte-associated protein 4 (anti-CTLA-4) for advanced-stage melanoma in 2011, ICIs—which now also include antibodies against programmed cell death 1 (PD-1) and its ligand (PD-L1)—quickly gained US Food and Drug Administration approval for the treatment of a wide array of cancer types, demonstrating unprecedented extension of patient survival. However, despite the success of ICIs, resistance to these agents restricts the number of patients able to achieve durable responses, and immune-related adverse events complicate treatment. Thus, a better understanding of the requirements for an effective and safe antitumor immune response following ICI therapy is needed. Studies of both tumoral and systemic changes in the immune system following ICI therapy have yielded insight into the basis for both efficacy and resistance. Ultimately, by building on these insights, researchers should be able to combine ICIs with other agents, or design new immunotherapies, to achieve broader and more durable efficacy as well as greater safety. Here, we review the history and clinical utility of ICIs, the mechanisms of resistance to therapy, and local and systemic immune cell changes associated with outcome.
Overview
Integrity signals
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Claims the paper makes
94 Not checked yet · 27 Own interpretation · 12 No basis given · 4 Partly supported · 1 Supported · 1 Supported so far · 1 Own result · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Examination of the lymphocytes that correlated with such beneficial outcomes has repeatedly implicated effector and memory CD8 + T cell and NK cell populations (136-141).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
- Not checked yetcites [136] source
- Partly supportedcites [137] sourceExperimental — accuracy not yet measured
The Results report that CD8+ effector-memory cells were significantly more frequent in anti-CTLA-4 responders, while the Discussion links activated NK-cell subsets to better anti-PD-1 response. The paper does not support the broader implication that terminal-effector CD8+ cells or NK cells generally correlate with benefit: terminal-effector CD8+ cells tended to be lower in responders without statistical significance, and overall NK-cell frequencies did not differ significantly. (LLM, conf=0.84)
- Partly supportedcites [138] sourceExperimental — accuracy not yet measured
The section “Clinical response is associated to the generation of memory T cells” reports a sustained increase in effector and terminal effector memory CD8+ T cells among patients with disease control after ipilimumab. The passages from our copy do not establish a corresponding link between NK cells and beneficial outcomes, so the NK-cell part is unsupported. (LLM, conf=0.87)
- Partly supportedcites [139] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports higher NK-cell frequency in responders, supporting the NK-cell portion. The Results (page unavailable) found no significant association between CD8+ effector-memory or other CD8+ subsets and clinical response, so this paper does not support that portion of the claim. (LLM, conf=0.90)
- Partly supportedcites [140] sourceExperimental — accuracy not yet measured
The Results section on tumor-infiltrating CD45RO+CD8+ T cells links CD8+ effector-memory cells to response to PD-1 blockade. But the Discussion says the authors could not document an increase in CD8+ cells with an effector phenotype, and the Results section on intratumoral leukocytes reports no significant change in NK cells on treatment. This source therefore supports the memory CD8+ portion, not the full list of populations implicated in beneficial outcomes. (LLM, conf=0.90)
- Not checked yetcites [141] source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“30-60% of patients experience irAEs of any grade”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > IMMUNE-RELATED ADVERSE EVENTS
What the sources say
- Partly supportedcites [114] sourceExperimental — accuracy not yet measured
Table 1 (page unavailable) reports any-grade irAE frequencies for individual toxicities in selected immune-checkpoint inhibitor cohorts, supporting that treated patients experience these events. It does not report that 30–60% of patients experience at least one irAE of any grade; its percentages are for specific toxicities, not overall patient incidence. (LLM, conf=0.78)
- Could not verifycites [115] sourceExperimental — accuracy not yet measured
The Abstract describes a review of 139 case reports of immune-related adverse events, not the proportion of all checkpoint-inhibitor recipients who experience them. The Literature Search section says severity grades were often unreported. Searches for the 30–60% figure and any-grade incidence found no passage establishing the claimed rate. (LLM, conf=0.76)
- Partly supportedcites [117] sourceExperimental — accuracy not yet measured
The Introduction (Anti-PD-1 and anti-PD-L1 antibodies; page unavailable) reports any-grade irAEs in 44% of one treated NSCLC cohort and irAEs in 39.3% and 57.7% of other treated cohorts. These figures support the approximate range for some groups, but the paper does not state a general 30–60% incidence across patients receiving immune checkpoint inhibitors; it also reports 20% in a treated renal-cell carcinoma cohort. (LLM, conf=0.83)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The increased abundance of ICOS + CD4 + T cells resulted in an increased ratio of these cells to Tregs (156) both in the tumor and in peripheral blood.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
- Supportedcites [156] source
The Discussion reports that anti-CTLA-4 treatment increased both CD4+ICOShi cells and their ratio to regulatory CD4+FOXP3+ T cells in peripheral blood and tumor tissues. The claim accurately paraphrases that finding in the treated bladder-cancer patients. (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
In the paper
“In a phase I clinical trial of patients with advanced-stage, ipilimumab-refractory melanoma, 26% of participants treated with pembrolizumab, an anti-PD-1 antibody, demonstrated either a complete or partial response (57).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > PD-1 and PD-L1
What the sources say
- Not checked yetcites [57] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Perhaps the most prominent predictive markers of effective ICI therapy are the compositions of immune cells within tumors and in the periphery in patients prior to and after therapy.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > INTRODUCTION
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“Atezolizumab was initially approved by the FDA for the treatment of localized and metastatic urothelial carcinoma on the basis of results of a phase II clinical trial that showed overall response rates of 10% in patients whose disease had progressed after platinumbased chemotherapy treatment (65).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > PD-1 and PD-L1
What the sources say
- Not checked yetcites [65] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In fact, peripheral immune responses are critical in achieving favorable clinical outcomes.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > INTRODUCTION
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“ICIs work not only by invigorating T cells but also by activating other cells of the innate and adaptive arms, all of which function in concert to orchestrate an effective response against tumors.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > INTRODUCTION
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Despite the fact that many patients experience dramatic tumor regression in response to ICIs, most patients and cancers do not respond to these therapies.”
- Also stated in: § RESISTANCE TO IMMUNE CHECKPOINT INHIBITORS · plain
“only a minority of patients treated with ICIs achieve a durable response.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > INTRODUCTION
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § RESISTANCE TO IMMUNE CHECKPOINT INHIBITORS · plain
None of the sources cited for this claim have been checked yet.
In the paper
“However, despite the success of ICIs, resistance to these agents restricts the number of patients able to achieve durable responses”
- Also stated in: § RESISTANCE TO IMMUNE CHECKPOINT INHIBITORS · plain
“only a minority of patients treated with ICIs achieve a durable response.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § RESISTANCE TO IMMUNE CHECKPOINT INHIBITORS · plain
- It may state two separate claims as one. 40
- Probably not a substantial claim. 5
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“CTLA-4, an inhibitory receptor expressed primarily by T cells, functions to dampen T cell activity and is upregulated upon T cell activation (1)(2)(3).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > CTLA-4
What the sources say
- Supportedcites [1] source
The Introduction identifies CTLA-4 as a T-cell co-receptor with a strong inhibitory role in T-cell activity. The section ‘Protein expression level of CTLA-4 in various cell subsets’ states that CTLA-4 levels are elevated in activated T cells compared with naïve T cells. Page numbers are not provided in our copy. (LLM, conf=0.92)
- Not checked yetcites [2] source
- Supportedcites [3] source
The opening summary (p. 459) describes CTLA-4 as a T-cell surface glycoprotein expressed at highest levels after activation and reports that its engagement inhibits T-cell proliferation and IL-2 secretion. The Results section (Fig. 1) also shows CTLA-4 becoming detectable on CD4 and CD8 T cells after stimulation. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Response rates to ICI treatment vary widely among different cancers, ranging from greater than 80% in patients with refractory Hodgkin's lymphoma to little or no response in patients with mismatch repair-proficient colorectal cancer (76, 77); many tumor indications fall within a response rate range of 20% to 40% (78).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
What the sources say
- Partly supportedcites [76] sourceExperimental — accuracy not yet measured
The Introduction notes activity of PD-1 blockade in classical Hodgkin lymphoma, supporting the qualitative point that it responds to treatment. It gives no response rate above 80%, and our copy does not address mismatch repair-proficient colorectal cancer (searched for that term). The 20–40% range is attached to a different citation in the citing sentence. (LLM, conf=0.78)
- Supportedcites [77] source
The Results (Primary End Point) report a 0% objective response rate in patients with mismatch repair–proficient colorectal cancer; the Radiographic Evaluation likewise reports no objective responses among 18 such patients. This supports the low-or-no-response portion of the sentence for which this paper is cited. The 20–40% statement is separately attributed to citation 78. (LLM, conf=0.92)
- Partly supportedcites [78] sourceExperimental — accuracy not yet measured
The citation to this paper is attached to the statement that many tumor indications have response rates of 20–40%. In “Clinical effects of PD-1/PD-L1 blockade therapy” (page unavailable), the paper reports 35–40% for common melanoma variants, but 15–25% for several other cancers. It supports variation across indications, not the stated range for all the examples it discusses. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Thus, it stands to reason that tumors with absent or low expression of PD-L1 are more likely to exhibit resistance to anti-PD-1 and anti-PD-L1 therapies, and this assertion is supported by response rates of only up to 10% in patients with PD-L1-low melanoma and patients with NSCLC treated with anti-PD-1 compared with 40-50% in patients with high PD-L1 expression (74,80).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
What the sources say
- Not checked yetcites [74] source
- Partly supportedcites [80] sourceExperimental — accuracy not yet measured
The Abstract and Relationship Between PD-L1 Expression and Efficacy section report that response to pembrolizumab in melanoma generally rose with PD-L1 expression, supporting the direction of the claim. The stated ranges are not exact: response was 8% at MEL score 0 but 12% at score 1, and 43%, 57%, and 53% at scores 3–5. This paper studied melanoma treated with anti-PD-1 pembrolizumab; it does not establish the NSCLC or anti-PD-L1 therapy portions of the sentence. (LLM, conf=0.88)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“At the end of the trial, progression-free survival was highest in patients who received the combination therapy, followed by patients treated with nivolumab alone, and was lowest in patients treated with ipilimumab alone (59).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > PD-1 and PD-L1
What the sources say
- Not checked yetcites [59] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“immune-related adverse events complicate treatment.”
- Also stated in: § PD-1 and PD-L1 · plain
“a large proportion of ICI-treated patients develop immune-related adverse events (irAEs), some of which can be life-threatening.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § PD-1 and PD-L1 · plain
None of the sources cited for this claim have been checked yet.
In the paper
“Once TCR signaling is induced, intracellularly stored CTLA-4 molecules traffic to the cell surface, where they can bind and compete for the same ligands as CD28, but with greater affinity, thereby dampening costimulation (7,8).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > CTLA-4
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Although PD-1 is expressed on the surface of most activated immune cells, such as macrophages, dendritic cells (DCs), Langerhans cells, B cells, and T cells, its expression is most highly upregulated on exhausted T cells (34,35).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > PD-1 and PD-L1
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“ICIs-which now also include antibodies against programmed cell death 1 (PD-1) and its ligand (PD-L1)-quickly gained US Food and Drug Administration approval for the treatment of a wide array of cancer types, demonstrating unprecedented extension of patient survival.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Abstract
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“ICIs work by releasing the inhibitory brakes of T cells, resulting in robust activation of the immune system and productive antitumor immune responses.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > INTRODUCTION
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Subsequent human studies have consistently shown that PD-L1 and PD-L2 expression not only increases in cancerous tissues but is also linked to poor disease prognosis in many cancer types (50)(51)(52)(53)(54)(55)(56).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > PD-1 and PD-L1
What the sources say
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Patients who never experience a therapeutic response are described as having primary resistance.”
- Also stated in: § RESISTANCE TO IMMUNE CHECKPOINT INHIBITORS · plain
“Primary resistance refers to those cases in which no initial response to checkpoint therapy was observed”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > INTRODUCTION
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Also stated in: § RESISTANCE TO IMMUNE CHECKPOINT INHIBITORS · plain
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This stratification in progression-free survival hinted at the possibility of combining ICIs to achieve maximum antitumor efficacy.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > PD-1 and PD-L1
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“Critically, analogous to what was observed in preclinical studies, the 20% of patients whose tumors were completely cleared maintained their response for the duration of the study, with a median follow-up time of approximately 30 months.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > CTLA-4
What the sources say
- Not checked yetcites [32] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Even among patients with melanoma, which has one of the highest rates of response to ICI, 60-70% of patients do not experience an objective response to anti-PD-1 therapy; of those that do, 20-30% demonstrate eventual tumor relapse and progression (74,75).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > RESISTANCE TO IMMUNE CHECKPOINT INHIBITORS
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For example, in preclinical models, the therapeutic response to anti-CTLA-4 therapy was found to be dependent on Bacteroides species, as germfree mice or antibiotic-treated mice did not respond to anti-CTLA-4, but response was rescued through gavage of Bacteroides fragilis (99).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
What the sources say
- Not checked yetcites [99] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, PD-L1-negative tumors can still occasionally respond to anti-PD-1 therapy, and high PD-L1 expression, although correlative, is by no means sufficient for generating a response following anti-PD-1 therapy, indicating that other factors are involved in determining response and nonresponse to ICIs (80)(81)(82).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The underlying cause of the high mutational burden is not important for determining whether a tumor will respond to ICIs, as melanoma and NSCLC, which acquire mutations through UV-and carcinogen-induced DNA damage, respectively, respond just as well to ICIs as do tumors that acquire mutations through genomic instability or deficient mismatch repair (74,80,87).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In another study, MHC I downregulation via transcriptional repression was associated with primary resistance to anti-CTLA-4 therapy but not to anti-PD-1 therapy, and the response to anti-PD-1 was more dependent on MHC II expression linked to an IFN-γ-regulated module of genes (97).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
What the sources say
- Not checked yetcites [97] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Some patients who receive ICIs do not respond to treatment (primary resistance), while others respond to initial therapy but eventually relapse (acquired resistance).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Figure 1
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Several studies have demonstrated that mutations in genes involved in the SWI-SNF chromatin remodeling complex may sensitize human tumors to ICIs and that treatment with an epigenetic modulator can potentiate the ICI-mediated antitumor response through increased production of chemokines responsible for recruiting CD8 + T cells (104-107).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
What the sources say
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Apart from atezolizumab, durvalumab and avelumab are also approved for use in patients with urothelial carcinoma (70)(71)(72), and avelumab is approved for use in patients with Merkel cell carcinoma (73).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > PD-1 and PD-L1
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This idea is further supported by reports of decreased overall survival and progression-free survival in ICI-treated patients who received antibiotics (101-103).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Interferon-γ (IFN-γ) is an important cytokine for initiating and maintaining a potent antitumor response not only through promoting CD8 + cytotoxic T cell activity and skewing toward a Th1 response but also through exerting antiproliferative, proapoptotic effects and inducing major histocompatibility complex class I (MHC I) upregulation in tumor cells (90,91).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Primary Resistance
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“the presence of CD8 + PD-1 hi T cells in the tumors of patients with melanoma and patients with NSCLC prior to anti-PD-1 administration was predictive of treatment response and correlated with overall survival (146, 147).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In patients with untreated melanoma, treatment with anti-CTLA-4 led to grade 3 or 4 irAEs in 27.3% of patients and treatment with anti-PD-1 led to such severe irAEs in only 16.3% of patients (59).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > IMMUNE-RELATED ADVERSE EVENTS
What the sources say
- Not checked yetcites [59] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This association may be stronger than those with other irAE manifestations due to the autoimmune reaction targeting shared antigens between healthy melanocytes and the melanoma cells, allowing the occurrence of vitiligo to serve as a surrogate measure of the developing antitumor response.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > IMMUNE-RELATED ADVERSE EVENTS
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although significant effort has been devoted to understanding the mechanisms of primary resistance, studies of acquired resistance have begun only recently.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Figure 1
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“increased lymphocyte counts in the blood are associated not only with favorable treatment outcome but also with increased overall survival in patients with melanoma treated with ICIs (132-135).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, there are exceptions, indicating that better understanding of the interplay between the developing antitumor response following ICI therapy and the use of immunosuppressive agents is needed (117, 122, 123).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > IMMUNE-RELATED ADVERSE EVENTS
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“a subset of peripheral effector-memorylike CD4 + T cells was associated with effective immunotherapy and could initiate an antitumor response upon adoptive transfer to untreated tumor-bearing mice (131).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
- Not checked yetcites [131] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Whereas CD45RA + naive CD8 + T cells negatively correlated with response with ipilimumab treatment, CD45RA -CD8 + T cells and CD8 + T effector memory cells (CD45RA -CCR7 -) were more abundant in responsive patients (137).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
- Not checked yetcites [137] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“anti-CTLA-4 resulting in more hypophysitis and more severe colitis cases and anti-PD-1 resulting in more pneumonitis, thyroiditis, and nephritis cases (114, 118).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > IMMUNE-RELATED ADVERSE EVENTS
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“These differences may be the result of the different mechanisms of T cell inhibition by CTLA-4 and PD-1, as the former is understood to function more proximally to T cell activation and the latter is thought to function at later stages in the periphery (119).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > IMMUNE-RELATED ADVERSE EVENTS
What the sources say
- Not checked yetcites [119] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The tumor rejection phase was characterized by proliferating immune cells in the draining lymph nodes but not in the tumor, suggesting that the immune response in the periphery is important for maintaining and activating immune cells participating in the antitumor response.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
- Not checked yetcites [131] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“a higher frequency of memory CD45RA -CD4 + T cells in the blood of patients with melanoma at baseline was associated with a favorable response to ipilimumab, whereas an increased presence of naive CD45RA + CD4 + T cells correlated with nonresponders (137).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
- Not checked yetcites [137] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“some studies have found that high TCR diversity in peripheral blood and tumors prior to ICI therapy is predictive of effective treatment, others have pointed to ICI therapy-associated increases in TCR clonality, that is, enrichment of T cells with the same TCRs, as a sign of effective therapy (150, 157-161).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“it is unlikely that quantifying a single cell population or parameter will accurately predict response or nonresponse to ICI treatment, and a more holistic approach encompassing multiple cell types will be necessary.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Controversial results
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“this study nonetheless points to the possibility that ICI therapy brings about similar tumoral and systemic changes in immune cells, suggesting that circulating immune cells may provide a window into changes in immune cells in the tumor.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“One study, for example, has suggested that anti-CTLA-4 induces mainly proliferation of ICOS + CD4 + effector T cells and that anti-PD-1 is associated primarily with reinvigoration CD8 + PD-1 hi T cells (175).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > Controversial results
What the sources say
- Not checked yetcites [175] source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“whereas the negative role for tissue macrophages and MDSCs in ICI treatment is well established, our understanding of the role of circulating monocytes remains blurred.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“an increased frequency of circulating monocytes at baseline, unlike macrophages and MDSCs in tumors and other tissues, predicts superior ICI responses (174).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > LOCAL AND SYSTEMIC IMMUNE RESPONSES TO IMMUNE CHECKPOINT INHIBITORS
What the sources say
- Not checked yetcites [174] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“A DC vaccine for the treatment of advanced prostate cancer and chimeric antigen receptor T cells for the treatment of several hematological malignancies are among other immunotherapies that have also received FDA approval (176, 177).”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > CONCLUDING REMARKS
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“the role of systemic immunity is not well understood in these modalities.”
§ Annual Review of Pathology: Mechanisms of Disease Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance > CONCLUDING REMARKS
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
The paper relies on this without support.
Lymphocytes, especially CD8+ T cells and NK cells, are critical for antitumor immunity.
“A paradigm in the field of tumor immunology is that lymphocytes, especially CD8 + T cells and NK cells, are critical for antitumor immunity.”
The paper relies on this without support.
For any T cell to become activated and acquire effector functions, its TCR must recognize its cognate antigen presented on an MHC molecule.
“For any T cell to become activated and acquire effector functions, its TCR must recognize its cognate antigen presented on an MHC molecule.”
The paper relies on this without support.
The antigen specificity of a T cell is determined by its TCR, and each cell expresses multiple copies of only a single TCR, making T cells highly specific.
“The antigen specificity of a T cell is determined by its TCR, and because each cell expresses multiple copies of only a single TCR, T cells are highly specific in their response.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Preclinical studies emphasizing the pivotal role of the PD-1/PD-L1 axis in suppressing effector T cell function led to FDA approval of nivolumab and pembrolizumab, monoclonal antibodies to PD-1, for various solid immunologically ‘hot’ cancers like melanoma, non-small cell lung cancer (NSCLC), and renal cell carcinoma (Bagchi et al., 2021).”
From Microphysiological systems as models for immunologically ‘cold’ tumors (2024) · cites this paper as Bagchi et al., 2021
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Ipilimumab, the first FDA-approved monoclonal antibody targeting the negative immune checkpoint protein CTLA-4, enhances T cell activation and depletes Tregs in the tumor bed (Bagchi et al., 2021).”
From Microphysiological systems as models for immunologically ‘cold’ tumors (2024) · cites this paper as Bagchi et al., 2021
Experimental — accuracy not yet measuredIn the citing paper
“Some studies reported that there might be phosphotyrosine‐independent cooperation among SHP2 and CTLA4 as alternated tyrosine CTLA4 could interact with SHP2 and inhibit TCRζ signaling pathways [299, 300].”
From Tumor microenvironment signaling and therapeutics in cancer progression (2023) · cites this paper as [299]
Citations
Cites
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Isobutyric acid enhances the anti-tumour effect of anti-PD-1 antibody
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The Evolving Landscape of Fecal Microbial Transplantation
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Metadata
- Authors
- Bagchi, S., Yuan, R., & Engleman, E. G.
- Affiliations
- Stanford Medicine (US)
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2021-01-24
- Volume
- 16
- Issue
- 1
- Pages
- 223-249
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- OpenAlex
- W3106005610
- Semantic Scholar
- 58a498a336df510986c6c2190384da22c7b34f10
- Cited by
- 2,189
- References
- 176
- Citations by year
- 2026: 259 · 2025: 425 · 2024: 548 · 2023: 514 · 2022: 377 · 2021: 64
- FWCI
- 25.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA233958, U54CA209971, R01CA222969)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- immune checkpoint inhibitors, cancer immunotherapy, CTLA-4, PD-1, PD-L1, immune resistance mechanisms, immune-related adverse events, antitumor immunity, combination immunotherapy, melanoma
- MeSH terms
- Immune Checkpoint Inhibitors, Animals, Humans, Immunotherapy, Neoplasms, Drug Resistance, Neoplasm
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